PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 33690674-5 2021 The objective of this study was to compare the propensity of ceftriaxone and temocillin to modify the abundance of ESBL-producing Escherichia coli in feces of colonized mice. Ceftriaxone 61-72 EsbL Escherichia coli 115-119 32558119-11 2021 Ceftriaxone reduced Fos expression in regions sending projections to the NA core (prefrontal cortex, basolateral amygdala, ventral tegmental area) and specifically reduced Fos in prelimbic cortex and not infralimbic cortex neurons projecting to the NA core. Ceftriaxone 0-11 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 20-23 32558119-11 2021 Ceftriaxone reduced Fos expression in regions sending projections to the NA core (prefrontal cortex, basolateral amygdala, ventral tegmental area) and specifically reduced Fos in prelimbic cortex and not infralimbic cortex neurons projecting to the NA core. Ceftriaxone 0-11 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 172-175 33559250-10 2021 Ceftriaxone, a selective activator of GLT-1, obviously increased the PWT of CFA rats. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 38-43 33688584-3 2021 Comparing to those under trial/temporarily used antivirus drugs (i.e., umifenovir, lopinavir), ceftriaxone, cefotaxime, and cefuroxime show higher binding affinities to the N-terminal domain of N protein (N-NTD), C-terminal domain of N protein (N-CTD), and receptor-binding domain of S protein (S-RBD). Ceftriaxone 95-106 nucleocapsid phosphoprotein Severe acute respiratory syndrome coronavirus 2 173-174 33688584-3 2021 Comparing to those under trial/temporarily used antivirus drugs (i.e., umifenovir, lopinavir), ceftriaxone, cefotaxime, and cefuroxime show higher binding affinities to the N-terminal domain of N protein (N-NTD), C-terminal domain of N protein (N-CTD), and receptor-binding domain of S protein (S-RBD). Ceftriaxone 95-106 nucleocapsid phosphoprotein Severe acute respiratory syndrome coronavirus 2 194-195 33688584-3 2021 Comparing to those under trial/temporarily used antivirus drugs (i.e., umifenovir, lopinavir), ceftriaxone, cefotaxime, and cefuroxime show higher binding affinities to the N-terminal domain of N protein (N-NTD), C-terminal domain of N protein (N-CTD), and receptor-binding domain of S protein (S-RBD). Ceftriaxone 95-106 nucleocapsid phosphoprotein Severe acute respiratory syndrome coronavirus 2 194-195 33688584-3 2021 Comparing to those under trial/temporarily used antivirus drugs (i.e., umifenovir, lopinavir), ceftriaxone, cefotaxime, and cefuroxime show higher binding affinities to the N-terminal domain of N protein (N-NTD), C-terminal domain of N protein (N-CTD), and receptor-binding domain of S protein (S-RBD). Ceftriaxone 95-106 surface glycoprotein Severe acute respiratory syndrome coronavirus 2 284-285 33568029-4 2021 RESULTS: Ceftriaxone achieved a peak mean plasma concentration of 131.67+-1.83 microg mL-1 at 5 min, which decreased sharply until 1 h (35.56+-0.44 microg mL-1) and was below detection limit at 24 h post drug administration in mastitic crossbred cows. Ceftriaxone 9-20 L1 cell adhesion molecule Mus musculus 86-90 33568029-5 2021 On the other hand, ceftizoxime (active metabolite of ceftriaxone) achieved a peak level of 55.42+-3.34 microg mL-1 at 72 h and could not be detected at 120 h post drug administration in the milk of thosemastitic crossbred cows. Ceftriaxone 53-64 L1 cell adhesion molecule Mus musculus 110-114 33507976-3 2021 Therefore, to assess the effect of glutamate uptake, pharmacological upregulation of GLT-1 using ceftriaxone administration (200 mg/kg/day, i.p, 5 days) was utilized in Li-PIL animal models of temporal lobe epilepsy (TLE). Ceftriaxone 97-108 solute carrier family 1 member 2 Homo sapiens 85-90 33507976-8 2021 Ceftriaxone administration in epileptic animals led to a reduction of glutamate along with elevation of the level of glutamine synthetase activity and GLT-1 expression in the acute phase. Ceftriaxone 0-11 glutamate-ammonia ligase Homo sapiens 117-137 33507976-8 2021 Ceftriaxone administration in epileptic animals led to a reduction of glutamate along with elevation of the level of glutamine synthetase activity and GLT-1 expression in the acute phase. Ceftriaxone 0-11 solute carrier family 1 member 2 Homo sapiens 151-156 33507976-10 2021 Ceftriaxone treatment increased the levels of GLT-1 expression. Ceftriaxone 0-11 solute carrier family 1 member 2 Homo sapiens 46-51 33585342-8 2021 LEARNING POINTS: Ceftriaxone-induced agranulocytosis is rare but may occur in patients with high cumulative doses.Prompt recognition, drug withdrawal and administration of recombinant human granulocyte colony-stimulating factor (rhG-CSF) are the mainstay approach. Ceftriaxone 17-28 colony stimulating factor 3 Homo sapiens 190-227 33075417-10 2020 Alternatively, treatment with ceftriaxone (CEF), a known GLT-1 upregulator, abolished the effect of chronic ethanol exposure on BDNF expression in the AcbSh. Ceftriaxone 30-41 solute carrier family 1 member 2 Rattus norvegicus 57-62 33069754-2 2021 Ceftriaxone (CEF) upregulates astrocytic GLT-1 expression/activity, which could counteract excessive glutamate levels and aggressive behavior induced by anabolic synthetic steroids such as nandrolone decanoate (ND). Ceftriaxone 0-11 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 41-46 33069754-2 2021 Ceftriaxone (CEF) upregulates astrocytic GLT-1 expression/activity, which could counteract excessive glutamate levels and aggressive behavior induced by anabolic synthetic steroids such as nandrolone decanoate (ND). Ceftriaxone 13-16 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 41-46 33322348-5 2020 To this aim, embryos expressing the human GFAP gene carrying the most severe p.R239C under the control of the zebrafish gfap gene promoter underwent functional validation to assess several features already observed in in vitro and other in vivo models of AxD, such as the localization of mutant GFAP inclusions, the ultrastructural analysis of cells expressing mutant GFAP, the effects of treatments with ceftriaxone, and the heat shock response. Ceftriaxone 405-416 glial fibrillary acidic protein Homo sapiens 42-46 33075417-10 2020 Alternatively, treatment with ceftriaxone (CEF), a known GLT-1 upregulator, abolished the effect of chronic ethanol exposure on BDNF expression in the AcbSh. Ceftriaxone 30-41 brain-derived neurotrophic factor Rattus norvegicus 128-132 33075417-10 2020 Alternatively, treatment with ceftriaxone (CEF), a known GLT-1 upregulator, abolished the effect of chronic ethanol exposure on BDNF expression in the AcbSh. Ceftriaxone 43-46 solute carrier family 1 member 2 Rattus norvegicus 57-62 33075417-10 2020 Alternatively, treatment with ceftriaxone (CEF), a known GLT-1 upregulator, abolished the effect of chronic ethanol exposure on BDNF expression in the AcbSh. Ceftriaxone 43-46 brain-derived neurotrophic factor Rattus norvegicus 128-132 32666660-1 2020 beta-Lactam antibiotics such as ceftriaxone, are potent stimulators of the expression of l-glutamate transporter GLT-1 and may exert neuroprotective effects when chronically used in rats and mice. Ceftriaxone 32-43 solute carrier family 1 member 2 Rattus norvegicus 113-118 32778543-7 2020 For elderly patients with moderate or severe renal impairment, 48-hourly dosing results in greater trough concentrations and total exposure than patients with normal renal function receiving 24-hourly dosing.Conclusions: Cystatin-C based measures of renal function improved predictions of ceftriaxone clearance in elderly patients. Ceftriaxone 289-300 cystatin C Homo sapiens 221-231 33196662-11 2020 AmpC strains (i.e., blaCMY-2) had distinctly less robust (p < 0.05) growth in ceftriaxone (4 mug/mL) compared to extended-spectrum beta-lactamase (ESBL) producers harboring blaCTX-M-*variants. Ceftriaxone 78-89 AmpC Escherichia coli 20-28 33120990-8 2020 Physicochemical features of ceftriaxone-loaded polymer nanoparticles were investigated by particle size distribution and zeta potential, Fourier-transform infrared spectroscopy (FTIR), Thermal Gravimetric Analysis (TG/TGA), Scanning Electron Microscopy (SEM) characteristics techniques. Ceftriaxone 28-39 T-box transcription factor 1 Homo sapiens 218-221 33132901-0 2020 GLT-1 Knockdown Inhibits Ceftriaxone-Mediated Improvements on Cognitive Deficits, and GLT-1 and xCT Expression and Activity in APP/PS1 AD Mice. Ceftriaxone 25-36 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 0-5 33132901-2 2020 Ceftriaxone has been reported to upregulate GLT-1 expression and improve cognitive decline in APP/PS1 mice. Ceftriaxone 0-11 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 44-49 33132901-2 2020 Ceftriaxone has been reported to upregulate GLT-1 expression and improve cognitive decline in APP/PS1 mice. Ceftriaxone 0-11 presenilin 1 Mus musculus 98-101 33132901-3 2020 The aim of the present study was to elucidate the role of GLT-1 in ceftriaxone-mediated improvement on cognitive deficits and associated changes in xCT (catalytic subunit of system x c -) expression and activity using GLT-1 knockdown APP/PS1 mice. Ceftriaxone 67-78 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 58-63 33132901-3 2020 The aim of the present study was to elucidate the role of GLT-1 in ceftriaxone-mediated improvement on cognitive deficits and associated changes in xCT (catalytic subunit of system x c -) expression and activity using GLT-1 knockdown APP/PS1 mice. Ceftriaxone 67-78 solute carrier family 7 (cationic amino acid transporter, y+ system), member 11 Mus musculus 148-151 33132901-3 2020 The aim of the present study was to elucidate the role of GLT-1 in ceftriaxone-mediated improvement on cognitive deficits and associated changes in xCT (catalytic subunit of system x c -) expression and activity using GLT-1 knockdown APP/PS1 mice. Ceftriaxone 67-78 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 218-223 33132901-3 2020 The aim of the present study was to elucidate the role of GLT-1 in ceftriaxone-mediated improvement on cognitive deficits and associated changes in xCT (catalytic subunit of system x c -) expression and activity using GLT-1 knockdown APP/PS1 mice. Ceftriaxone 67-78 presenilin 1 Mus musculus 238-241 33132901-8 2020 Ceftriaxone treatment significantly improved the above impairments in APP/PS1 mice, but had negligible impact in GLT-1+-APP/PS1 mice. Ceftriaxone 0-11 presenilin 1 Mus musculus 74-77 33132901-11 2020 Ceftriaxone treatment restored xCT expression in APP/PS1 mice, but not in GLT-1+-APP/PS1 mice. Ceftriaxone 0-11 solute carrier family 7 (cationic amino acid transporter, y+ system), member 11 Mus musculus 31-34 33132901-11 2020 Ceftriaxone treatment restored xCT expression in APP/PS1 mice, but not in GLT-1+-APP/PS1 mice. Ceftriaxone 0-11 presenilin 1 Mus musculus 53-56 33132901-13 2020 After ceftriaxone administration, the decline in glutathione level was restored in APP/PS1 mice, but not in GLT-1+-APP/PS1 mice. Ceftriaxone 6-17 presenilin 1 Mus musculus 87-90 33132901-14 2020 Conclusion: Ceftriaxone improves cognitive impairment of APP/PS1 mice by upregulating GLT-1-mediated uptake of glutamate and co-regulation of GLT-1 and xCT in APP/PS1 mice. Ceftriaxone 12-23 presenilin 1 Mus musculus 61-64 33132901-14 2020 Conclusion: Ceftriaxone improves cognitive impairment of APP/PS1 mice by upregulating GLT-1-mediated uptake of glutamate and co-regulation of GLT-1 and xCT in APP/PS1 mice. Ceftriaxone 12-23 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 86-91 33132901-14 2020 Conclusion: Ceftriaxone improves cognitive impairment of APP/PS1 mice by upregulating GLT-1-mediated uptake of glutamate and co-regulation of GLT-1 and xCT in APP/PS1 mice. Ceftriaxone 12-23 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 142-147 33132901-14 2020 Conclusion: Ceftriaxone improves cognitive impairment of APP/PS1 mice by upregulating GLT-1-mediated uptake of glutamate and co-regulation of GLT-1 and xCT in APP/PS1 mice. Ceftriaxone 12-23 solute carrier family 7 (cationic amino acid transporter, y+ system), member 11 Mus musculus 152-155 33132901-14 2020 Conclusion: Ceftriaxone improves cognitive impairment of APP/PS1 mice by upregulating GLT-1-mediated uptake of glutamate and co-regulation of GLT-1 and xCT in APP/PS1 mice. Ceftriaxone 12-23 presenilin 1 Mus musculus 163-166 32742338-0 2020 Ameliorative effects of ceftriaxone sodium combined with dexamethasone on infantile purulent meningitis and associated effects on brain-derived neurotrophic factor levels. Ceftriaxone 24-42 brain derived neurotrophic factor Homo sapiens 130-163 32566057-7 2020 Higher frequencies of MDR bacteria were found among ESBL-E. coli, with resistance to ampicillin (100%), ceftriaxone (96%), gentamicin (57%), ciprofloxacin (89%), and TMP/SMX (53%). Ceftriaxone 104-115 EsbL Escherichia coli 52-56 32485268-1 2020 Ceftriaxone is a beta-lactam antibiotic that increases the expression of the major glutamate transporter, GLT-1. Ceftriaxone 0-11 solute carrier family 1 member 2 Homo sapiens 106-111 32485268-5 2020 We find that ceftriaxone (200 mg/kg for at least two days) consistently restores GLT-1 expression in multiple rodent models of neurological disease, especially when GLT-1 is decreased in the disease model. Ceftriaxone 13-24 solute carrier family 1 member 2 Homo sapiens 81-86 32485268-5 2020 We find that ceftriaxone (200 mg/kg for at least two days) consistently restores GLT-1 expression in multiple rodent models of neurological disease, especially when GLT-1 is decreased in the disease model. Ceftriaxone 13-24 solute carrier family 1 member 2 Homo sapiens 165-170 32849376-0 2020 Genomic Surveillance of Ceftriaxone-Resistant Escherichia coli in Western New York Suggests the Extended-Spectrum beta-Lactamase bla CTX-M-27 Is Emerging on Distinct Plasmids in ST38. Ceftriaxone 24-35 EsbL Escherichia coli 96-128 32660552-10 2020 Treatment with CRO + DOX significantly diminished both the number of cerebral hemorrhages (p = 0.029) and the amount of MMP-9 in the brain (p = 0.046) compared to untreated controls, but not to CRO-treated animals (p > 0.05). Ceftriaxone 15-18 matrix metallopeptidase 9 Mus musculus 120-125 32695257-0 2020 Ceftriaxone Calcium Crystals Induce Acute Kidney Injury by NLRP3-Mediated Inflammation and Oxidative Stress Injury. Ceftriaxone 0-11 NLR family, pyrin domain containing 3 Rattus norvegicus 59-64 32695257-13 2020 Conclusions: Notably, we found that ceftriaxone-induced urolithiasis was associated with a high risk of AKI and NLRP3-mediated inflammasome and oxidative stress injury were of major importance in the pathogenesis. Ceftriaxone 36-47 NLR family, pyrin domain containing 3 Rattus norvegicus 112-117 32714875-0 2020 Long-Term Exposure to Ceftriaxone Sodium Induces Alteration of Gut Microbiota Accompanied by Abnormal Behaviors in Mice. Ceftriaxone 22-40 glucuronidase, beta Mus musculus 63-66 32382781-2 2020 While the restoration of nucleus accumbens core (NA core) GLT-1 expression is necessary for ceftriaxone to attenuate reinstatement, AAV-mediated GLT-1 overexpression is not sufficient to attenuate reinstatement and does not prevent glutamate efflux during reinstatement. Ceftriaxone 92-103 solute carrier family 1 member 2 Rattus norvegicus 58-63 32382781-3 2020 AIMS: Here, we test the hypothesis that ceftriaxone attenuates reinstatement through interactions with glutamate autoreceptors mGlu2 and mGlu3 in the NA core. Ceftriaxone 40-51 glutamate receptor, metabotropic 3 Mus musculus 137-142 32382781-7 2020 In experiment 2, we tested the hypothesis that mGlu2/3 signaling is necessary for ceftriaxone to attenuate cue- and cocaine-primed reinstatement by administering bilateral intra-NA core infusion of mGlu2/3 antagonist LY341495 or vehicle immediately prior to reinstatement testing. Ceftriaxone 82-93 glutamate receptor, metabotropic 3 Mus musculus 47-54 32382781-11 2020 The antagonism of mGlu2/3 in the NA core during both cue- and cocaine-primed reinstatement tests prevented ceftriaxone from attenuating reinstatement. Ceftriaxone 107-118 glutamate receptor, metabotropic 3 Mus musculus 18-25 32382781-12 2020 CONCLUSIONS: These results indicate that ceftriaxone"s effects depend on mGlu2/3 function and possibly mGlu2 receptor expression. Ceftriaxone 41-52 glutamate receptor, metabotropic 3 Mus musculus 73-80 32714151-0 2020 Ceftriaxone Relieves Trigeminal Neuropathic Pain Through Suppression of Spatiotemporal Synaptic Plasticity via Restoration of Glutamate Transporter 1 in the Medullary Dorsal Horn. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 126-149 32714151-4 2020 Western blot and immunofluorescent results demonstrated that 5-days administration of Cef resulted in the restoration of GLT-1 expression to a level equivalent to the sham control which was dramatically lost under the TNP condition. Ceftriaxone 86-89 solute carrier family 1 member 2 Rattus norvegicus 121-126 32714151-7 2020 Taken together, the results indicate that Cef can relieve TNP through suppression of spatiotemporal synaptic plasticity via GLT-1 restoration in the medullary dorsal horn of the trigeminal nerve. Ceftriaxone 42-45 solute carrier family 1 member 2 Rattus norvegicus 124-129 32366707-9 2020 The Vd for total drug concentrations for both drugs were significantly lower with albumin replacement.ConclusionsFor highly protein-bound drugs such as ceftriaxone and ertapenem, both hypoalbuminemia and albumin replacement may affect unbound drug exposure. Ceftriaxone 152-163 albumin Ovis aries 82-89 32366707-9 2020 The Vd for total drug concentrations for both drugs were significantly lower with albumin replacement.ConclusionsFor highly protein-bound drugs such as ceftriaxone and ertapenem, both hypoalbuminemia and albumin replacement may affect unbound drug exposure. Ceftriaxone 152-163 albumin Ovis aries 188-195 32440324-9 2020 We also found that Cef increases the activity of SOD, GPx, and CAT as well as decreasing the level of MDA in the brain of aged mice. Ceftriaxone 19-22 catalase Mus musculus 63-66 31955291-8 2020 Doxycycline in presence of ceftriaxone improved survival of septic mice by significantly reducing the plasma and lung pro-inflammatory cytokines and MPO levels. Ceftriaxone 27-38 myeloperoxidase Mus musculus 149-152 32354757-3 2020 Ceftriaxone, a beta-lactam antibiotic reported to increase GLT-1 expression, can exert neuroprotective effects in a variety of neurodegenerative diseases; however, many of these diseases do not exhibit uniform brain pathology. Ceftriaxone 0-11 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 59-64 32354757-4 2020 In contrast, as a drug that readily crosses the blood-brain barrier, ceftriaxone administration is likely to increase GLT-1 levels globally throughout the neuroaxis. Ceftriaxone 69-80 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 118-123 32354757-6 2020 While ceftriaxone was reported to increase striatal GLT-1 and ameliorate the motor symptoms in a mouse model of HD, the extrastriatal effects of ceftriaxone in HD are unknown. Ceftriaxone 6-17 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 52-57 32173352-8 2020 This reduction was positively modulated by ceftriaxone treatment, a beta-lactam antibiotic that promotes the expression of the glutamate transporter EAAT2. Ceftriaxone 43-54 solute carrier family 1 member 2b Danio rerio 149-154 31954597-4 2020 82.4% of isolates of ESBL-positive, carbapenemase-negative Enterobacteriaceae were susceptible to ceftolozane/tazobactam, compared to 1.5%, 7.8%, 20.3%, 71.1%, 94.7%, and 98.7%, respectively, for ceftriaxone, cefepime, ceftazidime, piperacillin-tazobactam, ertapenem, and meropenem. Ceftriaxone 196-207 EsbL Escherichia coli 21-25 32129853-8 2020 The pharmacokinetics of ceftriaxone was best described by a one-compartment model with non-linear saturable protein binding including the following covariates: body weight, estimated CLCR, serum albumin concentration and mode of administration. Ceftriaxone 24-35 chymotrypsin C Homo sapiens 183-187 32129853-11 2020 CONCLUSIONS: In the critically ill, the clearance of unbound ceftriaxone is closely related to CLCR. Ceftriaxone 61-72 chymotrypsin C Homo sapiens 95-99 32129853-13 2020 Intermittent dosing of 2 g/24 h ceftriaxone leads to subtherapeutic exposure in patients with a normal or increased CLCR. Ceftriaxone 32-43 chymotrypsin C Homo sapiens 116-120 32008166-5 2020 Ceftriaxone is a beta-lactam antibiotic that upregulates GLT1 expression. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 57-61 32008166-6 2020 Bilateral microinjection of ceftriaxone recovered GLT1 expression, decreased synaptic C1q production, suppressed microglial phagocytosis of glutamatergic synapses in the hippocampal CA1, and attenuated synaptic and cognitive deficits in rats microinjected with Abeta1-40. Ceftriaxone 28-39 solute carrier family 1 member 2 Rattus norvegicus 50-54 32169530-0 2021 Genetic analysis and plasmid-mediated blaCMY-2 in Salmonella and Shigella and the Ceftriaxone Susceptibility regulated by the ISEcp-1 tnpA-blaCMY-2-blc-sugE. Ceftriaxone 82-93 ISEcp1 Escherichia coli 126-133 31924036-5 2020 Four thermal degradation steps were characterized from the TGA of NBent-NTiO2-Chit with a total loss = 23.514% in the temperature range 30-600 C. The assembled nanocomposite enhanced the removal of two important classes of antibiotics including Levofloxacin (LEVO) Ceftriaxone (CFT) in the forms of Fluoroquinolone and Cephalosporin, respectively. Ceftriaxone 266-277 chitinase 1 Homo sapiens 78-82 31924036-5 2020 Four thermal degradation steps were characterized from the TGA of NBent-NTiO2-Chit with a total loss = 23.514% in the temperature range 30-600 C. The assembled nanocomposite enhanced the removal of two important classes of antibiotics including Levofloxacin (LEVO) Ceftriaxone (CFT) in the forms of Fluoroquinolone and Cephalosporin, respectively. Ceftriaxone 279-282 chitinase 1 Homo sapiens 78-82 31924036-12 2020 The kinetic studies of NBent-NTiO2-Chit with LEVO and CFT antibiotics were better fitted by the pseudo-second-order based on the acquired R2 values as 0.999 and 0.997 for LEVO and CFT, respectively. Ceftriaxone 54-57 chitinase 1 Homo sapiens 35-39 31924036-12 2020 The kinetic studies of NBent-NTiO2-Chit with LEVO and CFT antibiotics were better fitted by the pseudo-second-order based on the acquired R2 values as 0.999 and 0.997 for LEVO and CFT, respectively. Ceftriaxone 180-183 chitinase 1 Homo sapiens 35-39 31924036-13 2020 The results proved that the designed NBent-NTiO2-Chit was successively implemented for extraction of LEVO and CFT from industrial wastewater providing percentage values 83.2 and 79.0% using 10.0 and 150.0 +- 1.0 mg NBent-NTiO2-Chit, respectively. Ceftriaxone 110-113 chitinase 1 Homo sapiens 49-53 31924036-13 2020 The results proved that the designed NBent-NTiO2-Chit was successively implemented for extraction of LEVO and CFT from industrial wastewater providing percentage values 83.2 and 79.0% using 10.0 and 150.0 +- 1.0 mg NBent-NTiO2-Chit, respectively. Ceftriaxone 110-113 chitinase 1 Homo sapiens 227-231 32169530-0 2021 Genetic analysis and plasmid-mediated blaCMY-2 in Salmonella and Shigella and the Ceftriaxone Susceptibility regulated by the ISEcp-1 tnpA-blaCMY-2-blc-sugE. Ceftriaxone 82-93 outer membrane lipoprotein Blc Escherichia coli 148-151 31949454-5 2019 Results: ESBL-producing samples had higher antibiotic resistance rates than ESBL-non-producing samples: ceftriaxone (58.8% vs. 27.3%), cefotaxime (73.5% vs. 30.3%), ceftizoxime (76.5% vs. 33.3%), cefixime (79.4% vs. 40.9%), and cefpodoxime (73.5% vs. 53%), except for carbenicillin (29.4% vs. 48.5%). Ceftriaxone 104-115 EsbL Escherichia coli 9-13 31699822-6 2020 Ceftriaxone restored astrocytic GLT1 function and inhibited seizures in endothelial Cdk5-deficient mice, and these effects were also reversed after silencing Cxcl1 in endothelial cells and its receptor chemokine (C-X-C motif) receptor 2 (Cxcr2) in astrocytes, respectively, in the CA1 by AAV transfection. Ceftriaxone 0-11 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 32-36 31699822-6 2020 Ceftriaxone restored astrocytic GLT1 function and inhibited seizures in endothelial Cdk5-deficient mice, and these effects were also reversed after silencing Cxcl1 in endothelial cells and its receptor chemokine (C-X-C motif) receptor 2 (Cxcr2) in astrocytes, respectively, in the CA1 by AAV transfection. Ceftriaxone 0-11 cyclin-dependent kinase 5 Mus musculus 84-88 31699822-6 2020 Ceftriaxone restored astrocytic GLT1 function and inhibited seizures in endothelial Cdk5-deficient mice, and these effects were also reversed after silencing Cxcl1 in endothelial cells and its receptor chemokine (C-X-C motif) receptor 2 (Cxcr2) in astrocytes, respectively, in the CA1 by AAV transfection. Ceftriaxone 0-11 chemokine (C-X-C motif) ligand 1 Mus musculus 158-163 31699822-6 2020 Ceftriaxone restored astrocytic GLT1 function and inhibited seizures in endothelial Cdk5-deficient mice, and these effects were also reversed after silencing Cxcl1 in endothelial cells and its receptor chemokine (C-X-C motif) receptor 2 (Cxcr2) in astrocytes, respectively, in the CA1 by AAV transfection. Ceftriaxone 0-11 chemokine (C-X-C motif) receptor 2 Mus musculus 202-236 31699822-6 2020 Ceftriaxone restored astrocytic GLT1 function and inhibited seizures in endothelial Cdk5-deficient mice, and these effects were also reversed after silencing Cxcl1 in endothelial cells and its receptor chemokine (C-X-C motif) receptor 2 (Cxcr2) in astrocytes, respectively, in the CA1 by AAV transfection. Ceftriaxone 0-11 chemokine (C-X-C motif) receptor 2 Mus musculus 238-243 31699822-6 2020 Ceftriaxone restored astrocytic GLT1 function and inhibited seizures in endothelial Cdk5-deficient mice, and these effects were also reversed after silencing Cxcl1 in endothelial cells and its receptor chemokine (C-X-C motif) receptor 2 (Cxcr2) in astrocytes, respectively, in the CA1 by AAV transfection. Ceftriaxone 0-11 carbonic anhydrase 1 Mus musculus 281-284 30590449-0 2019 Ceftriaxone Treatment Preserves Cortical Inhibitory Interneuron Function via Transient Salvage of GLT-1 in a Rat Traumatic Brain Injury Model. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 98-103 30590449-5 2019 Ceftriaxone, a beta-lactam antibiotic, is a potent stimulator of the expression of rodent GLT-1 and would presumably decrease excitotoxic damage to GABAergic interneurons. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 90-95 30590449-8 2019 We show that neocortical GLT-1 gene and protein expression are significantly reduced 1 week after TBI, and this transient loss is mitigated by ceftriaxone. Ceftriaxone 143-154 solute carrier family 1 member 2 Rattus norvegicus 25-30 30590449-10 2019 This finding is accompanied by significantly higher parvalbumin gene and protein expression in ceftriaxone-treated injured rats. Ceftriaxone 95-106 parvalbumin Rattus norvegicus 52-63 30590449-11 2019 Our results highlight prospects for ceftriaxone as an intervention after TBI to prevent cortical inhibitory interneuron dysfunction, partly by preserving GLT-1 expression. Ceftriaxone 36-47 solute carrier family 1 member 2 Rattus norvegicus 154-159 31660887-11 2019 Among ESBL- producing strains, 85.7% were resistant for cefotaxime and ceftriaxone and 71.4% for ceftazidime. Ceftriaxone 71-82 EsbL Escherichia coli 6-10 31478210-5 2019 Ceftriaxone is known to increase the expression and/or activity of glutamate transporters in the brain and prevented both the decreases in glutamate aspartate transporter and the increases in basal extracellular glutamate when administered during EtOH drinking. Ceftriaxone 0-11 solute carrier family 1 member 3 Rattus norvegicus 139-170 31628912-3 2019 Ceftriaxone (CFT), a well-known upregulator of GLT-1, selectively induces the expression of glutamate transporter-1 (GLT-1) in different brain regions and therefore can be posed as a potential candidate for elimination of glutamate-induced excitotoxicity which is an early prominent event in AD brains. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 47-52 31628912-3 2019 Ceftriaxone (CFT), a well-known upregulator of GLT-1, selectively induces the expression of glutamate transporter-1 (GLT-1) in different brain regions and therefore can be posed as a potential candidate for elimination of glutamate-induced excitotoxicity which is an early prominent event in AD brains. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 92-115 31628912-3 2019 Ceftriaxone (CFT), a well-known upregulator of GLT-1, selectively induces the expression of glutamate transporter-1 (GLT-1) in different brain regions and therefore can be posed as a potential candidate for elimination of glutamate-induced excitotoxicity which is an early prominent event in AD brains. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 117-122 31628912-3 2019 Ceftriaxone (CFT), a well-known upregulator of GLT-1, selectively induces the expression of glutamate transporter-1 (GLT-1) in different brain regions and therefore can be posed as a potential candidate for elimination of glutamate-induced excitotoxicity which is an early prominent event in AD brains. Ceftriaxone 13-16 solute carrier family 1 member 2 Rattus norvegicus 47-52 31628912-3 2019 Ceftriaxone (CFT), a well-known upregulator of GLT-1, selectively induces the expression of glutamate transporter-1 (GLT-1) in different brain regions and therefore can be posed as a potential candidate for elimination of glutamate-induced excitotoxicity which is an early prominent event in AD brains. Ceftriaxone 13-16 solute carrier family 1 member 2 Rattus norvegicus 92-115 31628912-3 2019 Ceftriaxone (CFT), a well-known upregulator of GLT-1, selectively induces the expression of glutamate transporter-1 (GLT-1) in different brain regions and therefore can be posed as a potential candidate for elimination of glutamate-induced excitotoxicity which is an early prominent event in AD brains. Ceftriaxone 13-16 solute carrier family 1 member 2 Rattus norvegicus 117-122 31655628-7 2019 Among 17 isolates of Shigella spp, the most frequent drug resistant was observed in ampicillin (64.7%), nalidixic acid (58.8%), ceftriaxone (47%). Ceftriaxone 128-139 histocompatibility minor 13 Homo sapiens 30-33 31100299-10 2019 Moreover, repeated administrations of ceftriaxone during cocaine-free perios attenuated CPP persistence and normalized GLT-1 level in the NAc. Ceftriaxone 38-49 solute carrier family 1 member 2 Rattus norvegicus 119-124 31766528-0 2019 Ceftriaxone Treatment Affects EAAT2 Expression and Glutamatergic Neurotransmission and Exerts a Weak Anticonvulsant Effect in Young Rats. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 30-35 31766528-5 2019 Previous research showed that the antibiotic ceftriaxone (CTX) increased the expression and functional activity of excitatory amino acid transporter 2 (EAAT2) and exerted considerable anticonvulsant effects. Ceftriaxone 45-56 solute carrier family 1 member 2 Rattus norvegicus 115-150 31766528-5 2019 Previous research showed that the antibiotic ceftriaxone (CTX) increased the expression and functional activity of excitatory amino acid transporter 2 (EAAT2) and exerted considerable anticonvulsant effects. Ceftriaxone 45-56 solute carrier family 1 member 2 Rattus norvegicus 152-157 31641170-7 2019 Therefore, we investigated the role of glutamate in pregabalin-seeking behavior with ceftriaxone (CEF), a potent GLT-1 upregulator. Ceftriaxone 85-96 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 113-118 31100299-12 2019 Additionally, we are the first to report that ceftriaxone strongly upregulates the GLT-1 in the HIP in a transcriptional mechanism involving the Nf-kappaB transcription factor. Ceftriaxone 46-57 solute carrier family 1 member 2 Rattus norvegicus 83-88 30716289-3 2019 Ceftriaxone (CTX) restores xCT and GLT1 expression and effectively suppresses cocaine and ethanol reinstatement, however, the effects of CTX on amphetamine (AMP) reinstatement are not determined. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 35-39 30937933-4 2019 Finally, we demonstrate that treatment of a 20-month-old SLC1A2-related epilepsy patient with the SLC1A2-modulating agent ceftriaxone did not result in a significant change in daily spasm count. Ceftriaxone 122-133 solute carrier family 1 member 2 Homo sapiens 57-63 30937933-4 2019 Finally, we demonstrate that treatment of a 20-month-old SLC1A2-related epilepsy patient with the SLC1A2-modulating agent ceftriaxone did not result in a significant change in daily spasm count. Ceftriaxone 122-133 solute carrier family 1 member 2 Homo sapiens 98-104 31437166-11 2019 Ceftriaxone pretreatment significantly reinforced inflammation during experimental colitis 56 days after ceftriaxone withdrawal, which was confirmed by increased histopathology of colitis, Goblet cell dysfunction, colonic dilatation and wall thickening, and increased serum levels of inflammatory cytokines (TNF-alpha and IL-10). Ceftriaxone 0-11 tumor necrosis factor Rattus norvegicus 308-317 31437166-11 2019 Ceftriaxone pretreatment significantly reinforced inflammation during experimental colitis 56 days after ceftriaxone withdrawal, which was confirmed by increased histopathology of colitis, Goblet cell dysfunction, colonic dilatation and wall thickening, and increased serum levels of inflammatory cytokines (TNF-alpha and IL-10). Ceftriaxone 0-11 interleukin 10 Rattus norvegicus 322-327 31428078-11 2019 Results: All 18 ESBL-producing E. coli strains were resistant to ampicillin, cefazolin, and ceftriaxone. Ceftriaxone 92-103 EsbL Escherichia coli 16-20 30843538-4 2019 The highly selective response of this MOF probe to ceftriaxone sodium (an antibiotic) can reach up to the ppb level in water, along with a fast response time, acid and alkali resistance, and anti-interference ability. Ceftriaxone 51-69 lysine acetyltransferase 8 Homo sapiens 38-41 31178684-2 2019 Ceftriaxone (CEF) reduces excitotoxicity by increasing glutamate transporter 1 expression and glutamate reuptake. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 55-78 31178684-2 2019 Ceftriaxone (CEF) reduces excitotoxicity by increasing glutamate transporter 1 expression and glutamate reuptake. Ceftriaxone 13-16 solute carrier family 1 member 2 Rattus norvegicus 55-78 31171749-0 2019 Synergistic evaluation of AgO2 nanoparticles with ceftriaxone against CTXM and blaSHV genes positive ESBL producing clinical strains of Uro-pathogenic E. coli. Ceftriaxone 50-61 EsbL Escherichia coli 101-105 31171749-7 2019 This study also described the effect of AgO2-NPs having synergistic activity with beta lactam antibiotic i.e. ceftriaxone against ESBL generating Escherichia coli (E. coli). Ceftriaxone 110-121 EsbL Escherichia coli 130-134 31171749-9 2019 The synergistic activities of AgO2-NPs with ceftriaxone suggest that these combinations are effective against MDR-ESBL E. coli strains as evident by increase in zone sizes. Ceftriaxone 44-55 EsbL Escherichia coli 114-118 30843538-4 2019 The highly selective response of this MOF probe to ceftriaxone sodium (an antibiotic) can reach up to the ppb level in water, along with a fast response time, acid and alkali resistance, and anti-interference ability. Ceftriaxone 51-69 histatin 1 Homo sapiens 106-109 30654495-3 2019 Proof of concept for this approach was achieved with an orally-administered beta-lactamase enzyme, SYN-004 (ribaxamase), that was demonstrated to degrade ceftriaxone excreted into the GI tract and protect the gut microbiome from antibiotic-mediated dysbiosis. Ceftriaxone 154-165 synemin Homo sapiens 99-102 30805183-13 2019 Extended spectrum ss-lactamase (ESBL) -production was the most common mechanism for ceftriaxone resistance (89%, 341/382). Ceftriaxone 84-95 EsbL Escherichia coli 32-36 30714803-1 2019 Research using the cocaine self-administration and reinstatement animal model of relapse finds that the beta-lactam antibiotic, ceftriaxone, attenuates cocaine-primed reinstatement of cocaine seeking and upregulates two proteins that regulate glutamate release and reuptake (xCT and GLT-1, respectively) in the nucleus accumbens core (NAc). Ceftriaxone 128-139 solute carrier family 1 member 2 Rattus norvegicus 283-288 31019528-7 2019 Moreover, ceftriaxone can promote glutamate circulation and synaptic plasticity (all p < 0.05) by raising astroglial GLT-1 (p < 0.05) and then improve depressive behaviors of the CUMS-induced model rats (p < 0.05). Ceftriaxone 10-21 solute carrier family 1 member 2 Rattus norvegicus 117-122 30838143-0 2019 Ceftriaxone-Induced Immune Hemolytic Anemia: In Vitro Reversal with Peptide Inhibitor of Complement C1 (PIC1). Ceftriaxone 0-11 small ubiquitin like modifier 1 Homo sapiens 104-108 30838143-6 2019 We confirmed that ceftriaxone initiated a classical complement pathway-mediated hemolysis by in vitro reversal with peptide inhibitor of complement C1 (PIC1). Ceftriaxone 18-29 small ubiquitin like modifier 1 Homo sapiens 152-156 29873816-6 2018 At linear regression analysis, CSF-to-serum albumin ratio was an independent predictor of ceftriaxone CSF concentrations (P = .001; also in those with intact blood-brain barrier: P = .031) and CSF-to-plasma ratio (P = .001; also in those with blood-brain barrier impairment: P = .040). Ceftriaxone 90-101 albumin Homo sapiens 44-51 29873816-0 2018 Effect of ABCC2 and ABCG2 Gene Polymorphisms and CSF-to-Serum Albumin Ratio on Ceftriaxone Plasma and Cerebrospinal Fluid Concentrations. Ceftriaxone 79-90 albumin Homo sapiens 62-69 30259171-0 2018 SERS detection of ceftriaxone and sulfadimethoxine using copper nanoparticles temporally protected by porous calcium carbonate. Ceftriaxone 18-29 seryl-tRNA synthetase 1 Homo sapiens 0-4 29980462-1 2018 STUDY OBJECTIVE: Community-onset urinary tract infections (UTIs) caused by extended-spectrum beta-lactamase (ESBL)-producing Enterobacteriaceae, which are resistant to ceftriaxone and usually coresistant to fluoroquinolones, are increasing worldwide. Ceftriaxone 168-179 EsbL Escherichia coli 109-113 29980462-3 2018 METHODS: At an urban public hospital in Northern California, microbiology staff prospectively reviewed ED urine culture results weekly for 1 year and presumptively identified ESBL-producing isolates by ceftriaxone plus ceftazidime resistance. Ceftriaxone 202-213 EsbL Escherichia coli 175-179 30258039-8 2018 Lower MICs for ceftriaxone, cefepime, aztreonam, meropenem, and imipenem for the mutated KPC-2-producing isolates were observed compared to those of the isolates producing a wild-type KPC-2. Ceftriaxone 15-26 KPC-2 Escherichia coli 89-94 30172223-5 2018 Kainic acid-induced immobility was improved in wild-type mice following treatment with ceftriaxone, which upregulates glutamate transporter GLT-1. Ceftriaxone 87-98 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 140-145 30259171-4 2018 The composite was used for SERS detection of rhodamine 6G and two antibacterial drugs (ceftriaxone and sulfadimethoxine). Ceftriaxone 87-98 seryl-tRNA synthetase 1 Homo sapiens 27-31 29913736-0 2018 Effects of the excitatory amino acid transporter subtype 2 (EAAT-2) inducer ceftriaxone on different pain modalities in rat. Ceftriaxone 76-87 solute carrier family 1 member 2 Rattus norvegicus 60-66 29722912-8 2018 In addition, ceftriaxone upregulated GLT1 expression in the spinal cord, but not the PAG, of control mice and attenuated tactile hypersensitivity in nerve-injured control mice but not in nerve-injured spinal cord-specific GLT1 knockout mice. Ceftriaxone 13-24 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 37-41 29722912-9 2018 Based on these results, the anti-neuropathic pain effect of ceftriaxone is mediated by the upregulation of GLT1 expression in the spinal cord. Ceftriaxone 60-71 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 107-111 30154934-2 2018 Ceftriaxone (CEF), a beta-lactam antibiotic, has been suggested as a therapeutic agent in several neurodegenerative disorders for its abilities to counteract glutamate-mediated toxicity and to block alpha-synuclein polymerization. Ceftriaxone 0-11 synuclein alpha Rattus norvegicus 199-214 30154934-2 2018 Ceftriaxone (CEF), a beta-lactam antibiotic, has been suggested as a therapeutic agent in several neurodegenerative disorders for its abilities to counteract glutamate-mediated toxicity and to block alpha-synuclein polymerization. Ceftriaxone 13-16 synuclein alpha Rattus norvegicus 199-214 30154934-4 2018 The data showed that CEF corrected neuronal density and activity in the hippocampal CA1 area, suppressed hyperactivity in the subthalamic nucleus, and reduced alpha-synuclein accumulation, indicating that CEF is a potential agent in the treatment of DLB. Ceftriaxone 21-24 synuclein alpha Rattus norvegicus 159-174 30154934-4 2018 The data showed that CEF corrected neuronal density and activity in the hippocampal CA1 area, suppressed hyperactivity in the subthalamic nucleus, and reduced alpha-synuclein accumulation, indicating that CEF is a potential agent in the treatment of DLB. Ceftriaxone 205-208 synuclein alpha Rattus norvegicus 159-174 29604365-15 2018 Importantly, CEF treatment attenuated the reinstatement effect of HYD and normalized xCT expression in the affected brain regions. Ceftriaxone 13-16 solute carrier family 7 member 11 Homo sapiens 85-88 29604365-16 2018 These findings demonstrate that the attenuating effect of HYD reinstatement with CEF might be mediated through xCT. Ceftriaxone 81-84 solute carrier family 7 member 11 Homo sapiens 111-114 29701809-6 2018 After combining ceftriaxone with receptor blockade, using anti-pIgR and PECAM-1 antibodies, we found 100% survival after 5 and 10 days of infection, in contrast to 60% for ceftriaxone alone. Ceftriaxone 16-27 polymeric immunoglobulin receptor Mus musculus 63-67 29701809-6 2018 After combining ceftriaxone with receptor blockade, using anti-pIgR and PECAM-1 antibodies, we found 100% survival after 5 and 10 days of infection, in contrast to 60% for ceftriaxone alone. Ceftriaxone 16-27 platelet/endothelial cell adhesion molecule 1 Mus musculus 72-79 30068589-4 2018 E. coli cells carrying the beta-lactamase triple mutant G238S:E240:R241G show increased resistance to cefotaxime and ceftriaxone, two cephalosporins, compared with wild-type cells. Ceftriaxone 117-128 beta-lactamase Escherichia coli 27-41 30113467-6 2018 Resistance rates of ESBL-positive E coli ranged from 50.0% (ceftriaxone) to 88.1% (cefepime), and ESBL-negative E coli rates ranged from 3.4% (cefepime) to 64.4% (amikacin). Ceftriaxone 60-71 EsbL Escherichia coli 20-24 29913736-4 2018 Ceftriaxone, a beta-lactam, induces EAAT-2 and has proven effect for the treatment of neuropathic pain. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 36-42 29913738-0 2018 Effects of the excitatory amino acid transporter subtype 2 (EAAT-2) transporter inducer ceftriaxone (an antibiotic) on different pain modalities in rat. Ceftriaxone 88-99 solute carrier family 1 member 2 Rattus norvegicus 60-66 29524538-3 2018 We recently found that ceftriaxone, a beta-lactam antibiotic able to overcome the blood-brain barrier, successfully eliminated the cellular toxic effects of misfolded proteins as Glial Fibrillary Acidic Protein (GFAP) and alpha-synuclein. Ceftriaxone 23-34 glial fibrillary acidic protein Homo sapiens 179-210 29868674-3 2018 The substrate for the SWIP-10 protein remains unknown and to date no functional roles have been ascribed to MBLAC1, though we have shown that the protein binds the neuroprotective beta-lactam antibiotic, ceftriaxone. Ceftriaxone 204-215 Lactamase_B domain-containing protein Caenorhabditis elegans 22-29 29868674-3 2018 The substrate for the SWIP-10 protein remains unknown and to date no functional roles have been ascribed to MBLAC1, though we have shown that the protein binds the neuroprotective beta-lactam antibiotic, ceftriaxone. Ceftriaxone 204-215 metallo-beta-lactamase domain containing 1 Mus musculus 108-114 29524538-3 2018 We recently found that ceftriaxone, a beta-lactam antibiotic able to overcome the blood-brain barrier, successfully eliminated the cellular toxic effects of misfolded proteins as Glial Fibrillary Acidic Protein (GFAP) and alpha-synuclein. Ceftriaxone 23-34 glial fibrillary acidic protein Homo sapiens 212-216 29524538-3 2018 We recently found that ceftriaxone, a beta-lactam antibiotic able to overcome the blood-brain barrier, successfully eliminated the cellular toxic effects of misfolded proteins as Glial Fibrillary Acidic Protein (GFAP) and alpha-synuclein. Ceftriaxone 23-34 synuclein alpha Homo sapiens 222-237 29524538-4 2018 To further understand the anti-amyloidogenic properties of ceftriaxone, we studied its activity towards lysozyme aggregation with the aim to investigate a possible chaperone-like activity of this molecule. Ceftriaxone 59-70 lysozyme Homo sapiens 104-112 29524538-5 2018 METHODS: Here we present the results obtained from fluorescence and synchrotron radiation circular dichroism spectroscopies and from molecular docking and molecular dynamics about the lysozyme-ceftriaxone interaction at neutral and acidic pH values. Ceftriaxone 193-204 lysozyme Homo sapiens 184-192 29524538-6 2018 RESULTS: We found that ceftriaxone exhibits comparable affinity constants to lysozyme in both experimental pH conditions and that its addition enhanced lysozyme stability reducing its aggregation propensity in acidic conditions. Ceftriaxone 23-34 lysozyme Homo sapiens 77-85 29524538-6 2018 RESULTS: We found that ceftriaxone exhibits comparable affinity constants to lysozyme in both experimental pH conditions and that its addition enhanced lysozyme stability reducing its aggregation propensity in acidic conditions. Ceftriaxone 23-34 lysozyme Homo sapiens 152-160 29524538-9 2018 General significance These results, in addition to our previous studies on alpha-synuclein and GFAP, confirm the property of ceftriaxone to inhibit the pathological protein aggregation of lysozyme also by a chaperone-like mechanism, extending the potential therapeutic application of this molecule to some forms of human hereditary systemic amyloidosis. Ceftriaxone 125-136 synuclein alpha Homo sapiens 75-90 29524538-9 2018 General significance These results, in addition to our previous studies on alpha-synuclein and GFAP, confirm the property of ceftriaxone to inhibit the pathological protein aggregation of lysozyme also by a chaperone-like mechanism, extending the potential therapeutic application of this molecule to some forms of human hereditary systemic amyloidosis. Ceftriaxone 125-136 glial fibrillary acidic protein Homo sapiens 95-99 29524538-9 2018 General significance These results, in addition to our previous studies on alpha-synuclein and GFAP, confirm the property of ceftriaxone to inhibit the pathological protein aggregation of lysozyme also by a chaperone-like mechanism, extending the potential therapeutic application of this molecule to some forms of human hereditary systemic amyloidosis. Ceftriaxone 125-136 lysozyme Homo sapiens 188-196 29507072-4 2018 IL-8 levels were negatively correlated with the number of ceftriaxone doses administered (r = -0.315; P = 0.031). Ceftriaxone 58-69 C-X-C motif chemokine ligand 8 Homo sapiens 0-4 29567092-3 2018 Ceftriaxone restores cocaine-induced deficits in both system xc- and GLT-1 expression and function in the nucleus accumbens core (NAc). Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 69-74 29567092-4 2018 We recently demonstrated that restoration of GLT-1 expression in the NAc is necessary for ceftriaxone to attenuate reinstatement of cocaine-seeking. Ceftriaxone 90-101 solute carrier family 1 member 2 Rattus norvegicus 45-50 29626176-10 2018 The mean score on mRS was 2.38 (95% confidence interval [CI] 2.31-2.44) vs 2.44 (95% CI 2.37-2.51) in the ceftriaxone vs control group, the decrease by 0.06 (95% CI -0.04 to 0.16) in favor of ceftriaxone treatment being nonsignificant. Ceftriaxone 106-117 sterile alpha motif domain containing 11 Mus musculus 18-21 29626176-14 2018 CONCLUSIONS: Preventive ceftriaxone has a probability of 0.7 of being less costly than standard treatment per unit decrease in mRS and per QALY gained. Ceftriaxone 24-35 sterile alpha motif domain containing 11 Mus musculus 127-130 29745864-12 2018 Furthermore, CEF augmented Mme, Ide, and Epo mRNA levels in the amygdala as well as the levels of Ece1 and Aktb in the striatum. Ceftriaxone 13-16 membrane metallo-endopeptidase Rattus norvegicus 27-30 29745864-12 2018 Furthermore, CEF augmented Mme, Ide, and Epo mRNA levels in the amygdala as well as the levels of Ece1 and Aktb in the striatum. Ceftriaxone 13-16 insulin degrading enzyme Rattus norvegicus 32-35 29745864-12 2018 Furthermore, CEF augmented Mme, Ide, and Epo mRNA levels in the amygdala as well as the levels of Ece1 and Aktb in the striatum. Ceftriaxone 13-16 erythropoietin Rattus norvegicus 41-44 29197981-2 2018 In male rats, ceftriaxone attenuates the reinstatement of cocaine-seeking while increasing glutamate transporter-1 (GLT-1) and xCT expression in the nucleus accumbens core (NAc). Ceftriaxone 14-25 solute carrier family 1 member 2 Rattus norvegicus 91-114 29658459-7 2018 RESULTS: After 21 days of ceftriaxone intervention, the experimental group had a significant reduction in body weight, a significant reduction in the expression of Ki67 and ZO-1 and a significant increase in the expression of Muc2 in intestinal epithelial cells, a significant reduction in the overall concentration of fecal bacteria, and a significant increase in the diversity of fecal bacteria compared with the control group (P&lt;0.05). Ceftriaxone 26-37 antigen identified by monoclonal antibody Ki 67 Mus musculus 164-168 29658459-7 2018 RESULTS: After 21 days of ceftriaxone intervention, the experimental group had a significant reduction in body weight, a significant reduction in the expression of Ki67 and ZO-1 and a significant increase in the expression of Muc2 in intestinal epithelial cells, a significant reduction in the overall concentration of fecal bacteria, and a significant increase in the diversity of fecal bacteria compared with the control group (P&lt;0.05). Ceftriaxone 26-37 tight junction protein 1 Mus musculus 173-177 29658459-7 2018 RESULTS: After 21 days of ceftriaxone intervention, the experimental group had a significant reduction in body weight, a significant reduction in the expression of Ki67 and ZO-1 and a significant increase in the expression of Muc2 in intestinal epithelial cells, a significant reduction in the overall concentration of fecal bacteria, and a significant increase in the diversity of fecal bacteria compared with the control group (P&lt;0.05). Ceftriaxone 26-37 mucin 2 Mus musculus 226-230 29197981-2 2018 In male rats, ceftriaxone attenuates the reinstatement of cocaine-seeking while increasing glutamate transporter-1 (GLT-1) and xCT expression in the nucleus accumbens core (NAc). Ceftriaxone 14-25 solute carrier family 1 member 2 Rattus norvegicus 116-121 28984398-8 2018 However, both clavulanic acid and ceftriaxone up-regulated GLT1 expression in rat cortical and human spinal astrocyte cultures. Ceftriaxone 34-45 solute carrier family 1 member 2 Rattus norvegicus 59-63 29128307-7 2018 This reduction was restored by systemic administration of ceftriaxone, a beta-lactam antibiotic known to increase GLT-1 expression. Ceftriaxone 58-69 solute carrier family 1 member 2 Rattus norvegicus 114-119 29128307-9 2018 Finally, systemic administration of ceftriaxone alleviated depression- and anxiety-like behaviors, which was fully blocked by intra-LHb administrations of DHK, suggesting that GLT-1"s function in the LHb is critical. Ceftriaxone 36-47 solute carrier family 1 member 2 Rattus norvegicus 176-181 29949502-1 2018 PURPOSE: Ceftriaxone elimination occurs through breast cancer resistance transporter (BCRP) and multidrug resistance-associated protein 2 (MRP-2) which are expressed on the canalicular membrane of hepatocytes. Ceftriaxone 9-20 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 48-84 30452416-0 2018 Ceftriaxone Improves Cognitive Function and Upregulates GLT-1-Related Glutamate-Glutamine Cycle in APP/PS1 Mice. Ceftriaxone 0-11 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 56-61 30452416-0 2018 Ceftriaxone Improves Cognitive Function and Upregulates GLT-1-Related Glutamate-Glutamine Cycle in APP/PS1 Mice. Ceftriaxone 0-11 presenilin 1 Mus musculus 103-106 30452416-5 2018 Ceftriaxone (Cef) has been reported to upregulate the expression and uptake of GLT-1. Ceftriaxone 0-11 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 79-84 30452416-5 2018 Ceftriaxone (Cef) has been reported to upregulate the expression and uptake of GLT-1. Ceftriaxone 0-3 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 79-84 30452416-6 2018 Therefore, the present study was undertaken to explore whether Cef can improve cognitive deficits of APP/PS1 mice in early stage of AD by upregulating GLT-1 expression, and then promoting the glutamate-glutamine cycle. Ceftriaxone 63-66 presenilin 1 Mus musculus 105-108 30452416-6 2018 Therefore, the present study was undertaken to explore whether Cef can improve cognitive deficits of APP/PS1 mice in early stage of AD by upregulating GLT-1 expression, and then promoting the glutamate-glutamine cycle. Ceftriaxone 63-66 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 151-156 30452416-7 2018 It was shown that Cef treatment significantly alleviated the cognitive deficits measured by Morris water maze test and upregulated GLT-1 protein expression in the hippocampus of APP/PS1 mice. Ceftriaxone 18-21 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 131-136 30452416-7 2018 It was shown that Cef treatment significantly alleviated the cognitive deficits measured by Morris water maze test and upregulated GLT-1 protein expression in the hippocampus of APP/PS1 mice. Ceftriaxone 18-21 presenilin 1 Mus musculus 182-185 30452416-8 2018 Particularly, the activity of glutamine synthetase (GS) and the protein expression of system N glutamine transporter 1 (SN1), which are the key factors involved in the glutamate-glutamine cycle, were significantly upregulated as well after the Cef treatment. Ceftriaxone 244-247 glutamate-ammonia ligase (glutamine synthetase) Mus musculus 30-50 30452416-8 2018 Particularly, the activity of glutamine synthetase (GS) and the protein expression of system N glutamine transporter 1 (SN1), which are the key factors involved in the glutamate-glutamine cycle, were significantly upregulated as well after the Cef treatment. Ceftriaxone 244-247 glutamate-ammonia ligase (glutamine synthetase) Mus musculus 52-54 30452416-8 2018 Particularly, the activity of glutamine synthetase (GS) and the protein expression of system N glutamine transporter 1 (SN1), which are the key factors involved in the glutamate-glutamine cycle, were significantly upregulated as well after the Cef treatment. Ceftriaxone 244-247 solute carrier family 38, member 3 Mus musculus 86-118 30452416-8 2018 Particularly, the activity of glutamine synthetase (GS) and the protein expression of system N glutamine transporter 1 (SN1), which are the key factors involved in the glutamate-glutamine cycle, were significantly upregulated as well after the Cef treatment. Ceftriaxone 244-247 solute carrier family 38, member 3 Mus musculus 120-123 30452416-9 2018 Furthermore, inhibition of GLT-1 uptake activity by dihydrokainic acid, an inhibitor of GLT-1, blocked the Cef-induced improvement on the cognitive deficits, GS activity, and SN1 expression. Ceftriaxone 107-110 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 27-32 30452416-9 2018 Furthermore, inhibition of GLT-1 uptake activity by dihydrokainic acid, an inhibitor of GLT-1, blocked the Cef-induced improvement on the cognitive deficits, GS activity, and SN1 expression. Ceftriaxone 107-110 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 88-93 30452416-9 2018 Furthermore, inhibition of GLT-1 uptake activity by dihydrokainic acid, an inhibitor of GLT-1, blocked the Cef-induced improvement on the cognitive deficits, GS activity, and SN1 expression. Ceftriaxone 107-110 solute carrier family 38, member 3 Mus musculus 175-178 30452416-10 2018 The above results suggested that Cef could improve cognitive deficits of APP/PS1 mice in early stage of AD by upregulating the GLT-1 expression, GS activity, and SN1 expression, which would lead to stimulating the glutamate-glutamine cycle. Ceftriaxone 33-36 presenilin 1 Mus musculus 77-80 30452416-10 2018 The above results suggested that Cef could improve cognitive deficits of APP/PS1 mice in early stage of AD by upregulating the GLT-1 expression, GS activity, and SN1 expression, which would lead to stimulating the glutamate-glutamine cycle. Ceftriaxone 33-36 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 127-132 30452416-10 2018 The above results suggested that Cef could improve cognitive deficits of APP/PS1 mice in early stage of AD by upregulating the GLT-1 expression, GS activity, and SN1 expression, which would lead to stimulating the glutamate-glutamine cycle. Ceftriaxone 33-36 solute carrier family 38, member 3 Mus musculus 162-165 29949502-1 2018 PURPOSE: Ceftriaxone elimination occurs through breast cancer resistance transporter (BCRP) and multidrug resistance-associated protein 2 (MRP-2) which are expressed on the canalicular membrane of hepatocytes. Ceftriaxone 9-20 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 86-90 29949502-1 2018 PURPOSE: Ceftriaxone elimination occurs through breast cancer resistance transporter (BCRP) and multidrug resistance-associated protein 2 (MRP-2) which are expressed on the canalicular membrane of hepatocytes. Ceftriaxone 9-20 ATP binding cassette subfamily C member 2 Homo sapiens 96-137 29949502-1 2018 PURPOSE: Ceftriaxone elimination occurs through breast cancer resistance transporter (BCRP) and multidrug resistance-associated protein 2 (MRP-2) which are expressed on the canalicular membrane of hepatocytes. Ceftriaxone 9-20 ATP binding cassette subfamily C member 2 Homo sapiens 139-144 29402790-10 2018 Protein bioinformatics and validation studies supported heat stress response mediated by heat shock protein 70 (Hsp70) and downregulation of annexin A1 as the proposed pathophysiology of crystalline nephropathy in ceftriaxone-associated AKI, in which impaired proliferation and wound healing of crystal-induced distal tubular cells were outcomes. Ceftriaxone 214-225 heat shock 70 kDa protein 1 Canis lupus familiaris 89-110 29402790-10 2018 Protein bioinformatics and validation studies supported heat stress response mediated by heat shock protein 70 (Hsp70) and downregulation of annexin A1 as the proposed pathophysiology of crystalline nephropathy in ceftriaxone-associated AKI, in which impaired proliferation and wound healing of crystal-induced distal tubular cells were outcomes. Ceftriaxone 214-225 heat shock 70 kDa protein 1 Canis lupus familiaris 112-117 29402790-10 2018 Protein bioinformatics and validation studies supported heat stress response mediated by heat shock protein 70 (Hsp70) and downregulation of annexin A1 as the proposed pathophysiology of crystalline nephropathy in ceftriaxone-associated AKI, in which impaired proliferation and wound healing of crystal-induced distal tubular cells were outcomes. Ceftriaxone 214-225 annexin A1 Canis lupus familiaris 141-151 28826758-1 2017 Studies from our laboratory showed that upregulation of glutamate transporter 1 (GLT-1) and cystine-glutamate exchanger (xCT) expression with ceftriaxone, beta-lactam antibiotic, in the brain was associated with attenuation of ethanol consumption. Ceftriaxone 142-153 solute carrier family 1 member 2 Rattus norvegicus 56-79 29242830-5 2017 Ceftriaxone, ciprofloxacin, and azithromycin each demonstrated synergy with the human cathelicidin defense peptide LL-37 in killing Salmonella. Ceftriaxone 0-11 cathelicidin antimicrobial peptide Homo sapiens 115-120 29242830-6 2017 Exposure of Salmonella to sub-MICs of ceftriaxone resulted in enhanced susceptibility to LL-37, whole blood, and neutrophil killing. Ceftriaxone 38-49 cathelicidin antimicrobial peptide Homo sapiens 89-94 29319728-6 2017 In the group treated with ceftriaxone there was an increase in pro-caspase-3, gamma-glutamyl transpeptidase concentration, PCNA expression and in the number of cells positive for anti-CD68 (P<0.05). Ceftriaxone 26-37 proliferating cell nuclear antigen Oryctolagus cuniculus 123-127 29319728-6 2017 In the group treated with ceftriaxone there was an increase in pro-caspase-3, gamma-glutamyl transpeptidase concentration, PCNA expression and in the number of cells positive for anti-CD68 (P<0.05). Ceftriaxone 26-37 macrosialin Oryctolagus cuniculus 184-188 27774857-0 2017 In-vitro activity of ceftriaxone combined with newer agents against MRSA. Ceftriaxone 21-32 solute carrier family 9 member A6 Homo sapiens 68-72 28486078-4 2017 The highest beta-lactamase activity was observed in S. Typhimurium CCARM 8009 when exposed to ceftriaxone (8.2 mumol/min/ml), while the least beta-lactamase activity was observed in S. Typhimurium ATCC 19585. Ceftriaxone 94-105 Bla Salmonella enterica subsp. enterica serovar Typhimurium 12-26 28631864-4 2017 Initiation of a ceftriaxone regimen at the time of nigrostriatal lesion can attenuate tyrosine hydroxylase loss in conjunction with increased glutamate uptake and glutamate transporter GLT-1 expression in a rat 6-hydroxydopamine model. Ceftriaxone 16-27 solute carrier family 1 member 2 Rattus norvegicus 185-190 28631864-9 2017 The ceftriaxone-treated l-dopa group had significantly increased striatal GLT-1 expression and glutamate uptake. Ceftriaxone 4-15 solute carrier family 1 member 2 Rattus norvegicus 74-79 28783953-0 2017 Metallo-beta-lactamase Domain-Containing Protein 1 (MBLAC1) Is a Specific, High-Affinity Target for the Glutamate Transporter Inducer Ceftriaxone. Ceftriaxone 134-145 metallo-beta-lactamase domain containing 1 Homo sapiens 0-50 28783953-0 2017 Metallo-beta-lactamase Domain-Containing Protein 1 (MBLAC1) Is a Specific, High-Affinity Target for the Glutamate Transporter Inducer Ceftriaxone. Ceftriaxone 134-145 metallo-beta-lactamase domain containing 1 Homo sapiens 52-58 28783953-5 2017 Using cyanogen bromide immobilized ceftriaxone for affinity capture experiments and backscattering interferometry to monitor MBLAC1 binding of unmodified ceftriaxone, we obtained evidence for specific, high affinity (KD = 2.2 muM) binding of ceftriaxone to MBLAC1. Ceftriaxone 154-165 metallo-beta-lactamase domain containing 1 Homo sapiens 125-131 28783953-5 2017 Using cyanogen bromide immobilized ceftriaxone for affinity capture experiments and backscattering interferometry to monitor MBLAC1 binding of unmodified ceftriaxone, we obtained evidence for specific, high affinity (KD = 2.2 muM) binding of ceftriaxone to MBLAC1. Ceftriaxone 154-165 metallo-beta-lactamase domain containing 1 Homo sapiens 257-263 28783953-5 2017 Using cyanogen bromide immobilized ceftriaxone for affinity capture experiments and backscattering interferometry to monitor MBLAC1 binding of unmodified ceftriaxone, we obtained evidence for specific, high affinity (KD = 2.2 muM) binding of ceftriaxone to MBLAC1. Ceftriaxone 154-165 metallo-beta-lactamase domain containing 1 Homo sapiens 125-131 28783953-5 2017 Using cyanogen bromide immobilized ceftriaxone for affinity capture experiments and backscattering interferometry to monitor MBLAC1 binding of unmodified ceftriaxone, we obtained evidence for specific, high affinity (KD = 2.2 muM) binding of ceftriaxone to MBLAC1. Ceftriaxone 154-165 metallo-beta-lactamase domain containing 1 Homo sapiens 257-263 28783953-6 2017 We discuss our findings with respect to MBLAC1 as a potentially exclusive, high-affinity binding partner of ceftriaxone in the CNS, and the path forward in the development of novel, MBLAC1-based therapeutics. Ceftriaxone 108-119 metallo-beta-lactamase domain containing 1 Homo sapiens 40-46 28957452-5 2017 Furthermore, the administration of ceftriaxone, but not vancomycin, led to a significant reduction in the abundance of splenic CD4+CD25+Foxp3+ T cells. Ceftriaxone 35-46 CD4 antigen Mus musculus 127-130 28957452-5 2017 Furthermore, the administration of ceftriaxone, but not vancomycin, led to a significant reduction in the abundance of splenic CD4+CD25+Foxp3+ T cells. Ceftriaxone 35-46 forkhead box P3 Mus musculus 136-141 27796747-9 2017 We also found that the administration of beta-lactam antibiotic ceftriaxone increased glutamate transporter-1 protein expression and significantly reduced HI-induced WM injury in neonatal DEX-treated rats. Ceftriaxone 64-75 solute carrier family 1 member 2 Rattus norvegicus 86-109 29045497-13 2017 Moreover, our results suggest that CEF and NAC may induce brain tolerance to ischemia by influencing GLT-1 and system xc- expression levels. Ceftriaxone 35-38 solute carrier family 1 member 2 Rattus norvegicus 101-106 28826758-1 2017 Studies from our laboratory showed that upregulation of glutamate transporter 1 (GLT-1) and cystine-glutamate exchanger (xCT) expression with ceftriaxone, beta-lactam antibiotic, in the brain was associated with attenuation of ethanol consumption. Ceftriaxone 142-153 solute carrier family 1 member 2 Rattus norvegicus 81-86 28698584-2 2017 MRSA strains lacking STK1 become susceptible to failing cephalosporins, such as Ceftriaxone and Cefotaxime. Ceftriaxone 80-91 TEK receptor tyrosine kinase Mus musculus 21-25 28624317-3 2017 Ceftriaxone, a beta-lactam antibiotic, restored GLT-1 expression and consequently reduced cue-induced reinstatement of cocaine-seeking behavior. Ceftriaxone 0-11 solute carrier family 1 member 2 Homo sapiens 48-53 26452467-4 2017 RESULTS: The ceftriaxone group had the highest levels of TNF-alpha. Ceftriaxone 13-24 tumor necrosis factor Oryctolagus cuniculus 57-66 26452467-5 2017 TNF-alpha levels were significantly higher after ceftriaxone administration than in both daptomycin groups. Ceftriaxone 49-60 tumor necrosis factor Oryctolagus cuniculus 0-9 26452467-8 2017 CONCLUSION: CSF TNF-alpha levels were significantly lower in rabbits treated with daptomycin than in rabbits treated with ceftriaxone. Ceftriaxone 122-133 tumor necrosis factor Oryctolagus cuniculus 16-25 28495973-4 2017 Intra-NAc xCT knockdown prevented ceftriaxone from attenuating reinstatement and from upregulating GLT-1 and resulted in increased surface expression of AMPA receptor subunits GluA1 and GluA2. Ceftriaxone 34-45 solute carrier family 1 member 2 Rattus norvegicus 99-104 28620220-6 2017 Hence, it was chosen to investigate the proposed ability of Pep19-2.5-an anti-endotoxic peptide with high affinity to lipopolysaccharide and lipoprotein-to attenuate sepsis-associated pathologies in combination with an antibiotic (ceftriaxone). Ceftriaxone 231-242 Purkinje cell protein 4 Homo sapiens 60-65 28620220-7 2017 We demonstrate that a combination of Pep19-2.5 and ceftriaxone administered intravenously to the rabbits (1) kills bacteria and eliminates bacteremia 30 min post challenge; (2) inhibits Toll-like receptor 4 agonists in serum 90 min post challenge; (3) reduces serum levels of pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor alpha); and (4) reverts to hypothermia and gives rise to temperature values indistinguishable from basal levels 330 min post challenge. Ceftriaxone 51-62 Purkinje cell protein 4 Homo sapiens 37-42 28620220-7 2017 We demonstrate that a combination of Pep19-2.5 and ceftriaxone administered intravenously to the rabbits (1) kills bacteria and eliminates bacteremia 30 min post challenge; (2) inhibits Toll-like receptor 4 agonists in serum 90 min post challenge; (3) reduces serum levels of pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor alpha); and (4) reverts to hypothermia and gives rise to temperature values indistinguishable from basal levels 330 min post challenge. Ceftriaxone 51-62 toll-like receptor 4 Oryctolagus cuniculus 186-206 28620220-7 2017 We demonstrate that a combination of Pep19-2.5 and ceftriaxone administered intravenously to the rabbits (1) kills bacteria and eliminates bacteremia 30 min post challenge; (2) inhibits Toll-like receptor 4 agonists in serum 90 min post challenge; (3) reduces serum levels of pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor alpha); and (4) reverts to hypothermia and gives rise to temperature values indistinguishable from basal levels 330 min post challenge. Ceftriaxone 51-62 interleukin-6 Oryctolagus cuniculus 304-317 28620220-7 2017 We demonstrate that a combination of Pep19-2.5 and ceftriaxone administered intravenously to the rabbits (1) kills bacteria and eliminates bacteremia 30 min post challenge; (2) inhibits Toll-like receptor 4 agonists in serum 90 min post challenge; (3) reduces serum levels of pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor alpha); and (4) reverts to hypothermia and gives rise to temperature values indistinguishable from basal levels 330 min post challenge. Ceftriaxone 51-62 tumor necrosis factor Oryctolagus cuniculus 322-349 28620220-8 2017 The two components of the combination displayed synergism in some of these activities, and Pep19-2.5 notably counteracted the endotoxin-inducing potential of ceftriaxone. Ceftriaxone 158-169 Purkinje cell protein 4 Homo sapiens 91-96 28495973-0 2017 Contrasting the Role of xCT and GLT-1 Upregulation in the Ability of Ceftriaxone to Attenuate the Cue-Induced Reinstatement of Cocaine Seeking and Normalize AMPA Receptor Subunit Expression. Ceftriaxone 69-80 solute carrier family 1 member 2 Rattus norvegicus 32-37 28495973-1 2017 Long-term treatment with ceftriaxone attenuates the reinstatement of cocaine seeking while increasing the function of the glutamate transporter 1 (GLT-1) and system xC- (Sxc) in the nucleus accumbens core (NAc). Ceftriaxone 25-36 solute carrier family 1 member 2 Rattus norvegicus 122-145 28495973-1 2017 Long-term treatment with ceftriaxone attenuates the reinstatement of cocaine seeking while increasing the function of the glutamate transporter 1 (GLT-1) and system xC- (Sxc) in the nucleus accumbens core (NAc). Ceftriaxone 25-36 solute carrier family 1 member 2 Rattus norvegicus 147-152 28495973-5 2017 Intra-NAc GLT-1 knockdown also prevented ceftriaxone from attenuating reinstatement and from upregulating xCT expression, without affecting GluA1 and GluA2 expression. Ceftriaxone 41-52 solute carrier family 1 member 2 Rattus norvegicus 10-15 28495973-8 2017 These data support important and distinct roles for xCT and GLT-1 in the actions of ceftriaxone and add to a body of literature finding evidence for coregulation of these transporters. Ceftriaxone 84-95 solute carrier family 1 member 2 Rattus norvegicus 60-65 28495973-12 2017 While upregulation of both xCT and GLT-1 are essential to the ability of ceftriaxone to attenuate cue-induced reinstatement of cocaine seeking, each protein uniquely affects the expression of other glutamate receptor and transporter proteins. Ceftriaxone 73-84 solute carrier family 1 member 2 Rattus norvegicus 35-40 27888396-4 2017 We also tested the effects of ceftriaxone (CEF), known to upregulate GLT-1, in animals administered EtOH and MA. Ceftriaxone 30-41 solute carrier family 1 member 2 Rattus norvegicus 69-74 28245954-0 2017 Ceftriaxone attenuates glutamate-mediated neuro-inflammation and restores BDNF in MPTP model of Parkinson"s disease in rats. Ceftriaxone 0-11 brain-derived neurotrophic factor Rattus norvegicus 74-78 28245954-9 2017 In addition, Ceftriaxone also attenuated the marked increase of NFkappaB, TNF-alpha and IL-1beta in MPTP treated rats thus, conferring its neuro-inflammatory property. Ceftriaxone 13-24 tumor necrosis factor Rattus norvegicus 74-83 28245954-9 2017 In addition, Ceftriaxone also attenuated the marked increase of NFkappaB, TNF-alpha and IL-1beta in MPTP treated rats thus, conferring its neuro-inflammatory property. Ceftriaxone 13-24 interleukin 1 beta Rattus norvegicus 88-96 28245954-10 2017 Further, Ceftriaxone significantly restored the decreased activity of BDNF in striatum of MPTP treated rats. Ceftriaxone 9-20 brain-derived neurotrophic factor Rattus norvegicus 70-74 28257918-0 2017 Ceftriaxone-mediated upregulation of the glutamate transporter GLT-1 contrasts neurotoxicity evoked by kainate in rat organotypic spinal cord cultures. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 63-68 27993695-3 2017 Parenteral treatment with ceftriaxone, beta-lactam antibiotic, has been reported to attenuate ethanol consumption and reinstatement to cocaine-seeking behavior, in part, by restoring the expression of GLT-1 and xCT in mesocorticolimbic brain regions in rats. Ceftriaxone 26-37 solute carrier family 1 member 2 Rattus norvegicus 201-206 28345130-0 2017 Antiallodynic Activity of Ceftriaxone and Clavulanic Acid in Acute Administration is Associated with Serum TNF-alpha Modulation and Activation of Dopaminergic and Opioidergic Systems. Ceftriaxone 26-37 tumor necrosis factor Rattus norvegicus 107-116 28345130-8 2017 Additionally, serum TNF-alpha levels were attenuated following CFX and CLAV administration. Ceftriaxone 63-66 tumor necrosis factor Rattus norvegicus 20-29 28345130-9 2017 These results suggest that acute administration of CFX and CLAV may represent a promising approach for treating the acute allodynia of NP, and that the mechanisms involved in these effects involve activation of dopaminergic and opioidergic pathways as well as modulation of TNF-alpha production. Ceftriaxone 51-54 tumor necrosis factor Rattus norvegicus 274-283 27214038-10 2017 Quantitative real-time PCR showed that in basal level without antibiotic stress, SHV-148 expressed more, but with ceftriaxone stressed, expression of CTX-M-15 and SHV-148 was high. Ceftriaxone 114-125 hypothetical protein Escherichia coli 150-158 27888396-4 2017 We also tested the effects of ceftriaxone (CEF), known to upregulate GLT-1, in animals administered EtOH and MA. Ceftriaxone 43-46 solute carrier family 1 member 2 Rattus norvegicus 69-74 27888396-13 2017 These findings demonstrated that sequential exposure to EtOH and MA has additive effect in downregulation of GLT-1 and this effect can be attenuated by CEF treatment. Ceftriaxone 152-155 solute carrier family 1 member 2 Rattus norvegicus 109-114 28220870-9 2017 The IFN-gamma/IL-4 and CD4/CD8 ratios increased, the CD4+CD25+ cells reduced on days 30 and 60 after ceftriaxone administration. Ceftriaxone 101-112 CD4 antigen Mus musculus 53-56 28052855-0 2017 The Oral beta-Lactamase SYN-004 (Ribaxamase) Degrades Ceftriaxone Excreted into the Intestine in Phase 2a Clinical Studies. Ceftriaxone 54-65 synemin Homo sapiens 24-27 28220870-10 2017 However, after 90 days of ceftriaxone administration, the IFN-gamma/IL-4, CD4/CD8 ratios and CD4+CD25+ cells restored, which indicated a new balance of immune regulation had been formed. Ceftriaxone 26-37 interferon gamma Mus musculus 58-67 28220870-10 2017 However, after 90 days of ceftriaxone administration, the IFN-gamma/IL-4, CD4/CD8 ratios and CD4+CD25+ cells restored, which indicated a new balance of immune regulation had been formed. Ceftriaxone 26-37 interleukin 4 Mus musculus 68-72 28220870-10 2017 However, after 90 days of ceftriaxone administration, the IFN-gamma/IL-4, CD4/CD8 ratios and CD4+CD25+ cells restored, which indicated a new balance of immune regulation had been formed. Ceftriaxone 26-37 CD4 antigen Mus musculus 74-77 28220870-10 2017 However, after 90 days of ceftriaxone administration, the IFN-gamma/IL-4, CD4/CD8 ratios and CD4+CD25+ cells restored, which indicated a new balance of immune regulation had been formed. Ceftriaxone 26-37 CD4 antigen Mus musculus 93-96 27773601-6 2016 Administration of the NMDA antagonist MK-801 or the glutamate transporter type 1 (GLT-1) inducer ceftriaxone prevented both the MDMA-induced loss of GAD67-IR neurons and the increased vulnerability to kainic acid-induced seizures. Ceftriaxone 97-108 solute carrier family 1 member 2 Homo sapiens 52-87 27889371-5 2017 Analysis of blaSHV open-reading frame showed that blaSHV-5 had a high hydrolysis activity to the broad-spectrum penicillin (ampicillin or piperacillin), ceftazidime, ceftriaxone, cefotaxime and aztreonam. Ceftriaxone 166-177 BlaSHV-5 Escherichia coli 50-58 28828608-7 2017 One such compound, ceftriaxone, was recently tested in clinical trials but unfortunately did not modify disease course, though its effect on EAAT2 expression in patients was not measured. Ceftriaxone 19-30 solute carrier family 1 member 2 Homo sapiens 141-146 27599008-6 2016 The specific surface area of SnO2 modified anode was higher than that of TiO2/Nano-G anode and the degradation rate of ceftriaxone sodium within 120 min on SnO2-TiO2/Nano-G electrode was 98.7% at applied bias of 2.0 V. The highly efficient electro-chemical property of SnO2-TiO2/Nano-G electrode was attributed to the admirable conductive property of the Nano-G and SnO2-TiO2/Nano-G electrode. Ceftriaxone 119-137 Nanog homeobox Homo sapiens 78-84 27599008-6 2016 The specific surface area of SnO2 modified anode was higher than that of TiO2/Nano-G anode and the degradation rate of ceftriaxone sodium within 120 min on SnO2-TiO2/Nano-G electrode was 98.7% at applied bias of 2.0 V. The highly efficient electro-chemical property of SnO2-TiO2/Nano-G electrode was attributed to the admirable conductive property of the Nano-G and SnO2-TiO2/Nano-G electrode. Ceftriaxone 119-137 Nanog homeobox Homo sapiens 166-172 27599008-6 2016 The specific surface area of SnO2 modified anode was higher than that of TiO2/Nano-G anode and the degradation rate of ceftriaxone sodium within 120 min on SnO2-TiO2/Nano-G electrode was 98.7% at applied bias of 2.0 V. The highly efficient electro-chemical property of SnO2-TiO2/Nano-G electrode was attributed to the admirable conductive property of the Nano-G and SnO2-TiO2/Nano-G electrode. Ceftriaxone 119-137 Nanog homeobox Homo sapiens 166-172 27599008-6 2016 The specific surface area of SnO2 modified anode was higher than that of TiO2/Nano-G anode and the degradation rate of ceftriaxone sodium within 120 min on SnO2-TiO2/Nano-G electrode was 98.7% at applied bias of 2.0 V. The highly efficient electro-chemical property of SnO2-TiO2/Nano-G electrode was attributed to the admirable conductive property of the Nano-G and SnO2-TiO2/Nano-G electrode. Ceftriaxone 119-137 Nanog homeobox Homo sapiens 166-172 27599008-6 2016 The specific surface area of SnO2 modified anode was higher than that of TiO2/Nano-G anode and the degradation rate of ceftriaxone sodium within 120 min on SnO2-TiO2/Nano-G electrode was 98.7% at applied bias of 2.0 V. The highly efficient electro-chemical property of SnO2-TiO2/Nano-G electrode was attributed to the admirable conductive property of the Nano-G and SnO2-TiO2/Nano-G electrode. Ceftriaxone 119-137 Nanog homeobox Homo sapiens 166-172 27773601-6 2016 Administration of the NMDA antagonist MK-801 or the glutamate transporter type 1 (GLT-1) inducer ceftriaxone prevented both the MDMA-induced loss of GAD67-IR neurons and the increased vulnerability to kainic acid-induced seizures. Ceftriaxone 97-108 glutamate decarboxylase 1 Homo sapiens 149-154 27932896-6 2016 Furthermore, repeated intrathecal administrations of ceftriaxone dose-dependently prevented the development of mechanical hyperalgesia and allodynia in ZDF rats, which were correlated with enhanced GLT-1 expression without altering the basal glutamate levels in the spinal cord of ZDF rats. Ceftriaxone 53-64 solute carrier family 1 member 2 Rattus norvegicus 198-203 27932896-4 2016 Finally, the effects of repeated intrathecal injections of ceftriaxone, which was previously shown to enhance GLT-1 expression, on the development of mechanical allodynia and hyperalgesia as well as on basal extracellular level of glutamate and the expression of GLT-1 in the spinal cord of ZDF rats were evaluated. Ceftriaxone 59-70 solute carrier family 1 member 2 Rattus norvegicus 110-115 27133445-4 2016 METHODS: In this study, synchrotron radiation circular dichroism spectroscopy has been used to obtain structural information about the GFAP-ceftriaxone (phenytoin) interactions, while computational methods allowed the identification of the relevant putative binding site of either ceftriaxone or phenytoin on the dimer structure of GFAP, permitting to rationalize the spectroscopic experimental results. Ceftriaxone 281-292 glial fibrillary acidic protein Rattus norvegicus 135-139 27834383-4 2016 GLT-1 expression is reduced around Abeta plaques and upregulation of GLT-1 expression and activity by ceftriaxone partially restores glutamate dynamics to values in control regions. Ceftriaxone 102-113 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 69-74 27558732-7 2016 Finally, ceftriaxone pretreatment (200mg/kg/day, 5days) before the 15min BCCAO prevented the development of PPD, and prevented the reduction of GLT-1 expression in the mPFC. Ceftriaxone 9-20 solute carrier family 1 member 2 Rattus norvegicus 144-149 27558732-8 2016 CONCLUSIONS: Taken together, our results suggested that ceftriaxone pretreatment before brain ischemia during pregnancy may reduce the propensity for the development of PPD by preventing the loss of GLT-1 expression in the mPFC. Ceftriaxone 56-67 solute carrier family 1 member 2 Rattus norvegicus 199-204 27133445-0 2016 Interactions of GFAP with ceftriaxone and phenytoin: SRCD and molecular docking and dynamic simulation. Ceftriaxone 26-37 glial fibrillary acidic protein Homo sapiens 16-20 27133445-5 2016 RESULTS: We found that GFAP exhibited enhanced stability upon the addition of two equivalents of each ligands with ceftriaxone imparting a more spontaneous interactions and a more ordered complex system than phenytoin. Ceftriaxone 115-126 glial fibrillary acidic protein Rattus norvegicus 23-27 27133445-3 2016 Recently, ceftriaxone a multi-potent beta-lactam antibiotic able to overcome the blood-brain barrier, successfully eliminated the cellular toxic effects of misfolded mutated GFAP, similarly to phenytoin sodium, in a cellular model of Alexander"s disease and inhibited alpha-synuclein aggregation protecting PC12 cells from the exposure to 6-hydroxydopamine. Ceftriaxone 10-21 glial fibrillary acidic protein Rattus norvegicus 174-178 27133445-6 2016 CONCLUSIONS: SRCD data and MD models indicate a stronger protective effect of ceftriaxone in neurological disorders characterized by an increased production and polymerization of GFAP. Ceftriaxone 78-89 glial fibrillary acidic protein Rattus norvegicus 179-183 27133445-7 2016 GENERAL SIGNIFICANCE: This result, in addition to our previous works in which we documented that ceftriaxone interacts with alpha-synuclein inhibiting its pathological aggregation and that a cyclical treatment with this molecule in a patient with adult-onset Alexander"s disease halted, and partly reversed, the progression of neurodegeneration, suggests the possibility of a chaperone-like effect of ceftriaxone on protein involved in specific neurodegenerative diseases. Ceftriaxone 97-108 synuclein alpha Homo sapiens 124-139 27133445-3 2016 Recently, ceftriaxone a multi-potent beta-lactam antibiotic able to overcome the blood-brain barrier, successfully eliminated the cellular toxic effects of misfolded mutated GFAP, similarly to phenytoin sodium, in a cellular model of Alexander"s disease and inhibited alpha-synuclein aggregation protecting PC12 cells from the exposure to 6-hydroxydopamine. Ceftriaxone 10-21 synuclein alpha Rattus norvegicus 268-283 27133445-7 2016 GENERAL SIGNIFICANCE: This result, in addition to our previous works in which we documented that ceftriaxone interacts with alpha-synuclein inhibiting its pathological aggregation and that a cyclical treatment with this molecule in a patient with adult-onset Alexander"s disease halted, and partly reversed, the progression of neurodegeneration, suggests the possibility of a chaperone-like effect of ceftriaxone on protein involved in specific neurodegenerative diseases. Ceftriaxone 401-412 synuclein alpha Homo sapiens 124-139 27133445-4 2016 METHODS: In this study, synchrotron radiation circular dichroism spectroscopy has been used to obtain structural information about the GFAP-ceftriaxone (phenytoin) interactions, while computational methods allowed the identification of the relevant putative binding site of either ceftriaxone or phenytoin on the dimer structure of GFAP, permitting to rationalize the spectroscopic experimental results. Ceftriaxone 140-151 glial fibrillary acidic protein Rattus norvegicus 135-139 26677751-11 2016 Combined ROL and ceftriaxone treatment decreased lethality rates and was more efficient in reducing inflammation, by increasing proresolving protein annexin A1 (AnxA1) expression, and bacterial burden by enhancing phagocytosis. Ceftriaxone 17-28 annexin A1 Mus musculus 149-159 27133445-4 2016 METHODS: In this study, synchrotron radiation circular dichroism spectroscopy has been used to obtain structural information about the GFAP-ceftriaxone (phenytoin) interactions, while computational methods allowed the identification of the relevant putative binding site of either ceftriaxone or phenytoin on the dimer structure of GFAP, permitting to rationalize the spectroscopic experimental results. Ceftriaxone 140-151 glial fibrillary acidic protein Rattus norvegicus 332-336 27085607-3 2016 We hypothesized that repeated administration of the synthetic cathinone, MDPV (3,4-methylenedioxypyrovalerone), would affect GLT-1 expression in the corticolimbic circuit, and that a GLT-1 activator (ceftriaxone, CTX) would reduce rewarding and locomotor-stimulant effects of MDPV in rats. Ceftriaxone 200-211 solute carrier family 1 member 2 Homo sapiens 183-188 27383586-6 2016 Furthermore, ceftriaxone-mediated upregulation of surface GLT1 expression restores functional glutamate uptake and attenuates enhanced neuronal excitability in Fmr1 KO mice. Ceftriaxone 13-24 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 58-62 27383586-6 2016 Furthermore, ceftriaxone-mediated upregulation of surface GLT1 expression restores functional glutamate uptake and attenuates enhanced neuronal excitability in Fmr1 KO mice. Ceftriaxone 13-24 fragile X messenger ribonucleoprotein 1 Mus musculus 160-164 27383586-7 2016 In particular, ceftriaxone significantly decreases the growth rate of abnormally accelerated body weight and completely corrects spine abnormality in Fmr1 KO mice. Ceftriaxone 15-26 fragile X messenger ribonucleoprotein 1 Mus musculus 150-154 26677751-11 2016 Combined ROL and ceftriaxone treatment decreased lethality rates and was more efficient in reducing inflammation, by increasing proresolving protein annexin A1 (AnxA1) expression, and bacterial burden by enhancing phagocytosis. Ceftriaxone 17-28 annexin A1 Mus musculus 161-166 27060486-0 2016 Effects of ceftriaxone on ethanol, nicotine or sucrose intake by alcohol-preferring (P) rats and its association with GLT-1 expression. Ceftriaxone 11-22 solute carrier family 1 member 2 Rattus norvegicus 118-123 27390674-0 2016 Beta Lactams Antibiotic Ceftriaxone Modulates Seizures, Oxidative Stress and Connexin 43 Expression in Hippocampus of Pentylenetetrazole Kindled Rats. Ceftriaxone 24-35 gap junction protein, alpha 1 Rattus norvegicus 77-88 27390674-1 2016 BACKGROUND AND PURPOSE: This study aimed to investigate the effect of ceftriaxone on oxidative stress and gap junction protein (connexin 43, Cx-43) expression in pentylenetetrazole (PTZ) induced kindling model. Ceftriaxone 70-81 gap junction protein, alpha 1 Rattus norvegicus 128-139 27390674-9 2016 While, ceftriaxone treatment ameliorated, significantly, PTZ-induced convulsions and caused significant improvement in oxidative stress markers and Cx-43 expression in hippocamal regions (p < 0.05). Ceftriaxone 7-18 gap junction protein, alpha 1 Rattus norvegicus 148-153 27060486-2 2016 We have shown that administration of ceftriaxone (CEF), a beta-lactam antibiotic, reduced EtOH intake and increased glutamate transporter 1 (GLT-1) expression in mesocorticolimbic regions of male and female alcohol-preferring (P) rats. Ceftriaxone 37-48 solute carrier family 1 member 2 Rattus norvegicus 116-139 27060486-2 2016 We have shown that administration of ceftriaxone (CEF), a beta-lactam antibiotic, reduced EtOH intake and increased glutamate transporter 1 (GLT-1) expression in mesocorticolimbic regions of male and female alcohol-preferring (P) rats. Ceftriaxone 37-48 solute carrier family 1 member 2 Rattus norvegicus 141-146 27060486-2 2016 We have shown that administration of ceftriaxone (CEF), a beta-lactam antibiotic, reduced EtOH intake and increased glutamate transporter 1 (GLT-1) expression in mesocorticolimbic regions of male and female alcohol-preferring (P) rats. Ceftriaxone 50-53 solute carrier family 1 member 2 Rattus norvegicus 116-139 27060486-2 2016 We have shown that administration of ceftriaxone (CEF), a beta-lactam antibiotic, reduced EtOH intake and increased glutamate transporter 1 (GLT-1) expression in mesocorticolimbic regions of male and female alcohol-preferring (P) rats. Ceftriaxone 50-53 solute carrier family 1 member 2 Rattus norvegicus 141-146 27060486-11 2016 The present results along with previous reports of CEF"s efficacy in reducing cocaine self-administration in rats suggest that modulation of GLT-1 expression and/or activity is an important pharmacological target for treating polysubstance abuse and dependence. Ceftriaxone 51-54 solute carrier family 1 member 2 Rattus norvegicus 141-146 25092605-4 2016 METHODS: A retrospective chart review was conducted on chronic warfarin patients with a diagnosis of UTI treated with ceftriaxone, a first-generation cephalosporin, penicillin, or ciprofloxacin. Ceftriaxone 118-129 alpha-1-microglobulin/bikunin precursor Homo sapiens 101-104 26700136-9 2016 Coadministration of oral SYN-004 with intravenous ceftriaxone was safe and well tolerated, with SYN-004 having no noticeable effect on the plasma pharmacokinetics of ceftriaxone. Ceftriaxone 50-61 synemin Homo sapiens 25-28 26697981-8 2016 We also examined the influence of dihydrokainate (DHK) and ceftriaxone (CTX), which downregulate and upregulate Glt1, respectively, on pain development. Ceftriaxone 59-70 solute carrier family 1 member 2 Rattus norvegicus 112-116 26931569-7 2016 Excitotoxic neuronal death is ameliorated by ceftriaxone, which stimulates astrocytic glutamate uptake via the transporter EAAT2/GLT1. Ceftriaxone 45-56 solute carrier family 1 member 2 Homo sapiens 123-128 26931569-7 2016 Excitotoxic neuronal death is ameliorated by ceftriaxone, which stimulates astrocytic glutamate uptake via the transporter EAAT2/GLT1. Ceftriaxone 45-56 solute carrier family 1 member 2 Homo sapiens 129-133 26899719-6 2016 The gentamicin, vancomycin, amikacin and ceftriaxone beads all inhibited growth of the MRSA on the TSB and agar plates, both before and after gas sterilisation. Ceftriaxone 41-52 solute carrier family 9 member A6 Homo sapiens 87-91 25092605-7 2016 CONCLUSION: Ceftriaxone interacts with warfarin to increase a patient"s INR value more than other commonly administered antibiotics for UTI treatment. Ceftriaxone 12-23 alpha-1-microglobulin/bikunin precursor Homo sapiens 136-139 26543027-1 2016 The beta-lactam antibiotic ceftriaxone (CTX) reduces cocaine reinforcement and relapse in preclinical assays through a mechanism involving activation of glutamate transporter subtype 1 (GLT-1). Ceftriaxone 27-38 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 153-191 26706696-8 2016 GluA1 was reduced in the NAc by both doses of ceftriaxone while GluA2 expression was unchanged, indicating that ceftriaxone altered AMPA subunit composition following cocaine. Ceftriaxone 46-57 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 0-5 26706696-3 2016 We have demonstrated that the mechanism of action by which ceftriaxone attenuates reinstatement involves increased NAc GLT-1 expression and a reduction in NAc glutamate efflux during reinstatement. Ceftriaxone 59-70 solute carrier family 1 member 2 Homo sapiens 119-124 26706696-8 2016 GluA1 was reduced in the NAc by both doses of ceftriaxone while GluA2 expression was unchanged, indicating that ceftriaxone altered AMPA subunit composition following cocaine. Ceftriaxone 112-123 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 0-5 24657069-11 2016 A blaCMY-2 gene, carried by a 120-kb conjugative IncI1 plasmid of the sequence type 53, was identified in the two ceftriaxone-resistant isolates. Ceftriaxone 114-125 beta-lactamase Salmonella enterica 2-10 24657069-14 2016 Pediatricians should be aware of the possibility of resistance development during therapy, especially in areas with a widespread of ceftriaxone resistance genes that are carried by a self-transferrable plasmid, such as the blaCMY-2-carrying IncI1 plasmid identified herein. Ceftriaxone 132-143 beta-lactamase Salmonella enterica 223-231 26721358-0 2016 Ameliorative potential of pioglitazone and ceftriaxone alone and in combination in rat model of neuropathic pain: Targeting PPARgamma and GLT-1 pathways. Ceftriaxone 43-54 peroxisome proliferator-activated receptor gamma Rattus norvegicus 124-133 26721358-0 2016 Ameliorative potential of pioglitazone and ceftriaxone alone and in combination in rat model of neuropathic pain: Targeting PPARgamma and GLT-1 pathways. Ceftriaxone 43-54 solute carrier family 1 member 2 Rattus norvegicus 138-143 26721358-2 2016 Present study has been designed to elucidate the interaction between the GLT-1 activator (ceftriaxone) and PPAR gamma agonist (pioglitazone) in the spinal nerve ligation induced neuropathic pain. Ceftriaxone 90-101 solute carrier family 1 member 2 Rattus norvegicus 73-78 26518125-11 2015 iha and afa/draBC genes were more frequent in resistant isolates than the susceptible ones; for iha, in ampicillin, amoxicillin/clavulanic acid, nalidixic acid, cefuroxime, ceftriaxone resistant and ESBL and MDR positive isolates; for afa/draBC, in cefotaxime, cefuroxime, ciprofloxacin, trimethoprim/sulfamethoxazole resistant and ESBL and MDR positive isolates, this trend was observed. Ceftriaxone 173-184 AFA Homo sapiens 8-11 26825984-0 2015 Characterization of ceftriaxone-resistant Aeromonas spp. Ceftriaxone 20-31 histocompatibility minor 13 Homo sapiens 52-55 26619231-11 2016 Glutamate transporter-1 (GLT-1) selective antagonist ceftriaxone prolonged CNS-OT latency, whereas GLT-1 selective inhibitor dihydrokainate shortened CNS-OT latency. Ceftriaxone 53-64 solute carrier family 1 member 2 Rattus norvegicus 0-23 26619231-11 2016 Glutamate transporter-1 (GLT-1) selective antagonist ceftriaxone prolonged CNS-OT latency, whereas GLT-1 selective inhibitor dihydrokainate shortened CNS-OT latency. Ceftriaxone 53-64 solute carrier family 1 member 2 Rattus norvegicus 25-30 26518125-11 2015 iha and afa/draBC genes were more frequent in resistant isolates than the susceptible ones; for iha, in ampicillin, amoxicillin/clavulanic acid, nalidixic acid, cefuroxime, ceftriaxone resistant and ESBL and MDR positive isolates; for afa/draBC, in cefotaxime, cefuroxime, ciprofloxacin, trimethoprim/sulfamethoxazole resistant and ESBL and MDR positive isolates, this trend was observed. Ceftriaxone 173-184 AFA Homo sapiens 235-238 26617578-5 2015 The biological nature of ceftriaxone degradation in soil was supported by microcosm experiments that amended model Escherichia coli strains to sterile and non-sterile soils in the presence and absence of ceftriaxone and by the ubiquitous presence of ESBL genes (blaTEM, blaCTX-M, and blaOXA) in soil DNA extracts. Ceftriaxone 25-36 EsbL Escherichia coli 250-254 26296668-2 2015 The present study was aimed at clarifying whether combined treatment with CEF and EPO (CEF+EPO) had superior neuroprotective and behavioral effects than treatment with CEF or EPO alone in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson"s disease (PD) rat model. Ceftriaxone 74-77 erythropoietin Rattus norvegicus 87-94 26539828-1 2015 We characterized 12 clinical isolates of Klebsiella oxytoca with the extended-spectrum beta-lactamase (ESBL) phenotype (high minimum inhibitory concentration [MIC] values of ceftriaxone) recovered over 9 months at a university hospital in Japan. Ceftriaxone 174-185 EsbL Klebsiella oxytoca 69-101 26296668-5 2015 Lesioning also caused neurodegeneration in the nigrostriatal dopaminergic system and the hippocampal CA1 area and these changes were reduced or eliminated by treatment with CEF, EPO, or CEF+EPO, with the combination having a greater effect than single treatment in the densities of DAergic terminals in the striatum and neurons in the hippocampal CA1 area. Ceftriaxone 173-176 carbonic anhydrase 1 Rattus norvegicus 101-104 26296668-5 2015 Lesioning also caused neurodegeneration in the nigrostriatal dopaminergic system and the hippocampal CA1 area and these changes were reduced or eliminated by treatment with CEF, EPO, or CEF+EPO, with the combination having a greater effect than single treatment in the densities of DAergic terminals in the striatum and neurons in the hippocampal CA1 area. Ceftriaxone 173-176 carbonic anhydrase 1 Rattus norvegicus 347-350 26296668-5 2015 Lesioning also caused neurodegeneration in the nigrostriatal dopaminergic system and the hippocampal CA1 area and these changes were reduced or eliminated by treatment with CEF, EPO, or CEF+EPO, with the combination having a greater effect than single treatment in the densities of DAergic terminals in the striatum and neurons in the hippocampal CA1 area. Ceftriaxone 186-189 carbonic anhydrase 1 Rattus norvegicus 101-104 26296668-5 2015 Lesioning also caused neurodegeneration in the nigrostriatal dopaminergic system and the hippocampal CA1 area and these changes were reduced or eliminated by treatment with CEF, EPO, or CEF+EPO, with the combination having a greater effect than single treatment in the densities of DAergic terminals in the striatum and neurons in the hippocampal CA1 area. Ceftriaxone 186-189 carbonic anhydrase 1 Rattus norvegicus 347-350 26296668-6 2015 Thus, compared to treatment with CEF or EPO alone, combined treatment with CEF+EPO had a greater inhibitory effect on the lesion-induced behavioral and neuronal deficits. Ceftriaxone 33-36 erythropoietin Rattus norvegicus 75-82 26442907-8 2015 Additionally, the beta lactam antibiotic ceftriaxone increased expression of EAAT2. Ceftriaxone 41-52 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 77-82 26375494-9 2015 Pretreatment with ceftriaxone increased Akt/GSK3beta signalling in the nucleus accumbens and reduced levels of dopamine transporter, TH and phosphorylated alpha-synuclein, indicating that ceftriaxone affects numerous proteins involved in dopaminergic transmission. Ceftriaxone 18-29 AKT serine/threonine kinase 1 Rattus norvegicus 40-43 26375494-9 2015 Pretreatment with ceftriaxone increased Akt/GSK3beta signalling in the nucleus accumbens and reduced levels of dopamine transporter, TH and phosphorylated alpha-synuclein, indicating that ceftriaxone affects numerous proteins involved in dopaminergic transmission. Ceftriaxone 18-29 glycogen synthase kinase 3 beta Rattus norvegicus 44-52 26375494-9 2015 Pretreatment with ceftriaxone increased Akt/GSK3beta signalling in the nucleus accumbens and reduced levels of dopamine transporter, TH and phosphorylated alpha-synuclein, indicating that ceftriaxone affects numerous proteins involved in dopaminergic transmission. Ceftriaxone 18-29 tyrosine hydroxylase Rattus norvegicus 133-135 26375494-9 2015 Pretreatment with ceftriaxone increased Akt/GSK3beta signalling in the nucleus accumbens and reduced levels of dopamine transporter, TH and phosphorylated alpha-synuclein, indicating that ceftriaxone affects numerous proteins involved in dopaminergic transmission. Ceftriaxone 18-29 synuclein alpha Rattus norvegicus 155-170 26442907-9 2015 As EAAT2 is a principal mechanism of glutamate clearance from the synapse, the current study tests the hypothesis that ceftriaxone may reverse functional consequences of ketamine exposure. Ceftriaxone 119-130 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 3-8 26002627-0 2015 Ceftriaxone attenuates ethanol drinking and restores extracellular glutamate concentration through normalization of GLT-1 in nucleus accumbens of male alcohol-preferring rats. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 116-121 26168897-1 2015 Studies have shown that administration of the beta-lactam antibiotic ceftriaxone (CEF) attenuates ethanol consumption and cocaine seeking behavior as well as prevents ethanol-induced downregulation of glutamate transporter 1 (GLT-1) expression in central reward brain regions. Ceftriaxone 69-80 solute carrier family 1 member 2 Homo sapiens 201-224 26168897-1 2015 Studies have shown that administration of the beta-lactam antibiotic ceftriaxone (CEF) attenuates ethanol consumption and cocaine seeking behavior as well as prevents ethanol-induced downregulation of glutamate transporter 1 (GLT-1) expression in central reward brain regions. Ceftriaxone 69-80 solute carrier family 1 member 2 Homo sapiens 226-231 26168897-1 2015 Studies have shown that administration of the beta-lactam antibiotic ceftriaxone (CEF) attenuates ethanol consumption and cocaine seeking behavior as well as prevents ethanol-induced downregulation of glutamate transporter 1 (GLT-1) expression in central reward brain regions. Ceftriaxone 82-85 solute carrier family 1 member 2 Homo sapiens 201-224 26168897-1 2015 Studies have shown that administration of the beta-lactam antibiotic ceftriaxone (CEF) attenuates ethanol consumption and cocaine seeking behavior as well as prevents ethanol-induced downregulation of glutamate transporter 1 (GLT-1) expression in central reward brain regions. Ceftriaxone 82-85 solute carrier family 1 member 2 Homo sapiens 226-231 26002627-10 2015 Blockade of GLT-1 by DHK reversed the effects of ceftriaxone on glutamate and implicated the role of GLT-1 in the normalization of extracellular glutamate by ceftriaxone. Ceftriaxone 158-169 solute carrier family 1 member 2 Rattus norvegicus 12-17 26002627-10 2015 Blockade of GLT-1 by DHK reversed the effects of ceftriaxone on glutamate and implicated the role of GLT-1 in the normalization of extracellular glutamate by ceftriaxone. Ceftriaxone 158-169 solute carrier family 1 member 2 Rattus norvegicus 101-106 26002627-2 2015 We have previously reported that chronic ethanol-drinking downregulated glutamate transporter 1 (GLT-1) in nucleus accumbens (NAc) in male P rats in a manner that was reversed by ceftriaxone treatment. Ceftriaxone 179-190 solute carrier family 1 member 2 Rattus norvegicus 72-95 26002627-12 2015 Ceftriaxone treatment also increased glutamine synthetase activity in NAc but not in PFC as compared to ethanol drinking saline-treated rats. Ceftriaxone 0-11 glutamate-ammonia ligase Rattus norvegicus 37-57 26002627-13 2015 Our present study demonstrates that ceftriaxone treatment prevents ethanol drinking in part through normalization of extracellular glutamate concentrations in NAc of male P rats via GLT-1. Ceftriaxone 36-47 solute carrier family 1 member 2 Rattus norvegicus 182-187 26002627-2 2015 We have previously reported that chronic ethanol-drinking downregulated glutamate transporter 1 (GLT-1) in nucleus accumbens (NAc) in male P rats in a manner that was reversed by ceftriaxone treatment. Ceftriaxone 179-190 solute carrier family 1 member 2 Rattus norvegicus 97-102 26002627-6 2015 In vivo microdialysis was performed to measure the extracellular glutamate concentrations in NAc and the effect of blockade of GLT-1 with dihydrokainic acid (DHK) on extracellular glutamate in NAc of ceftriaxone-treated rats was determined. Ceftriaxone 200-211 solute carrier family 1 member 2 Rattus norvegicus 127-132 26002627-10 2015 Blockade of GLT-1 by DHK reversed the effects of ceftriaxone on glutamate and implicated the role of GLT-1 in the normalization of extracellular glutamate by ceftriaxone. Ceftriaxone 49-60 solute carrier family 1 member 2 Rattus norvegicus 12-17 25994587-7 2015 EAAT-2 induction by CEF reduced SNL-induced neuropathic pain in both NTg and GET-1 mice. Ceftriaxone 20-23 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 0-6 26031379-6 2015 Immunoblotting analysis showed that the expression of autophagy-related gene Beclin-1 in the hippocampus post-TBI were decreased in response to treatment with CBX, the P2X7 receptor (P2X7R) antagonist Oxidized ATP (OxATP) or ceftriaxone (Cef) which increased the expression and activity of the glutamate transporter (GLT-1) in the central nervous system (CNS). Ceftriaxone 225-236 beclin 1 Rattus norvegicus 77-85 26031379-6 2015 Immunoblotting analysis showed that the expression of autophagy-related gene Beclin-1 in the hippocampus post-TBI were decreased in response to treatment with CBX, the P2X7 receptor (P2X7R) antagonist Oxidized ATP (OxATP) or ceftriaxone (Cef) which increased the expression and activity of the glutamate transporter (GLT-1) in the central nervous system (CNS). Ceftriaxone 238-241 beclin 1 Rattus norvegicus 77-85 25994587-7 2015 EAAT-2 induction by CEF reduced SNL-induced neuropathic pain in both NTg and GET-1 mice. Ceftriaxone 20-23 activating transcription factor 7 interacting protein 2 Mus musculus 77-82 26037843-3 2015 The present study was carried out to investigate the effect of ceftriaxone (GLT-1 upregulator) and Brilliant Blue G (P2X7 antagonist) against PTZ-induced kindling in rats. Ceftriaxone 63-74 solute carrier family 1 member 2 Rattus norvegicus 76-81 25112679-0 2015 Ceftriaxone Protects Astrocytes from MPP(+) via Suppression of NF-kappaB/JNK/c-Jun Signaling. Ceftriaxone 0-11 nuclear factor kappa B subunit 1 Homo sapiens 63-72 25112679-0 2015 Ceftriaxone Protects Astrocytes from MPP(+) via Suppression of NF-kappaB/JNK/c-Jun Signaling. Ceftriaxone 0-11 mitogen-activated protein kinase 8 Homo sapiens 73-76 25112679-0 2015 Ceftriaxone Protects Astrocytes from MPP(+) via Suppression of NF-kappaB/JNK/c-Jun Signaling. Ceftriaxone 0-11 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-82 25112679-1 2015 Ceftriaxone has been shown to attenuate the dopaminergic neuron death and alleviate behavioral disorders in Parkinson"s disease models via upregulation of glutamate transporter-1 (GLT-1) and decreases in extracellular glutamate. Ceftriaxone 0-11 solute carrier family 1 member 2 Homo sapiens 155-178 26096891-6 2015 Translational activators of EAAT2/GLT-1, such as ceftriaxone and LDN/OSU-0212320, have been described to have significant protective effects in animal models of amyotrophic lateral sclerosis and epilepsy. Ceftriaxone 49-60 solute carrier family 1 member 2 Homo sapiens 28-33 26096891-6 2015 Translational activators of EAAT2/GLT-1, such as ceftriaxone and LDN/OSU-0212320, have been described to have significant protective effects in animal models of amyotrophic lateral sclerosis and epilepsy. Ceftriaxone 49-60 solute carrier family 1 member 2 Homo sapiens 34-39 25112679-1 2015 Ceftriaxone has been shown to attenuate the dopaminergic neuron death and alleviate behavioral disorders in Parkinson"s disease models via upregulation of glutamate transporter-1 (GLT-1) and decreases in extracellular glutamate. Ceftriaxone 0-11 solute carrier family 1 member 2 Homo sapiens 180-185 25112679-3 2015 We hypothesized that cytoprotection by ceftriaxone in astrocytes exposed to 1-methyl-4-phenylpyridinium (MPP(+)) involves suppression of the NF-kappaB/JNK/c-Jun signaling pathway. Ceftriaxone 39-50 nuclear factor kappa B subunit 1 Homo sapiens 141-150 25112679-3 2015 We hypothesized that cytoprotection by ceftriaxone in astrocytes exposed to 1-methyl-4-phenylpyridinium (MPP(+)) involves suppression of the NF-kappaB/JNK/c-Jun signaling pathway. Ceftriaxone 39-50 mitogen-activated protein kinase 8 Homo sapiens 151-154 25112679-3 2015 We hypothesized that cytoprotection by ceftriaxone in astrocytes exposed to 1-methyl-4-phenylpyridinium (MPP(+)) involves suppression of the NF-kappaB/JNK/c-Jun signaling pathway. Ceftriaxone 39-50 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 155-160 25112679-6 2015 Ceftriaxone enhances glutamate uptake via upregulation of GLT-1 in the plasma membrane, and alleviates MPP(+)-induced neurotoxicity via suppression of NF-kappaB/JNK/c-Jun signaling. Ceftriaxone 0-11 solute carrier family 1 member 2 Homo sapiens 58-63 25112679-6 2015 Ceftriaxone enhances glutamate uptake via upregulation of GLT-1 in the plasma membrane, and alleviates MPP(+)-induced neurotoxicity via suppression of NF-kappaB/JNK/c-Jun signaling. Ceftriaxone 0-11 nuclear factor kappa B subunit 1 Homo sapiens 151-160 25112679-6 2015 Ceftriaxone enhances glutamate uptake via upregulation of GLT-1 in the plasma membrane, and alleviates MPP(+)-induced neurotoxicity via suppression of NF-kappaB/JNK/c-Jun signaling. Ceftriaxone 0-11 mitogen-activated protein kinase 8 Homo sapiens 161-164 25112679-6 2015 Ceftriaxone enhances glutamate uptake via upregulation of GLT-1 in the plasma membrane, and alleviates MPP(+)-induced neurotoxicity via suppression of NF-kappaB/JNK/c-Jun signaling. Ceftriaxone 0-11 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 165-170 25112679-7 2015 Collectively, our data offer evidence that increased expression and function of GLT-1 are involved in the protective mechanism of ceftriaxone in astrocytes exposed to MPP(+) in vitro, and we offer insight into the potential therapeutic role of ceftriaxone in treatment of Parkinson"s disease. Ceftriaxone 130-141 solute carrier family 1 member 2 Homo sapiens 80-85 25112679-7 2015 Collectively, our data offer evidence that increased expression and function of GLT-1 are involved in the protective mechanism of ceftriaxone in astrocytes exposed to MPP(+) in vitro, and we offer insight into the potential therapeutic role of ceftriaxone in treatment of Parkinson"s disease. Ceftriaxone 244-255 solute carrier family 1 member 2 Homo sapiens 80-85 25619881-8 2015 The reduction in ethanol intake was associated with significantly enhanced expression of GLT1, GLT1a, GLT1b, and xCT in the nucleus accumbens (NAc) and prefrontal cortex (PFC) of 5-day ceftriaxone-treated P rats. Ceftriaxone 185-196 solute carrier family 1 member 2 Homo sapiens 89-93 25806702-0 2015 Imaging in vivo glutamate fluctuations with [(11)C]ABP688: a GLT-1 challenge with ceftriaxone. Ceftriaxone 82-93 solute carrier family 1 member 2 Rattus norvegicus 61-66 25806702-3 2015 For this, we used ceftriaxone (CEF) administration in rats, an activator of the GLT-1 transporter (EAAT2), which is known to decrease extracellular levels of glutamate. Ceftriaxone 18-29 solute carrier family 1 member 2 Rattus norvegicus 80-85 25806702-3 2015 For this, we used ceftriaxone (CEF) administration in rats, an activator of the GLT-1 transporter (EAAT2), which is known to decrease extracellular levels of glutamate. Ceftriaxone 18-29 solute carrier family 1 member 2 Rattus norvegicus 99-104 25806702-3 2015 For this, we used ceftriaxone (CEF) administration in rats, an activator of the GLT-1 transporter (EAAT2), which is known to decrease extracellular levels of glutamate. Ceftriaxone 31-34 solute carrier family 1 member 2 Rattus norvegicus 80-85 25806702-3 2015 For this, we used ceftriaxone (CEF) administration in rats, an activator of the GLT-1 transporter (EAAT2), which is known to decrease extracellular levels of glutamate. Ceftriaxone 31-34 solute carrier family 1 member 2 Rattus norvegicus 99-104 25619881-0 2015 Effects of ceftriaxone on GLT1 isoforms, xCT and associated signaling pathways in P rats exposed to ethanol. Ceftriaxone 11-22 solute carrier family 1 member 2 Homo sapiens 26-30 25619881-5 2015 OBJECTIVES: We focus in this study to determine the effects of ceftriaxone, beta-lactam antibiotic, on glial proteins such as GLT1 isoforms, xCT, glutamate aspartate transporter (GLAST), and several associated signaling pathways as well as ethanol intake in P rats. Ceftriaxone 63-74 solute carrier family 1 member 2 Homo sapiens 126-130 25619881-5 2015 OBJECTIVES: We focus in this study to determine the effects of ceftriaxone, beta-lactam antibiotic, on glial proteins such as GLT1 isoforms, xCT, glutamate aspartate transporter (GLAST), and several associated signaling pathways as well as ethanol intake in P rats. Ceftriaxone 63-74 solute carrier family 1 member 3 Homo sapiens 179-184 25619881-8 2015 The reduction in ethanol intake was associated with significantly enhanced expression of GLT1, GLT1a, GLT1b, and xCT in the nucleus accumbens (NAc) and prefrontal cortex (PFC) of 5-day ceftriaxone-treated P rats. Ceftriaxone 185-196 solute carrier family 7 member 11 Homo sapiens 113-116 25619881-10 2015 Importantly, ceftriaxone-treated P rats (2 and 5 days) demonstrated enhanced phosphorylation of Akt and nuclear translocation of nuclear factor kappaB (NFkappaB) in the NAc and PFC compared to control animals. Ceftriaxone 13-24 AKT serine/threonine kinase 1 Homo sapiens 96-99 25619881-10 2015 Importantly, ceftriaxone-treated P rats (2 and 5 days) demonstrated enhanced phosphorylation of Akt and nuclear translocation of nuclear factor kappaB (NFkappaB) in the NAc and PFC compared to control animals. Ceftriaxone 13-24 nuclear factor kappa B subunit 1 Homo sapiens 129-150 25619881-10 2015 Importantly, ceftriaxone-treated P rats (2 and 5 days) demonstrated enhanced phosphorylation of Akt and nuclear translocation of nuclear factor kappaB (NFkappaB) in the NAc and PFC compared to control animals. Ceftriaxone 13-24 nuclear factor kappa B subunit 1 Homo sapiens 152-160 25619881-11 2015 CONCLUSIONS: These findings demonstrate that ceftriaxone treatment induced upregulation of GLT1, GLT1 isoforms, and xCT in association with activation of the Akt-NFkappaB signaling pathway. Ceftriaxone 45-56 solute carrier family 1 member 2 Homo sapiens 91-95 25619881-11 2015 CONCLUSIONS: These findings demonstrate that ceftriaxone treatment induced upregulation of GLT1, GLT1 isoforms, and xCT in association with activation of the Akt-NFkappaB signaling pathway. Ceftriaxone 45-56 solute carrier family 1 member 2 Homo sapiens 97-101 25619881-11 2015 CONCLUSIONS: These findings demonstrate that ceftriaxone treatment induced upregulation of GLT1, GLT1 isoforms, and xCT in association with activation of the Akt-NFkappaB signaling pathway. Ceftriaxone 45-56 solute carrier family 7 member 11 Homo sapiens 116-119 25619881-11 2015 CONCLUSIONS: These findings demonstrate that ceftriaxone treatment induced upregulation of GLT1, GLT1 isoforms, and xCT in association with activation of the Akt-NFkappaB signaling pathway. Ceftriaxone 45-56 AKT serine/threonine kinase 1 Homo sapiens 158-161 25619881-11 2015 CONCLUSIONS: These findings demonstrate that ceftriaxone treatment induced upregulation of GLT1, GLT1 isoforms, and xCT in association with activation of the Akt-NFkappaB signaling pathway. Ceftriaxone 45-56 nuclear factor kappa B subunit 1 Homo sapiens 162-170 25399934-5 2015 In comparison, C. difficile infection following ceftriaxone treatment was associated with increased expression of inflammatory cytokines and chemokines including Cxcl1, Cxcl2, Il1b, Il17f and Tnfa, as well as robust recruitment of Ly6C(Mid) Gr-1(High) neutrophils and Ly6C(High) Gr-1(Mid) monocytes and the development of severe colonic histopathology. Ceftriaxone 48-59 lymphocyte antigen 6 complex, locus G Mus musculus 242-246 26387186-5 2015 This sequence showed similar inhibition on the expression of GLT-la in sham and ceftriaxone (Cef)-treated rats. Ceftriaxone 80-91 solute carrier family 1 member 2 Rattus norvegicus 61-64 26387186-5 2015 This sequence showed similar inhibition on the expression of GLT-la in sham and ceftriaxone (Cef)-treated rats. Ceftriaxone 93-96 solute carrier family 1 member 2 Rattus norvegicus 61-64 25954150-8 2015 Regarding glutamatergic homeostasis, ceftriaxone, MS-153, and GPI-1046, which upregulate glutamate transporter 1 (GLT1) expression in mesocorticolimbic brain regions, reduce alcohol intake in genetic animal models of alcoholism. Ceftriaxone 37-48 solute carrier family 1 member 2 Homo sapiens 89-112 25954150-8 2015 Regarding glutamatergic homeostasis, ceftriaxone, MS-153, and GPI-1046, which upregulate glutamate transporter 1 (GLT1) expression in mesocorticolimbic brain regions, reduce alcohol intake in genetic animal models of alcoholism. Ceftriaxone 37-48 solute carrier family 1 member 2 Homo sapiens 114-118 26082590-2 2015 Although usually idiopathic, IgA antibody is occasionally induced by drugs (e.g., vancomycin, carbamazepine, ceftriaxone, and cyclosporine), malignancies, infections, and other causes. Ceftriaxone 109-120 CD79a molecule Homo sapiens 29-32 25399934-5 2015 In comparison, C. difficile infection following ceftriaxone treatment was associated with increased expression of inflammatory cytokines and chemokines including Cxcl1, Cxcl2, Il1b, Il17f and Tnfa, as well as robust recruitment of Ly6C(Mid) Gr-1(High) neutrophils and Ly6C(High) Gr-1(Mid) monocytes and the development of severe colonic histopathology. Ceftriaxone 48-59 lymphocyte antigen 6 complex, locus G Mus musculus 280-284 25710192-4 2015 OXA-160 and OXA-225 possess greatly enhanced hydrolytic activities against aztreonam, ceftazidime, cefotaxime, and ceftriaxone when compared to OXA-24/40 and OXA-23. Ceftriaxone 115-126 class D beta-lactamase OXA-23 Acinetobacter baumannii 158-164 25499022-2 2015 Ceftriaxone increases expression of glutamate transporter 1 (GLT-1) and affords neuroprotection. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 36-59 25499022-2 2015 Ceftriaxone increases expression of glutamate transporter 1 (GLT-1) and affords neuroprotection. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 61-66 25499022-8 2015 Lesioning also caused neurodegeneration in the hippocampal CA1 area and induced glutamatergic hyperactivity in the subthalamic nucleus, and both changes were suppressed by ceftriaxone. Ceftriaxone 172-183 carbonic anhydrase 1 Rattus norvegicus 59-62 25499022-9 2015 Increased GLT-1 expression and its co-localization with astrocytes were observed in the striatum and hippocampus in the ceftriaxone-treated animals. Ceftriaxone 120-131 solute carrier family 1 member 2 Rattus norvegicus 10-15 25499022-10 2015 To our knowledge, this is the first study showing a relationship between ceftriaxone-induced GLT-1 expression, neuroprotection, and improved cognition in a PD rat model. Ceftriaxone 73-84 solute carrier family 1 member 2 Rattus norvegicus 93-98 25816291-9 2015 Importantly, among ceftriaxone treated mice, B. burgdorferi DNA was detected by PCR uniformly in joint samples of mice infected with DbpA and B expressing bacteria, while this was not observed in mice infected with the DbpA and B deficient strain. Ceftriaxone 19-30 Y box protein 3 Mus musculus 133-137 25446343-5 2015 Changes in mechanical sensitivity were verified in bortezomib-treated animals, and these changes were prevented by co-treatment with a glial activation inhibitor (minocycline), a gap junction decoupler (carbenoxolone), and by a glutamate transporter upregulator (ceftriaxone). Ceftriaxone 263-274 solute carrier family 1 member 3 Rattus norvegicus 228-249 25297012-2 2014 In animal models, decreased excitatory aminoacid transporter 2 (EAAT2) overexpression delays disease onset and prolongs survival, and ceftriaxone increases EAAT2 activity. Ceftriaxone 134-145 solute carrier family 1 member 2 Homo sapiens 156-161 25905696-9 2015 After implementation of HAP a decreased use of ceftriaxone and cefuroxime was observed. Ceftriaxone 47-58 scaffold attachment factor B Homo sapiens 24-27 25270764-1 2015 Ceftriaxone(Cef) selectively increases the expression of glial glutamate transporter-1 (GLT-1), which was thought to be neuroprotective in some circumstances. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 57-93 25270764-12 2015 Ceftriaxone up-regulates GLT-1 expression and uptake of glutamate, diminishes the excitotoxicity of glutamate and then protects neurons against global brain ischemia. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 25-30 26635971-4 2015 GLT1 upregulators including ceftriaxone, a beta-lactam antibiotic, have been effective in attenuating drug-seeking and drug-consumption behavior in rodent models. Ceftriaxone 28-39 solute carrier family 1 member 2 Homo sapiens 0-4 25779570-0 2015 Ceftriaxone-resistant Salmonella enterica serotype typhimurium sequence type 313 from Kenyan patients is associated with the blaCTX-M-15 gene on a novel IncHI2 plasmid. Ceftriaxone 0-11 Beta-lactamase CTX-M-15 Salmonella enterica subsp. enterica serovar Typhimurium 125-136 25779570-5 2015 Resistance to beta-lactams, including to ceftriaxone, was associated with carriage of a combination of blaCTX-M-15, blaOXA-1, and blaTEM-1 genes. Ceftriaxone 41-52 Beta-lactamase CTX-M-15 Salmonella enterica subsp. enterica serovar Typhimurium 103-114 25779570-5 2015 Resistance to beta-lactams, including to ceftriaxone, was associated with carriage of a combination of blaCTX-M-15, blaOXA-1, and blaTEM-1 genes. Ceftriaxone 41-52 TEM-1 Salmonella enterica subsp. enterica serovar Typhimurium 130-138 26430455-2 2015 The purpose of the present study was to evaluate anti-hyperalgesic effect of repeated administration of ceftriaxone, which selectively activates and increases the expression of glutamate transporter, as well as minocycline, a selective inhibitor of microglia activation, either alone or together in Wistar rats subjected to the chronic constriction injury (CCI) of sciatic nerve. Ceftriaxone 104-115 solute carrier family 1 member 3 Rattus norvegicus 177-198 25312503-7 2014 GLT-1 translational activators such as ceftriaxone are found to have significant protective effects in ALS and epilepsy animal models, suggesting that this translational activation approach works well in rodents and that these compounds are worth further pursuit for various neurological disorders. Ceftriaxone 39-50 solute carrier family 1 member 2 Homo sapiens 0-5 25285631-5 2014 Here, we investigated whether SIRT2 deacetylates BubR1, which is a core component of the SAC; acetylation of BubR1 at lysine 250 (K250) during prometaphase inhibits its APC/C-dependent proteolysis and thus regulates timing in anaphase entry. Ceftriaxone 130-134 BUB1 mitotic checkpoint serine/threonine kinase B Homo sapiens 109-114 24535561-2 2014 We have previously shown that ceftriaxone, a beta-lactam antibiotic known to upregulate glutamate transporter 1 (GLT1), reduced ethanol intake after 5 weeks of free choice ethanol drinking paradigm in male alcohol-preferring (P) rats. Ceftriaxone 30-41 solute carrier family 1 member 2 Homo sapiens 88-111 24687412-2 2014 We have recently demonstrated that ceftriaxone treatment induced upregulation of GLT1 levels and attenuated ethanol intake; however, less is known about the involvement of xCT on ethanol intake. Ceftriaxone 35-46 solute carrier family 1 member 2 Rattus norvegicus 81-85 24776520-11 2014 Serotype 19A decreased 27% in the post-PCV13 period (P = 0.007), but accounted for all the isolates with penicillin minimal inhibitory concentration >= 4 mug/mL and ceftriaxone minimal inhibitory concentration >= 2 mug/mL. Ceftriaxone 168-179 SLAM family member 7 Homo sapiens 9-12 24985046-0 2014 Ceftriaxone pretreatment protects rats against cerebral ischemic injury by attenuating microglial activation-induced IL-1beta expression. Ceftriaxone 0-11 interleukin 1 beta Rattus norvegicus 117-125 24535561-9 2014 Western blot analysis of brain samples from animals euthanized 24 h after treatment with the last dose of ceftriaxone revealed a significant upregulation of cystine/glutamate exchanger (xCT) and GLT1 levels in prefrontal cortex, nucleus accumbens, and amygdala as compared to saline vehicle-treated group. Ceftriaxone 106-117 solute carrier family 7 member 11 Homo sapiens 186-189 24535561-9 2014 Western blot analysis of brain samples from animals euthanized 24 h after treatment with the last dose of ceftriaxone revealed a significant upregulation of cystine/glutamate exchanger (xCT) and GLT1 levels in prefrontal cortex, nucleus accumbens, and amygdala as compared to saline vehicle-treated group. Ceftriaxone 106-117 solute carrier family 1 member 2 Homo sapiens 195-199 24535561-2 2014 We have previously shown that ceftriaxone, a beta-lactam antibiotic known to upregulate glutamate transporter 1 (GLT1), reduced ethanol intake after 5 weeks of free choice ethanol drinking paradigm in male alcohol-preferring (P) rats. Ceftriaxone 30-41 solute carrier family 1 member 2 Homo sapiens 113-117 25053526-8 2014 However, post treatment with Ceftriaxone (100 and 200mg/kg) significantly improved the motor deficits and attenuated the oxidative damage indicating decreased rise of LPO and nitrite concentration and restored the decreased activities of endogenous antioxidant enzyme (Glutathione, Catalase, SOD). Ceftriaxone 29-40 lactoperoxidase Rattus norvegicus 167-170 25053526-8 2014 However, post treatment with Ceftriaxone (100 and 200mg/kg) significantly improved the motor deficits and attenuated the oxidative damage indicating decreased rise of LPO and nitrite concentration and restored the decreased activities of endogenous antioxidant enzyme (Glutathione, Catalase, SOD). Ceftriaxone 29-40 catalase Rattus norvegicus 282-290 25053526-9 2014 In addition Ceftriaxone also attenuates the pro-inflammatory cytokines like TNF-alpha and IL-beta in striatum region of MPTP induced PD in rats. Ceftriaxone 12-23 tumor necrosis factor Rattus norvegicus 76-85 25120981-4 2014 OBJECTIVE: This study is to find the susceptibility pattern of the novel adjuvant antimicrobial CSE 1034 a combination of Ceftriaxone+sulbactam+disodium edetate for the current ESBL and MBL isolates in a tertiary care centre. Ceftriaxone 122-133 EsbL Escherichia coli 177-181 24755306-9 2014 Furthermore, this study provides evidence that ceftriaxone inhibits MPTP lesion-induced dopaminergic degeneration in the nigrostriatal system, microglial activation in the SNc, and cell loss in the hippocampal CA1 area. Ceftriaxone 47-58 carbonic anhydrase 1 Rattus norvegicus 210-213 24743029-4 2014 RESULTS: A significant increase in the plasma level of anti-inflammatory cytokine IL-10 was observed in the ceftriaxone-treated group when compared with the saline-treated group in both the 2-day and 5-day treatments. Ceftriaxone 108-119 interleukin 10 Homo sapiens 82-87 24743029-5 2014 Furthermore, ceftriaxone treatment for 2 days induced reduction in TNFalpha level in both plasma and PFC. Ceftriaxone 13-24 tumor necrosis factor Homo sapiens 67-75 24743029-6 2014 Additionally, ceftriaxone treatment for 2 days significantly reduced the IFNgamma level in PFC. Ceftriaxone 14-25 interferon gamma Homo sapiens 73-81 24650590-0 2014 Ceftriaxone, a GLT-1 transporter activator, disrupts hippocampal learning in rats. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 15-20 24650590-3 2014 It has been shown that the beta-lactam antibiotic ceftriaxone (Rocephin) induces an up-regulation of the glutamate transporter GLT-1. Ceftriaxone 50-61 solute carrier family 1 member 2 Rattus norvegicus 127-132 24650590-3 2014 It has been shown that the beta-lactam antibiotic ceftriaxone (Rocephin) induces an up-regulation of the glutamate transporter GLT-1. Ceftriaxone 63-71 solute carrier family 1 member 2 Rattus norvegicus 127-132 24650590-11 2014 Our findings show that a potential up-regulation of GLT-1 via ceftriaxone administration has detrimental effects on spatial learning and memory in rats. Ceftriaxone 62-73 solute carrier family 1 member 2 Rattus norvegicus 52-57 24863918-4 2014 The stable high-affinity binding of CaMKII to distinct sites on nano-C60, mediated by amino acid residues D246 and K250 within the catalytic domain of CaMKIIalpha, but not the nonspecific adsorption of CaMKII to diamond nanoparticles, leads to functional consequences reminiscent of the NR2B-CaMKII interaction, including generation of autonomous CaMKII activity after Ca(2+) withdrawal, calmodulin trapping and CaMKII translocation to postsynaptic sites. Ceftriaxone 115-119 calcium/calmodulin dependent protein kinase II gamma Homo sapiens 36-42 24297323-3 2014 The beta-lactam antibiotic, ceftriaxone, increases the expression of glutamate transporter 1 (GLT-1), a glutamate transporter that plays a major role in glutamate clearance in central nervous system and may attenuate adverse behavioral or neurobiological function in other neurodegenerative disease models. Ceftriaxone 28-39 solute carrier family 1 member 2 Rattus norvegicus 69-92 24297323-3 2014 The beta-lactam antibiotic, ceftriaxone, increases the expression of glutamate transporter 1 (GLT-1), a glutamate transporter that plays a major role in glutamate clearance in central nervous system and may attenuate adverse behavioral or neurobiological function in other neurodegenerative disease models. Ceftriaxone 28-39 solute carrier family 1 member 2 Rattus norvegicus 94-99 24297323-7 2014 When ceftriaxone was given at the time of 6-OHDA, TH loss was ~57% compared to ~85% in temporally matched vehicle-injected controls and amphetamine-induced rotation was reduced about 2-fold. Ceftriaxone 5-16 tyrosine hydroxylase Rattus norvegicus 50-52 24297323-0 2014 Ceftriaxone increases glutamate uptake and reduces striatal tyrosine hydroxylase loss in 6-OHDA Parkinson"s model. Ceftriaxone 0-11 tyrosine hydroxylase Rattus norvegicus 60-80 25120981-11 2014 CSE 1034 (Ceftriaxone+sulbactam+disodium edetate) showed fairly good in-vitro susceptibility for these ESBL and MBL producing isolates. Ceftriaxone 10-21 EsbL Escherichia coli 103-107 24503119-6 2014 IL-18(+/+) mice cured of pneumococcal meningitis with four doses of ceftriaxone, initiated at 20 h post-inoculation, showed enduring sequelae. Ceftriaxone 68-79 interleukin 18 Mus musculus 0-5 24452391-9 2014 Finally, ceftriaxone treatment was associated with lasting upregulation of ethanol withdrawal-induced downregulation of EAAT2 in the striatum. Ceftriaxone 9-20 solute carrier family 1 member 2 Rattus norvegicus 120-125 24402134-2 2014 Recent evidence suggests that upregulation of the major glutamate transporter, GLT-1, by the beta-lactam antibiotic, ceftriaxone, can increase the removal of synaptic glutamate without producing noticeable side effects, and may provide an effective alternative to receptor antagonists for several neurodegenerative diseases. Ceftriaxone 117-128 solute carrier family 1 member 2 Homo sapiens 79-84 24402134-7 2014 These therapeutic effects of ceftriaxone were decreased by an injection of 10 mg/kg of the selective GLT-1 antagonist, dihydrokainate (DHK), and were still evident 69 days after the cessation of ceftriaxone injections. Ceftriaxone 29-40 solute carrier family 1 member 2 Homo sapiens 101-106 24402134-9 2014 CONCLUSIONS: These data suggest that ceftriaxone, by producing a long-term increase in GLT-1 function and increasing the removal of synaptic glutamate, may offer several advantages over L-DOPA as therapy for PD. Ceftriaxone 37-48 solute carrier family 1 member 2 Homo sapiens 87-92 24631672-0 2014 Ceftriaxone alleviates early brain injury after subarachnoid hemorrhage by increasing excitatory amino acid transporter 2 expression via the PI3K/Akt/NF-kappaB signaling pathway. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 86-121 24631672-0 2014 Ceftriaxone alleviates early brain injury after subarachnoid hemorrhage by increasing excitatory amino acid transporter 2 expression via the PI3K/Akt/NF-kappaB signaling pathway. Ceftriaxone 0-11 AKT serine/threonine kinase 1 Rattus norvegicus 146-149 24631672-2 2014 The aim of this study was to explore the neuroprotective effect of ceftriaxone (CEF), a potent compound that up-regulates EAAT2, against EBI and the potential mechanisms using in vitro experiments and a rat model of SAH. Ceftriaxone 67-78 solute carrier family 1 member 2 Rattus norvegicus 122-127 24631672-2 2014 The aim of this study was to explore the neuroprotective effect of ceftriaxone (CEF), a potent compound that up-regulates EAAT2, against EBI and the potential mechanisms using in vitro experiments and a rat model of SAH. Ceftriaxone 80-83 solute carrier family 1 member 2 Rattus norvegicus 122-127 24631672-8 2014 These findings suggest that CEF may exert significant protective effects against EBI following SAH by modulating the PI3K/Akt/NF-kappaB signaling pathway. Ceftriaxone 28-31 AKT serine/threonine kinase 1 Rattus norvegicus 122-125 24452391-0 2014 Attenuation of ethanol withdrawal by ceftriaxone-induced upregulation of glutamate transporter EAAT2. Ceftriaxone 37-48 solute carrier family 1 member 2 Rattus norvegicus 95-100 24452391-3 2014 Using a rat model of ethanol withdrawal, we tested whether ceftriaxone, a beta-lactam antibiotic known to increase the expression and activity of glutamate uptake transporter EAAT2, reduces the occurrence or severity of ethanol withdrawal manifestations. Ceftriaxone 59-70 solute carrier family 1 member 2 Rattus norvegicus 175-180 25146518-2 2014 METHODS: A beta-lactam antibiotic, ceftriaxone (CTX) was used to selectively induce transcription of the gene encoding GLT-1 and upregulate GLT-1 expression as an agonist. Ceftriaxone 35-46 solute carrier family 1 member 2 Rattus norvegicus 119-124 25146518-2 2014 METHODS: A beta-lactam antibiotic, ceftriaxone (CTX) was used to selectively induce transcription of the gene encoding GLT-1 and upregulate GLT-1 expression as an agonist. Ceftriaxone 35-46 solute carrier family 1 member 2 Rattus norvegicus 140-145 24277205-3 2014 The beta-lactam antibiotic ceftriaxone (CTX) has been reported to induce neuroprotection in animal models of diverse neurologic diseases via up-regulation of GLT-1. Ceftriaxone 27-38 solute carrier family 1 member 2 Rattus norvegicus 158-163 23941639-10 2014 CONCLUSION: Empirical ceftriaxone therapy for APN caused by ESBL-producing E. coli is inappropriate, and consequently can delay recovery and result in longer hospitalization. Ceftriaxone 22-33 EsbL Escherichia coli 60-64 24071615-1 2014 BACKGROUND: The beta-lactam antibiotic ceftriaxone stimulates glutamate transporter GLT-1 expression and is effective in neuropathic and visceral pain models. Ceftriaxone 39-50 solute carrier family 1 member 2 Rattus norvegicus 84-89 24741055-8 2014 Ceftriaxone-induced inhibition of reinstated heroin seeking was blocked by morpholino-antisense targeting GLT-1 synthesis. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 106-111 23941639-1 2014 BACKGROUND: Ceftriaxone is frequently administered empirically for hospitalized patients with acute pyelonephritis (APN) due to prevalent quinolone resistance in our hospital; however, its use is inappropriate for extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli, an increasing problem. Ceftriaxone 12-23 EsbL Escherichia coli 248-252 24099687-0 2014 Ceftriaxone blocks the polymerization of alpha-synuclein and exerts neuroprotective effects in vitro. Ceftriaxone 0-11 synuclein alpha Rattus norvegicus 41-56 23941639-2 2014 METHODS: A retrospective, 1:2 matched cohort study was performed to evaluate the impact of ESBL on APN treated with empirical ceftriaxone. Ceftriaxone 126-137 EsbL Escherichia coli 91-95 24234454-5 2014 By NMR structure determination and docking approaches, we built a 3D model of the Snup13p-Rsa1p interface, suggesting that residues R249, R246 and K250 in Rsa1p and E72 and D73 in Snu13p form a network of electrostatic interactions shielded from the solvent by hydrophobic residues from both proteins and that residue W253 of Rsa1p is inserted in a hydrophobic cavity of Snu13p. Ceftriaxone 147-151 Rsa1p Saccharomyces cerevisiae S288C 90-95 24234454-5 2014 By NMR structure determination and docking approaches, we built a 3D model of the Snup13p-Rsa1p interface, suggesting that residues R249, R246 and K250 in Rsa1p and E72 and D73 in Snu13p form a network of electrostatic interactions shielded from the solvent by hydrophobic residues from both proteins and that residue W253 of Rsa1p is inserted in a hydrophobic cavity of Snu13p. Ceftriaxone 147-151 Rsa1p Saccharomyces cerevisiae S288C 155-160 24234454-5 2014 By NMR structure determination and docking approaches, we built a 3D model of the Snup13p-Rsa1p interface, suggesting that residues R249, R246 and K250 in Rsa1p and E72 and D73 in Snu13p form a network of electrostatic interactions shielded from the solvent by hydrophobic residues from both proteins and that residue W253 of Rsa1p is inserted in a hydrophobic cavity of Snu13p. Ceftriaxone 147-151 Rsa1p Saccharomyces cerevisiae S288C 155-160 24234454-5 2014 By NMR structure determination and docking approaches, we built a 3D model of the Snup13p-Rsa1p interface, suggesting that residues R249, R246 and K250 in Rsa1p and E72 and D73 in Snu13p form a network of electrostatic interactions shielded from the solvent by hydrophobic residues from both proteins and that residue W253 of Rsa1p is inserted in a hydrophobic cavity of Snu13p. Ceftriaxone 147-151 RNA binding protein SNU13 Saccharomyces cerevisiae S288C 371-377 24099687-4 2014 Since, at the molecular level, neuronal alpha-synuclein inclusions and pathological alpha-synuclein transmission play a leading role in initiation of Parkinson-like neurodegeneration, we thought of investigating, by circular dichroism spectroscopy, the capability of ceftriaxone to interact with alpha-synuclein. Ceftriaxone 267-278 synuclein alpha Rattus norvegicus 40-55 24099687-5 2014 We found that ceftriaxone binds with good affinity to alpha-synuclein and blocks its in vitro polymerization. Ceftriaxone 14-25 synuclein alpha Rattus norvegicus 54-69 24696553-12 2014 All ESBL producers demonstrated minimum inhibitory concentration levels >=2 mug/ml towards cefotaxime, ceftazidime and ceftriaxone. Ceftriaxone 122-133 EsbL Escherichia coli 4-8 25028668-7 2014 Ceftriaxone attenuated the increased levels of Bax and cleaved forms of caspases 3 and 9, while it increased Bcl2 levels. Ceftriaxone 0-11 BCL2 associated X, apoptosis regulator Rattus norvegicus 47-50 25028668-7 2014 Ceftriaxone attenuated the increased levels of Bax and cleaved forms of caspases 3 and 9, while it increased Bcl2 levels. Ceftriaxone 0-11 caspase 9 Rattus norvegicus 72-88 25028668-7 2014 Ceftriaxone attenuated the increased levels of Bax and cleaved forms of caspases 3 and 9, while it increased Bcl2 levels. Ceftriaxone 0-11 BCL2, apoptosis regulator Rattus norvegicus 109-113 25028668-11 2014 CONCLUSION: Our results suggest that ceftriaxone, an upregulator/activator of GLT1, could concomitantly reduce oxidative stress and apoptosis and producing its new analogs lacking antimicrobial activity may represent a novel approach for neuropathic pain treatment. Ceftriaxone 37-48 solute carrier family 1 member 2 Rattus norvegicus 78-82 24123246-11 2014 Ceftriaxone also reduced (P < 0.024) spinal GFAP and GLAST expression, and neuronal hyperexcitability in the spinal dorsal horn, restoring the proportion of spinal neurons classified as wide dynamic range to that of normal. Ceftriaxone 0-11 solute carrier family 1 member 3 Rattus norvegicus 56-61 23510201-0 2013 Ceftriaxone treatment after traumatic brain injury restores expression of the glutamate transporter, GLT-1, reduces regional gliosis, and reduces post-traumatic seizures in the rat. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 101-106 24123246-11 2014 Ceftriaxone also reduced (P < 0.024) spinal GFAP and GLAST expression, and neuronal hyperexcitability in the spinal dorsal horn, restoring the proportion of spinal neurons classified as wide dynamic range to that of normal. Ceftriaxone 0-11 glial fibrillary acidic protein Rattus norvegicus 47-51 24123246-0 2014 Upregulation of GLT-1 by treatment with ceftriaxone alleviates radicular pain by reducing spinal astrocyte activation and neuronal hyperexcitability. Ceftriaxone 40-51 solute carrier family 1 member 2 Rattus norvegicus 16-21 23973312-3 2013 The impairment of LTP and memory formation of AQP4 knockout (KO) mice was mediated by the downregulation of glutamate transporter-1 (GLT-1) expression/function, since it can be rescued by beta-lactam antibiotic ceftriaxone (Cef), a potent GLT-1 stimulator. Ceftriaxone 211-222 aquaporin 4 Mus musculus 46-50 23973312-3 2013 The impairment of LTP and memory formation of AQP4 knockout (KO) mice was mediated by the downregulation of glutamate transporter-1 (GLT-1) expression/function, since it can be rescued by beta-lactam antibiotic ceftriaxone (Cef), a potent GLT-1 stimulator. Ceftriaxone 211-222 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 133-138 23973312-3 2013 The impairment of LTP and memory formation of AQP4 knockout (KO) mice was mediated by the downregulation of glutamate transporter-1 (GLT-1) expression/function, since it can be rescued by beta-lactam antibiotic ceftriaxone (Cef), a potent GLT-1 stimulator. Ceftriaxone 224-227 aquaporin 4 Mus musculus 46-50 23973312-3 2013 The impairment of LTP and memory formation of AQP4 knockout (KO) mice was mediated by the downregulation of glutamate transporter-1 (GLT-1) expression/function, since it can be rescued by beta-lactam antibiotic ceftriaxone (Cef), a potent GLT-1 stimulator. Ceftriaxone 224-227 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 108-131 23973312-3 2013 The impairment of LTP and memory formation of AQP4 knockout (KO) mice was mediated by the downregulation of glutamate transporter-1 (GLT-1) expression/function, since it can be rescued by beta-lactam antibiotic ceftriaxone (Cef), a potent GLT-1 stimulator. Ceftriaxone 224-227 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 133-138 24274894-9 2013 On initial screening with ceftriaxone (30 mug) disc showing resistance was then confirmed for ESBL production by phenotypic confirmatory disc diffusion test (PCDDT) using ceftazidime (30 ug) and ceftazidime + clavulanic acid (30 mug + 10ug) disc as per guidelines of CLSI (2011). Ceftriaxone 26-37 EsbL Escherichia coli 94-98 24274894-13 2013 These ESBL - producer uropathogens showed high degree of resistance to ceftriaxone (100.0%), amoxycillin, fluoroquinolones and co-trimoxazole. Ceftriaxone 71-82 EsbL Escherichia coli 6-10 24071028-10 2013 In addition, there was a significant reduction in rates of susceptibility of serotype 19A isolates to penicillin, cefotaxime and ceftriaxone but not to azithromycin or any quinolone tested compared with those of non-19A isolates. Ceftriaxone 129-140 SLAM family member 7 Homo sapiens 86-89 23893122-0 2013 Ceftriaxone treatment affects the levels of GLT1 and ENT1 as well as ethanol intake in alcohol-preferring rats. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 44-48 23893122-0 2013 Ceftriaxone treatment affects the levels of GLT1 and ENT1 as well as ethanol intake in alcohol-preferring rats. Ceftriaxone 0-11 solute carrier family 29 member 1 Rattus norvegicus 53-57 23510201-6 2013 However, the loss of GLT-1 expression was reversed by treatment with ceftriaxone (200 mg/kg, daily, intraperitoneally). Ceftriaxone 69-80 solute carrier family 1 member 2 Rattus norvegicus 21-26 23510201-7 2013 We found that ceftriaxone treatment also decreased the level of regional GFAP expression by 43% in the lesioned cortex, relative to control treatment with saline (n=7 per group; p<0.05), and, 12 weeks after injury, reduced cumulative post-traumatic seizure duration (n=6 rats in the ceftriaxone treatment group and n=5 rats in the saline control group; p<0.001). Ceftriaxone 14-25 glial fibrillary acidic protein Rattus norvegicus 73-77 23985782-2 2014 In particular, compounds that increase expression of the astroglial glutamate transporter GLT-1 (N-acetylcysteine and ceftriaxone) can decrease measures of drug seeking. Ceftriaxone 118-129 solute carrier family 1 member 2 Rattus norvegicus 90-95 23642110-5 2013 RECENT ADVANCES: Increased expression of GLT1 following treatment with ceftriaxone, a beta-lactam antibiotic, increases striatal glutamate uptake and AA release and also improves the HD behavioral phenotype. Ceftriaxone 71-82 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 41-45 23973312-0 2013 Chronic ceftriaxone treatment rescues hippocampal memory deficit in AQP4 knockout mice via activation of GLT-1. Ceftriaxone 8-19 aquaporin 4 Mus musculus 68-72 23973312-0 2013 Chronic ceftriaxone treatment rescues hippocampal memory deficit in AQP4 knockout mice via activation of GLT-1. Ceftriaxone 8-19 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 105-110 23893122-3 2013 We examined, then, whether ceftriaxone (CEF) would affect both GLT1 and ENT1 levels in these brain regions. Ceftriaxone 27-38 solute carrier family 1 member 2 Rattus norvegicus 63-67 23893122-3 2013 We examined, then, whether ceftriaxone (CEF) would affect both GLT1 and ENT1 levels in these brain regions. Ceftriaxone 27-38 solute carrier family 29 member 1 Rattus norvegicus 72-76 23893122-3 2013 We examined, then, whether ceftriaxone (CEF) would affect both GLT1 and ENT1 levels in these brain regions. Ceftriaxone 40-43 solute carrier family 1 member 2 Rattus norvegicus 63-67 23893122-3 2013 We examined, then, whether ceftriaxone (CEF) would affect both GLT1 and ENT1 levels in these brain regions. Ceftriaxone 40-43 solute carrier family 29 member 1 Rattus norvegicus 72-76 23893122-11 2013 These findings provide evidence for potential regulatory effects of CEF on both GLT1 and ENT1 expression in reducing ethanol intake. Ceftriaxone 68-71 solute carrier family 1 member 2 Rattus norvegicus 80-84 23893122-11 2013 These findings provide evidence for potential regulatory effects of CEF on both GLT1 and ENT1 expression in reducing ethanol intake. Ceftriaxone 68-71 solute carrier family 29 member 1 Rattus norvegicus 89-93 23510201-3 2013 We tested, by immunoblot, in the rat lateral fluid percussion injury TBI model whether GLT-1 expression is depressed in the cortex after TBI, and whether GLT-1 expression after TBI is restored after treatment with ceftriaxone, a well-tolerated beta-lactam antibiotic previously shown to enhance GLT-1 expression in noninjured animals. Ceftriaxone 214-225 solute carrier family 1 member 2 Rattus norvegicus 154-159 23510201-3 2013 We tested, by immunoblot, in the rat lateral fluid percussion injury TBI model whether GLT-1 expression is depressed in the cortex after TBI, and whether GLT-1 expression after TBI is restored after treatment with ceftriaxone, a well-tolerated beta-lactam antibiotic previously shown to enhance GLT-1 expression in noninjured animals. Ceftriaxone 214-225 solute carrier family 1 member 2 Rattus norvegicus 154-159 23638698-8 2013 Chronic treatment with ceftriaxone (200 mg kg(-1) i.p., once daily, 7 days), an EAAT2 expression enhancer, increased the actions of glutamate and DHK, suggesting a functional impact of EAAT2 up-regulation on the glutamatergic system. Ceftriaxone 23-34 solute carrier family 1 member 2 Rattus norvegicus 80-85 23638698-8 2013 Chronic treatment with ceftriaxone (200 mg kg(-1) i.p., once daily, 7 days), an EAAT2 expression enhancer, increased the actions of glutamate and DHK, suggesting a functional impact of EAAT2 up-regulation on the glutamatergic system. Ceftriaxone 23-34 solute carrier family 1 member 2 Rattus norvegicus 185-190 23628489-10 2013 Our immunohistochemistry findings indicate that ceftriaxone increases GLT-1 expression in CA1, CA3 and DG regions of hippocampus, especially with the dose of 200 mg/kg. Ceftriaxone 48-59 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 70-75 23586612-5 2013 Administration of ceftriaxone, an antibiotic that increases the functional expression of GLT-1, can improve the behavioral phenotype of the R6/2 mouse model of HD. Ceftriaxone 18-29 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 89-94 23503685-3 2013 We hypothesized that ceftriaxone, a GLT-1 and system xC- activator, would decrease murine behavioral aspects of nicotine dependence. Ceftriaxone 21-32 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 36-41 23523747-3 2013 Recently, a neuroprotective effect of preconditioning with a beta-lactam antibiotic ceftriaxone (CTX) that increases expression of GLT-1 has been reported in animal models of focal ischemia. Ceftriaxone 84-95 solute carrier family 1 member 2 Rattus norvegicus 131-136 23628489-10 2013 Our immunohistochemistry findings indicate that ceftriaxone increases GLT-1 expression in CA1, CA3 and DG regions of hippocampus, especially with the dose of 200 mg/kg. Ceftriaxone 48-59 carbonic anhydrase 3 Mus musculus 95-98 23628489-10 2013 Our immunohistochemistry findings indicate that ceftriaxone increases GLT-1 expression in CA1, CA3 and DG regions of hippocampus, especially with the dose of 200 mg/kg. Ceftriaxone 48-59 carbonic anhydrase 1 Mus musculus 90-93 23719800-2 2013 Decreased expression of glutamate type I transporter (GLT1), which is responsible for >90% of glutamate clearance, occurs in the core of rats withdrawn from cocaine self-administration, while treatment with ceftriaxone, a beta-lactam antibiotic previously shown to increase GLT1 expression and function in rodents, upregulates GLT1 and attenuates cue-induced cocaine reinstatement. Ceftriaxone 210-221 solute carrier family 1 member 2 Rattus norvegicus 54-58 23537837-2 2013 We recently reported that the administration of ceftriaxone (CEF), a beta-lactam antibiotic known to upregulate glutamate transporter 1 (GLT1) levels/activity, decreased the maintenance of EtOH intake in adult male alcohol-preferring (P) rats. Ceftriaxone 48-59 solute carrier family 1 member 2 Rattus norvegicus 112-135 23537837-2 2013 We recently reported that the administration of ceftriaxone (CEF), a beta-lactam antibiotic known to upregulate glutamate transporter 1 (GLT1) levels/activity, decreased the maintenance of EtOH intake in adult male alcohol-preferring (P) rats. Ceftriaxone 48-59 solute carrier family 1 member 2 Rattus norvegicus 137-141 23537837-2 2013 We recently reported that the administration of ceftriaxone (CEF), a beta-lactam antibiotic known to upregulate glutamate transporter 1 (GLT1) levels/activity, decreased the maintenance of EtOH intake in adult male alcohol-preferring (P) rats. Ceftriaxone 61-64 solute carrier family 1 member 2 Rattus norvegicus 112-135 23537837-2 2013 We recently reported that the administration of ceftriaxone (CEF), a beta-lactam antibiotic known to upregulate glutamate transporter 1 (GLT1) levels/activity, decreased the maintenance of EtOH intake in adult male alcohol-preferring (P) rats. Ceftriaxone 61-64 solute carrier family 1 member 2 Rattus norvegicus 137-141 23725677-1 2013 UNLABELLED: Repeated injections of the antibiotic ceftriaxone cause analgesia in rodents by upregulating the glutamate transporter, GLT-1. Ceftriaxone 50-61 solute carrier family 1 member 2 Homo sapiens 132-137 23725677-9 2013 A single intraperitoneal injection of ceftriaxone (200 mg/kg), but not cefazoline (200 mg/kg), caused analgesia in mouse models of inflammatory or postsurgical pain, and upregulated GLT-1 in the spinal cord. Ceftriaxone 38-49 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 182-187 23725677-13 2013 A single dose of ceftriaxone could also relieve inflammatory and postsurgical pain and upregulate GLT-1 expression in mice. Ceftriaxone 17-28 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 98-103 23719800-2 2013 Decreased expression of glutamate type I transporter (GLT1), which is responsible for >90% of glutamate clearance, occurs in the core of rats withdrawn from cocaine self-administration, while treatment with ceftriaxone, a beta-lactam antibiotic previously shown to increase GLT1 expression and function in rodents, upregulates GLT1 and attenuates cue-induced cocaine reinstatement. Ceftriaxone 210-221 solute carrier family 1 member 2 Rattus norvegicus 277-281 23719800-2 2013 Decreased expression of glutamate type I transporter (GLT1), which is responsible for >90% of glutamate clearance, occurs in the core of rats withdrawn from cocaine self-administration, while treatment with ceftriaxone, a beta-lactam antibiotic previously shown to increase GLT1 expression and function in rodents, upregulates GLT1 and attenuates cue-induced cocaine reinstatement. Ceftriaxone 210-221 solute carrier family 1 member 2 Rattus norvegicus 277-281 23719800-7 2013 To localize the effects of GLT1 upregulation within NAc, we tested the hypothesis that blockade of GLT1 in NAc core, but not shell, would reverse the ceftriaxone-mediated effect. Ceftriaxone 150-161 solute carrier family 1 member 2 Rattus norvegicus 99-103 23719800-9 2013 Our results reveal that the ceftriaxone-mediated attenuation of cue-induced cocaine reinstatement is reversed by GLT1 blockade in core, but not shell, and further implicate core GLT1 as a potential therapeutic target for cocaine relapse. Ceftriaxone 28-39 solute carrier family 1 member 2 Rattus norvegicus 113-117 23719800-9 2013 Our results reveal that the ceftriaxone-mediated attenuation of cue-induced cocaine reinstatement is reversed by GLT1 blockade in core, but not shell, and further implicate core GLT1 as a potential therapeutic target for cocaine relapse. Ceftriaxone 28-39 solute carrier family 1 member 2 Rattus norvegicus 178-182 23047495-1 2013 PURPOSE: Ceftriaxone, a beta-lactam antibiotic, can selectively enhance the expression of glutamate transporter 1 (GLT1), the most abundant astrocytic glutamate transporter expressed in the cortex. Ceftriaxone 9-20 solute carrier family 1 member 2 Rattus norvegicus 90-113 23594486-8 2013 We also found that the administration of beta-lactam antibiotic ceftriaxone increased GLT-1 protein expression and significantly reduced HI-induced brain injury in neonatal DEX-treated rats. Ceftriaxone 64-75 solute carrier family 1 member 2 Rattus norvegicus 86-91 24589574-10 2013 The logistic regression analysis revealed the associations between CTX-M-15 and resistance to ceftriaxone, between CTX-M-14 and resistance to cefoxitin, aztreonam, ampicillin/sulbactam, ticarcillin/clavulanic acid, and tobramycin, and between CTX-M-92 and resistance to cefepime, piperacillin/tazobactam, gentamicin, and tobramycin. Ceftriaxone 94-105 hypothetical protein Escherichia coli 67-75 23527251-7 2013 Serum TNF-alpha decreased significantly in surviving rats treated with ceftriaxone plus anti-TNF-alpha mAb but not in treated with antibiotics alone. Ceftriaxone 71-82 tumor necrosis factor Rattus norvegicus 6-15 23613806-1 2013 OBJECTIVES: Ceftriaxone increases expression of the astrocytic glutamate transporter, EAAT2, which might protect from glutamate-mediated excitotoxicity. Ceftriaxone 12-23 solute carrier family 1 member 2 Homo sapiens 86-91 23529866-18 2013 Ceftriaxone, cefotaxime, ceftazidime, cefixime and cefepime have been studied in children and are all able to adequately penetrate the CSF. Ceftriaxone 0-11 colony stimulating factor 2 Homo sapiens 135-138 23291347-7 2013 To determine if changes in the levels of EAAT-2 were responsible for the observed changes in nociceptive sensitivity and cognitive deficits, we treated EAE mice with the beta-lactam antibiotic ceftriaxone, an agent known to increase glutamate transporter levels in vivo. Ceftriaxone 193-204 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 41-47 23032072-9 2013 Ceftriaxone, an antibiotic compound known to increase EAAT2 expression and function, elevated not only EAAT2 but also AQP4 expression in the striatum. Ceftriaxone 0-11 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 54-59 23032072-9 2013 Ceftriaxone, an antibiotic compound known to increase EAAT2 expression and function, elevated not only EAAT2 but also AQP4 expression in the striatum. Ceftriaxone 0-11 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 103-108 23032072-9 2013 Ceftriaxone, an antibiotic compound known to increase EAAT2 expression and function, elevated not only EAAT2 but also AQP4 expression in the striatum. Ceftriaxone 0-11 aquaporin 4 Mus musculus 118-122 23032072-10 2013 Furthermore, ceftriaxone reduced ethanol drinking, suggesting that ENT1-mediated downregulation of EAAT2 and AQP4 expression contributes to excessive ethanol consumption in our mouse model. Ceftriaxone 13-24 solute carrier family 29 (nucleoside transporters), member 1 Mus musculus 67-71 23032072-10 2013 Furthermore, ceftriaxone reduced ethanol drinking, suggesting that ENT1-mediated downregulation of EAAT2 and AQP4 expression contributes to excessive ethanol consumption in our mouse model. Ceftriaxone 13-24 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 99-104 23032072-10 2013 Furthermore, ceftriaxone reduced ethanol drinking, suggesting that ENT1-mediated downregulation of EAAT2 and AQP4 expression contributes to excessive ethanol consumption in our mouse model. Ceftriaxone 13-24 aquaporin 4 Mus musculus 109-113 22998524-3 2013 In this study, GLT-1 up-regulation was induced by ceftriaxone, and L-glutamate was added to induce glutamate toxicity in primary cultured rat cortical cells. Ceftriaxone 50-61 solute carrier family 1 member 2 Rattus norvegicus 15-20 22998524-4 2013 The results showed that up-regulated GLT-1 induced by 1 muM ceftriaxone for 2 days markedly increased cell viability, decreased apoptotic cell death and alleviated ultrastructural damage induced by 50 muM glutamate 15 min. Ceftriaxone 60-71 solute carrier family 1 member 2 Rattus norvegicus 37-42 22998524-9 2013 In conclusion, GLT-1 up-regulation induced by ceftriaxone plays a positive glutamate transporting role against glutamate toxicity in primary cultured rat cortical cells. Ceftriaxone 46-57 solute carrier family 1 member 2 Rattus norvegicus 15-20 24409344-6 2013 We recently reported that treatment of alcohol-preferring rats with compounds ceftriaxone and GPI-1046, known to upregulate GLT1 levels, showed reduction in alcohol intake and attenuation of relapse-like ethanol-drinking behaviour. Ceftriaxone 78-89 solute carrier family 1 member 2 Rattus norvegicus 124-128 23047495-1 2013 PURPOSE: Ceftriaxone, a beta-lactam antibiotic, can selectively enhance the expression of glutamate transporter 1 (GLT1), the most abundant astrocytic glutamate transporter expressed in the cortex. Ceftriaxone 9-20 solute carrier family 1 member 2 Rattus norvegicus 115-119 23047495-4 2013 In adult male rats, ceftriaxone (200 mg/kg) or vehicle was intraperitoneally injected daily for 5 days, a treatment regime previously established to upregulate GLT-1. Ceftriaxone 20-31 solute carrier family 1 member 2 Rattus norvegicus 160-165 27335870-0 2013 Characterization of the Visceral Antinociceptive Effect of Glial Glutamate Transporter GLT-1 Upregulation by Ceftriaxone. Ceftriaxone 109-120 solute carrier family 1 member 2 Homo sapiens 87-92 23059796-1 2012 We have previously shown that ceftriaxone, beta-lactam antibiotic known to upregulate glutamate transporter 1 (GLT1), reduced ethanol intake in alcohol-preferring (P) rats. Ceftriaxone 30-41 solute carrier family 1 member 2 Rattus norvegicus 86-109 23059796-1 2012 We have previously shown that ceftriaxone, beta-lactam antibiotic known to upregulate glutamate transporter 1 (GLT1), reduced ethanol intake in alcohol-preferring (P) rats. Ceftriaxone 30-41 solute carrier family 1 member 2 Rattus norvegicus 111-115 22982625-8 2012 Administration of ceftriaxone, an astrocyte glutamate transporter enhancer, to axotomized mice significantly decreased the immunoreactivity for S100A6. Ceftriaxone 18-29 S100 calcium binding protein A6 (calcyclin) Mus musculus 144-150 27335870-2 2013 The present work further characterized the effect of ceftriaxone- (CTX-) mediated GLT-1 upregulation on visceral hyperalgesia. Ceftriaxone 53-64 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 67-70 27335870-2 2013 The present work further characterized the effect of ceftriaxone- (CTX-) mediated GLT-1 upregulation on visceral hyperalgesia. Ceftriaxone 53-64 solute carrier family 1 member 2 Homo sapiens 82-87 22978524-6 2012 This process was inhibited by the simultaneous injection of unlabeled PGE(2) and beta-lactam antibiotics, such as benzylpenicillin, cefazolin, and ceftriaxone, which are substrates and/or inhibitors of organic anion transporter 3 (OAT3). Ceftriaxone 148-159 solute carrier family 22 member 8 Homo sapiens 203-230 22962305-0 2012 Ceftriaxone, an FDA-approved cephalosporin antibiotic, suppresses lung cancer growth by targeting Aurora B. Ceftriaxone 0-11 aurora kinase B Homo sapiens 98-106 22962305-6 2012 Kinase profiling results predicted that Aurora B might be a potential "off" target of ceftriaxone. Ceftriaxone 86-97 aurora kinase B Homo sapiens 40-48 22962305-7 2012 Pull-down assay data confirmed that ceftriaxone could bind with Aurora B in vitro and in A549 cells. Ceftriaxone 36-47 aurora kinase B Homo sapiens 64-72 22962305-8 2012 Furthermore, ceftriaxone (500 microM) suppressed anchorage-independent cell growth by targeting Aurora B in A549, H520 and H1650 lung cancer cells. Ceftriaxone 13-24 aurora kinase B Homo sapiens 96-104 22962305-9 2012 Importantly, in vivo xenograft animal model results showed that ceftriaxone effectively suppressed A549 and H520 lung tumor growth by inhibiting Aurora B. Ceftriaxone 64-75 aurora kinase B Homo sapiens 145-153 22962305-10 2012 These data suggest the anticancer efficacy of ceftriaxone for the treatment of lung cancers through its inhibition of Aurora B. Ceftriaxone 46-57 aurora kinase B Homo sapiens 118-126 23169700-0 2012 Biophysical study on the interaction of ceftriaxone sodium with bovine serum albumin using spectroscopic methods. Ceftriaxone 40-58 albumin Homo sapiens 71-84 23169700-1 2012 The interaction of ceftriaxone sodium (CS), a cephalosporin antibiotic, with the major transport protein, bovine serum albumin (BSA), was investigated using different spectroscopic techniques such as fluorescence, circular dichroism (CD), and UV-vis spectroscopy. Ceftriaxone 19-37 albumin Homo sapiens 113-126 23169700-1 2012 The interaction of ceftriaxone sodium (CS), a cephalosporin antibiotic, with the major transport protein, bovine serum albumin (BSA), was investigated using different spectroscopic techniques such as fluorescence, circular dichroism (CD), and UV-vis spectroscopy. Ceftriaxone 39-41 albumin Homo sapiens 113-126 22978524-6 2012 This process was inhibited by the simultaneous injection of unlabeled PGE(2) and beta-lactam antibiotics, such as benzylpenicillin, cefazolin, and ceftriaxone, which are substrates and/or inhibitors of organic anion transporter 3 (OAT3). Ceftriaxone 148-159 solute carrier family 22 member 8 Homo sapiens 232-236 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 35-46 interleukin 10 Rattus norvegicus 219-224 23021150-9 2012 Treatment with the beta-lactam antibiotic ceftriaxone increased the expression of glutamate transporter 1 (Glt1) in the dorsal horn after SNI, raised transmitter uptake, and lowered extracellular glutamate. Ceftriaxone 42-53 solute carrier family 1 member 2 Rattus norvegicus 82-105 23021150-9 2012 Treatment with the beta-lactam antibiotic ceftriaxone increased the expression of glutamate transporter 1 (Glt1) in the dorsal horn after SNI, raised transmitter uptake, and lowered extracellular glutamate. Ceftriaxone 42-53 solute carrier family 1 member 2 Rattus norvegicus 107-111 22871519-3 2012 This investigation was designed to evaluate the interaction between co-administration of ceftriaxone, a specific GLT1 activator and minocycline, a specific microglia inhibitor, on the mechanical and cold allodynia of chronic constriction injury model (CCI) in rats. Ceftriaxone 89-100 solute carrier family 1 member 2 Rattus norvegicus 113-117 23413710-3 2012 All isolates susceptible to ceftriaxone were ESBL-negative. Ceftriaxone 28-39 EsbL Escherichia coli 45-49 23413710-4 2012 Nearly all isolates non-susceptible to ceftriaxone, ceftazidime and cefepime produced ESBL; the presence of CTX-M genes in the isolates correlated with a ceftriaxone non-susceptible phenotype. Ceftriaxone 39-50 EsbL Escherichia coli 86-90 22927394-5 2012 Cell wall-targeting antibiotics, such as vancomycin and ceftriaxone, inhibit the kinase activity of Stk1 and lead to decreased Cys-phosphorylation of SarA and MgrA. Ceftriaxone 56-67 TEK receptor tyrosine kinase Mus musculus 100-104 22927394-5 2012 Cell wall-targeting antibiotics, such as vancomycin and ceftriaxone, inhibit the kinase activity of Stk1 and lead to decreased Cys-phosphorylation of SarA and MgrA. Ceftriaxone 56-67 secretion associated Ras related GTPase 1A Mus musculus 150-154 22927394-5 2012 Cell wall-targeting antibiotics, such as vancomycin and ceftriaxone, inhibit the kinase activity of Stk1 and lead to decreased Cys-phosphorylation of SarA and MgrA. Ceftriaxone 56-67 MAS1 oncogene Mus musculus 159-163 23054634-2 2012 Specifically, NMDAR antagonists such as MK-801, and an inducer of the expression of glutamate transporter subtype-1 (GLT-1) (ceftriaxone) are known to inhibit addictive behavior. Ceftriaxone 125-136 solute carrier family 1 member 2 Rattus norvegicus 84-115 23054634-2 2012 Specifically, NMDAR antagonists such as MK-801, and an inducer of the expression of glutamate transporter subtype-1 (GLT-1) (ceftriaxone) are known to inhibit addictive behavior. Ceftriaxone 125-136 solute carrier family 1 member 2 Rattus norvegicus 117-122 23054634-10 2012 CONCLUSION: The combined action of a low dose of an NMDAR antagonist (MK-801) and GLT-1 activation by ceftriaxone effectively changed different phases of CPP behavior. Ceftriaxone 102-113 solute carrier family 1 member 2 Rattus norvegicus 82-87 22956831-4 2012 We have previously shown that chronic treatment with the antibiotic ceftriaxone restores xCT and GLT-1 expression following cocaine self-administration and attenuates both cue- and cocaine-primed reinstatement. Ceftriaxone 68-79 solute carrier family 7 member 11 Homo sapiens 89-92 22956831-4 2012 We have previously shown that chronic treatment with the antibiotic ceftriaxone restores xCT and GLT-1 expression following cocaine self-administration and attenuates both cue- and cocaine-primed reinstatement. Ceftriaxone 68-79 solute carrier family 1 member 2 Homo sapiens 97-102 22956831-5 2012 Here we used a (3)H-glutamate uptake assay and microdialysis to test the hypothesis that ceftriaxone restores the function of both GLT-1 and xCT (glutamate reuptake and export, respectively) in the NA core following cocaine self-administration. Ceftriaxone 89-100 solute carrier family 1 member 2 Homo sapiens 131-136 22956831-5 2012 Here we used a (3)H-glutamate uptake assay and microdialysis to test the hypothesis that ceftriaxone restores the function of both GLT-1 and xCT (glutamate reuptake and export, respectively) in the NA core following cocaine self-administration. Ceftriaxone 89-100 solute carrier family 7 member 11 Homo sapiens 141-144 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 16-27 C-C motif chemokine ligand 2 Rattus norvegicus 105-139 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 16-27 C-C motif chemokine ligand 2 Rattus norvegicus 141-146 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 16-27 C-C motif chemokine ligand 3 Rattus norvegicus 149-159 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 16-27 interleukin 6 Rattus norvegicus 165-178 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 16-27 interleukin 6 Rattus norvegicus 180-184 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 16-27 C-C motif chemokine ligand 3 Rattus norvegicus 197-207 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 16-27 interleukin 6 Rattus norvegicus 209-213 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 16-27 interleukin 10 Rattus norvegicus 219-224 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 35-46 C-C motif chemokine ligand 2 Rattus norvegicus 105-139 22644021-11 2012 While rifampin plus ceftriaxone versus ceftriaxone also led to lower CSF inflammation (P < 0.02 for IL-6 at 6 h), it had no significant effect on apoptosis and hearing capacity. Ceftriaxone 20-31 interleukin 6 Rattus norvegicus 103-107 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 35-46 C-C motif chemokine ligand 2 Rattus norvegicus 141-146 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 35-46 C-C motif chemokine ligand 3 Rattus norvegicus 149-159 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 35-46 interleukin 6 Rattus norvegicus 165-178 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 35-46 interleukin 6 Rattus norvegicus 180-184 22644021-11 2012 While rifampin plus ceftriaxone versus ceftriaxone also led to lower CSF inflammation (P < 0.02 for IL-6 at 6 h), it had no significant effect on apoptosis and hearing capacity. Ceftriaxone 39-50 interleukin 6 Rattus norvegicus 103-107 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 35-46 C-C motif chemokine ligand 3 Rattus norvegicus 197-207 22521042-2 2012 Using reinstatement of conditioned place preference (CPP), we determined whether ceftriaxone, a beta-lactam antibiotic known to increase the expression and activity of the glutamate transporter (EAAT2) on glial cells, blocks methamphetamine-triggered reinstatement of CPP. Ceftriaxone 81-92 solute carrier family 1 member 2 Rattus norvegicus 195-200 22644021-10 2012 Daptomycin plus ceftriaxone versus ceftriaxone significantly (P < 0.04) lowered CSF concentrations of monocyte chemoattractant protein 1 (MCP-1), MIP-1alpha, and interleukin 6 (IL-6) at 6 h and MIP-1alpha, IL-6, and IL-10 at 22 h after initiation of therapy, led to significantly (P < 0.01) less apoptosis, and significantly (P < 0.01) improved hearing capacity. Ceftriaxone 35-46 interleukin 6 Rattus norvegicus 209-213 22473056-9 2012 Upregulating GLT-1 expression by chronic treatment with ceftriaxone also reversed the impairment of LTP and fear memory in KO mice. Ceftriaxone 56-67 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 13-18 22521042-7 2012 Using real time PCR, EAAT2 mRNA levels in the nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) were quantified in response to ceftriaxone. Ceftriaxone 137-148 solute carrier family 1 member 2 Rattus norvegicus 21-26 22521042-8 2012 Ceftriaxone blocked methamphetamine-triggered reinstatement of CPP and significantly increased EAAT2 mRNA levels in the mPFC, with a trend towards significance in the NAc. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 95-100 23569940-3 2012 The blood culture reports, however, were reported to grow colonies of Salmonella paratyphi A; thus the diagnosis of the patient was changed to enteric fever, and the patient improved on the subsequently started therapy of ceftriaxone 2,000 mg bid. Ceftriaxone 222-233 BH3 interacting domain death agonist Homo sapiens 243-246 22826985-0 2012 In vivo susceptibility of ESBL producing Escherichia coli to ceftriaxone in children with acute pyelonephritis. Ceftriaxone 61-72 EsbL Escherichia coli 26-30 22826985-2 2012 OBJECTIVE: To examine in vivo susceptibility of ESBL (+) E. coli to ceftriaxone (CTX), and to evaluate the options for empiric therapy for APN in children. Ceftriaxone 68-79 EsbL Escherichia coli 48-52 22076500-1 2012 Several studies showed that the up-regulation of glial glutamate transporter-1 (GLT-1) participates in the acquisition of brain ischemic tolerance induced by cerebral ischemic preconditioning or ceftriaxone pretreatment in rats. Ceftriaxone 195-206 solute carrier family 1 member 2 Rattus norvegicus 49-85 22212402-6 2012 Correlating with the behavioral effects, ceftriaxone reversed downregulation of GLT-1 expression that was induced by OIH. Ceftriaxone 41-52 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 80-85 22212402-7 2012 These results suggest that ceftriaxone inhibited the development of OIH by up-regulating spinal GLT-1 expression. Ceftriaxone 27-38 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 96-101 21824497-1 2011 Ceftriaxone is a beta-lactam antibiotic which has been found to increase the expression and function of the major glutamate transporter, GLT-1. Ceftriaxone 0-11 solute carrier family 1 member 2 Homo sapiens 137-142 22680643-6 2012 We and others have recently found that ceftriaxone, an FDA-approved drug known to elevate GLT1 expression, attenuates cue-induced cocaine relapse. Ceftriaxone 39-50 solute carrier family 1 member 2 Rattus norvegicus 90-94 22680643-8 2012 We also demonstrated that ceftriaxone-induced upregulation of GLT1 expression was associated with increases in glutamate uptake in Huntington"s disease mouse model. Ceftriaxone 26-37 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 62-66 21693777-0 2011 Ceftriaxone preconditioning confers neuroprotection in neonatal rats through glutamate transporter 1 upregulation. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 77-100 21693777-1 2011 OBJECTIVE: This study investigated the hypothesis that ceftriaxone preconditioning ameliorates brain damage in neonatal animals through glutamate transporter 1 (GLT-1) upregulation. Ceftriaxone 55-66 solute carrier family 1 member 2 Rattus norvegicus 136-159 21693777-1 2011 OBJECTIVE: This study investigated the hypothesis that ceftriaxone preconditioning ameliorates brain damage in neonatal animals through glutamate transporter 1 (GLT-1) upregulation. Ceftriaxone 55-66 solute carrier family 1 member 2 Rattus norvegicus 161-166 21693777-5 2011 RESULTS: Repeated ceftriaxone injections significantly increased GLT-1 mRNA and protein levels but not GLAST. Ceftriaxone 18-29 solute carrier family 1 member 2 Rattus norvegicus 65-70 22374677-2 2012 We recently demonstrated that BubR1 was modified by sumoylation, and that lysine 250 (K250) functions as the crucial site for this modification. Ceftriaxone 86-90 BUB1 mitotic checkpoint serine/threonine kinase B Homo sapiens 30-35 22479544-2 2012 Recently, it has been demonstrated that ceftriaxone (CEF) robustly increases GLT-1 expression. Ceftriaxone 40-51 solute carrier family 1 member 2 Rattus norvegicus 77-82 22479544-2 2012 Recently, it has been demonstrated that ceftriaxone (CEF) robustly increases GLT-1 expression. Ceftriaxone 53-56 solute carrier family 1 member 2 Rattus norvegicus 77-82 21536061-0 2011 Role of GLT-1 transporter activation in prevention of cannabinoid tolerance by the beta-lactam antibiotic, ceftriaxone, in mice. Ceftriaxone 107-118 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 8-13 21524862-0 2011 Glutamate transporter subtype 1 (GLT-1) activator ceftriaxone attenuates amphetamine-induced hyperactivity and behavioral sensitization in rats. Ceftriaxone 50-61 solute carrier family 1 member 2 Rattus norvegicus 0-38 21524862-1 2011 BACKGROUND: The beta-lactam antibiotic and glutamate transporter subtype 1 (GLT-1) activator ceftriaxone prevents relapse to cocaine-seeking and inhibits morphine-induced physical dependence and tolerance in rats, but its efficacy against amphetamine-induced behaviors is unknown. Ceftriaxone 93-104 solute carrier family 1 member 2 Rattus norvegicus 43-81 21792905-7 2011 Treatment of animals with ceftriaxone (CEF), a beta-lactam antibiotic, led to an increase of EAAT2 expression and glutamate transport activity in the brain. Ceftriaxone 26-37 solute carrier family 1 member 2 Homo sapiens 93-98 21792905-7 2011 Treatment of animals with ceftriaxone (CEF), a beta-lactam antibiotic, led to an increase of EAAT2 expression and glutamate transport activity in the brain. Ceftriaxone 39-42 solute carrier family 1 member 2 Homo sapiens 93-98 21933448-5 2011 Compounds, such as ceftriaxone, that enhance the expression of GLT1 may exert neuroprotective effect in HIE. Ceftriaxone 19-30 solute carrier family 1 member 2 Rattus norvegicus 63-67 21933448-11 2011 RESULTS: Pre-treatment with 200 mg/kg ceftriaxone significantly reduced the brain injury scores and apoptotic cells in the hippocampus, restored myelination in the external capsule of P14 rats, and improved the hypoxia-ischemia induced learning and memory deficit of P23-24 rats. Ceftriaxone 38-49 S100 calcium binding protein A9 Rattus norvegicus 184-187 21933448-12 2011 GLT1 expression was observed in the cortical neurons of ceftriaxone treated rats. Ceftriaxone 56-67 solute carrier family 1 member 2 Rattus norvegicus 0-4 21970974-3 2011 Ceftriaxone delays loss of neurons in genetic animal models of amyotrophic lateral sclerosis through upregulation of astrocytic glutamate transporter expression (GLT-1). Ceftriaxone 0-11 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 162-167 21970974-9 2011 Ceftriaxone administration increased the expression of GLT-1 in the hypoglossal nucleus, while it suppressed the reactive increase of glial fibrillary acidic protein (GFAP) expression to control level. Ceftriaxone 0-11 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 55-60 21970974-9 2011 Ceftriaxone administration increased the expression of GLT-1 in the hypoglossal nucleus, while it suppressed the reactive increase of glial fibrillary acidic protein (GFAP) expression to control level. Ceftriaxone 0-11 glial fibrillary acidic protein Mus musculus 134-165 21970974-9 2011 Ceftriaxone administration increased the expression of GLT-1 in the hypoglossal nucleus, while it suppressed the reactive increase of glial fibrillary acidic protein (GFAP) expression to control level. Ceftriaxone 0-11 glial fibrillary acidic protein Mus musculus 167-171 21536061-7 2011 Dihydrokainic acid (10mg/kg), a GLT-1 transporter inhibitor, prevented this effect of ceftriaxone. Ceftriaxone 86-97 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 32-37 21422004-15 2011 CONCLUSIONS: These results indicate that CEF effectively reduces ethanol intake, possibly through activation of GLT1, and may be a potential therapeutic drug for alcohol addiction treatment. Ceftriaxone 41-44 solute carrier family 1 member 2 Rattus norvegicus 112-116 21034752-4 2011 The recent discovery of the neuroprotective properties of ceftriaxone, a beta lactam antibiotic, suggested that increasing EAAT2/GLT-1 gene expression might be beneficial in ALS and other neurological/psychiatric disorders by augmenting astrocytic glutamate uptake. Ceftriaxone 58-69 solute carrier family 1 member 2 Homo sapiens 123-128 21034752-4 2011 The recent discovery of the neuroprotective properties of ceftriaxone, a beta lactam antibiotic, suggested that increasing EAAT2/GLT-1 gene expression might be beneficial in ALS and other neurological/psychiatric disorders by augmenting astrocytic glutamate uptake. Ceftriaxone 58-69 solute carrier family 1 member 2 Homo sapiens 129-134 21518570-8 2011 RESULTS: The expressions of CXCL16 mRNA were significantly higher in the model group and the ceftriaxone group than in the control group and the cefodizime group (P < 0.05), indicating the mice in the model group and the ceftriaxone group were immunodeficient. Ceftriaxone 93-104 chemokine (C-X-C motif) ligand 16 Mus musculus 28-34 21256174-2 2011 Recent investigations suggest that ceftriaxone, a beta-lactam antibiotic, stimulates GLT-1 expression and confers neuroprotection against ischemic and motor neuron degeneration. Ceftriaxone 35-46 solute carrier family 1 member 2 Rattus norvegicus 85-90 21211547-11 2011 ), a selective GLT-1 transporter inhibitor, reversed the anti-allodynic and anti-hyperalgesic effects of ceftriaxone, at doses that produced no effect on its own. Ceftriaxone 105-116 solute carrier family 1 member 2 Rattus norvegicus 15-20 21518570-8 2011 RESULTS: The expressions of CXCL16 mRNA were significantly higher in the model group and the ceftriaxone group than in the control group and the cefodizime group (P < 0.05), indicating the mice in the model group and the ceftriaxone group were immunodeficient. Ceftriaxone 224-235 chemokine (C-X-C motif) ligand 16 Mus musculus 28-34 22110515-0 2011 Is Ceftriaxone-Induced Biliary Pseudolithiasis Influenced by UDP-Glucuronosyltransferase 1A1 Gene Polymorphisms? Ceftriaxone 3-14 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 61-92 21287576-11 2011 Ceftriaxone administration recovered also CycA-induced atrophy, vacuolization and exfoliations of tubular epithelium and glomerular collapse in histopathological evaluation of kidney. Ceftriaxone 0-11 peptidylprolyl isomerase A Rattus norvegicus 42-46 21287576-12 2011 In conclusion, we observed that ceftriaxone is beneficial on CycA-induced oxidative stress in kidney of rats by modulating oxidative and antioxidant system. Ceftriaxone 32-43 peptidylprolyl isomerase A Rattus norvegicus 61-65 21372390-8 2011 Moreover, OATP1B3 was involved in the transport of ceftriaxone, cefmetazole, cefoperazone, and cefotaxime. Ceftriaxone 51-62 solute carrier organic anion transporter family member 1B3 Homo sapiens 10-17 21287576-3 2011 The aim of this study was to evaluate whether ceftriaxone protects CycA-induced oxidative stress kidney injury in rats. Ceftriaxone 46-57 peptidylprolyl isomerase A Rattus norvegicus 67-71 22110515-3 2011 We describe 3 children with ceftriaxone-induced pseudolithiasis, who were also carriers of the A(TA)(7)TAA polymorphism of the UGT1A1 gene, implying that a cause and effect relation may exist. Ceftriaxone 28-39 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 127-133 22098637-6 2011 Ceftizoxime was also available from 72 h to 360 h post-dosing in milk in the presence of Fibrosin( ) following intramammary administration of ceftriaxone suggesting the polyherbal drug played a major role in the penetration of ceftriaxone from milk to systemic circulation. Ceftriaxone 142-153 LOW QUALITY PROTEIN: probable fibrosin-1 Capra hircus 89-98 22098637-6 2011 Ceftizoxime was also available from 72 h to 360 h post-dosing in milk in the presence of Fibrosin( ) following intramammary administration of ceftriaxone suggesting the polyherbal drug played a major role in the penetration of ceftriaxone from milk to systemic circulation. Ceftriaxone 227-238 LOW QUALITY PROTEIN: probable fibrosin-1 Capra hircus 89-98 22098637-8 2011 CONCLUSIONS: Polyherbal drug (Fibrosin( )) plays a major role in the penetration of ceftriaxone from milk to systemic circulation and may be responsible for increased bioavailability of its metabolite in the mammary gland resulting in higher concentration and longer persistence of the drug in milk. Ceftriaxone 84-95 LOW QUALITY PROTEIN: probable fibrosin-1 Capra hircus 30-39 22098637-1 2011 BACKGROUND: The aim of the present study was to determine pharmacokinetic interaction of ceftriaxone and polyherbal drug (Fibrosin( )) in lactating goats following single dose intramammary administration of ceftriaxone with 1 h pre-single dose oral administration of Fibrosin( ). Ceftriaxone 207-218 LOW QUALITY PROTEIN: probable fibrosin-1 Capra hircus 122-131 21029363-9 2011 RESULTS: Rh-TFPI reduced pneumonia-induced coagulation; rh-TFPI with ceftriaxone further attenuated coagulation relative to ceftriaxone alone. Ceftriaxone 69-80 tissue factor pathway inhibitor Mus musculus 59-63 22098637-1 2011 BACKGROUND: The aim of the present study was to determine pharmacokinetic interaction of ceftriaxone and polyherbal drug (Fibrosin( )) in lactating goats following single dose intramammary administration of ceftriaxone with 1 h pre-single dose oral administration of Fibrosin( ). Ceftriaxone 207-218 LOW QUALITY PROTEIN: probable fibrosin-1 Capra hircus 122-130 22098637-4 2011 RESULTS: Fibrosin( ) treated goats showed a typical absorption-reabsorption phase of ceftriaxone in plasma following intramammary administration. Ceftriaxone 85-96 LOW QUALITY PROTEIN: probable fibrosin-1 Capra hircus 9-18 20624078-8 2010 Ceftriaxone may be the recommended substance for monitoring because of some ability in separating ampC hyper-producing E. coli from ESBL and plasmidic AmpC isolates. Ceftriaxone 0-11 EsbL Escherichia coli 132-136 21846950-4 2011 Protein levels of GLAST and GLT-1 glutamate transporters were quantified using In-Cell Western techniques after acute or 5-day treatment with either ceftriaxone or APDC. Ceftriaxone 149-160 solute carrier family 1 member 3 Rattus norvegicus 18-23 21846950-7 2011 RESULTS: Five-day treatment with 100 muM ceftriaxone significantly increased both GLAST and GLT-1 protein levels 31.3% and 47.5% above control, respectively, increased the Vmax 29.3%, increased the Km of glutamate uptake 117.9%, and reduced neuronal death 22.0% after a 1 mM glutamate challenge. Ceftriaxone 41-52 solute carrier family 1 member 3 Rattus norvegicus 82-87 21846950-7 2011 RESULTS: Five-day treatment with 100 muM ceftriaxone significantly increased both GLAST and GLT-1 protein levels 31.3% and 47.5% above control, respectively, increased the Vmax 29.3%, increased the Km of glutamate uptake 117.9%, and reduced neuronal death 22.0% after a 1 mM glutamate challenge. Ceftriaxone 41-52 solute carrier family 1 member 2 Rattus norvegicus 92-97 21846950-9 2011 CONCLUSIONS: Chronic treatment with ceftriaxone or APDC provided neuroprotection from glutamate excitotoxicity while increasing GLAST and GLT-1 protein levels and increasing glutamate uptake. Ceftriaxone 36-47 solute carrier family 1 member 3 Rattus norvegicus 128-133 21846950-9 2011 CONCLUSIONS: Chronic treatment with ceftriaxone or APDC provided neuroprotection from glutamate excitotoxicity while increasing GLAST and GLT-1 protein levels and increasing glutamate uptake. Ceftriaxone 36-47 solute carrier family 1 member 2 Rattus norvegicus 138-143 21846950-2 2011 In the present study, the effects of ceftriaxone and (2R, 4R)-APDC (APDC) on the protein expression of GLAST and GLT-1, the rate of glutamate uptake, and neuroprotection were evaluated in a cell culture model of glutamate excitotoxicity. Ceftriaxone 37-48 solute carrier family 1 member 3 Rattus norvegicus 103-108 21846950-2 2011 In the present study, the effects of ceftriaxone and (2R, 4R)-APDC (APDC) on the protein expression of GLAST and GLT-1, the rate of glutamate uptake, and neuroprotection were evaluated in a cell culture model of glutamate excitotoxicity. Ceftriaxone 37-48 solute carrier family 1 member 2 Rattus norvegicus 113-118 20471977-6 2010 Ceftriaxone has also been shown to modulate the proteasome system, thus decreasing NF-kappaB activation and GFAP promoter transcriptional regulation, which further accounts for the down-modulation of GFAP protein levels. Ceftriaxone 0-11 glial fibrillary acidic protein Homo sapiens 108-112 20547213-0 2010 Spinal upregulation of glutamate transporter GLT-1 by ceftriaxone: therapeutic efficacy in a range of experimental nervous system disorders. Ceftriaxone 54-65 solute carrier family 1 member 2 Homo sapiens 45-50 20547213-6 2010 The present studies explored whether daily intrathecal treatment of rats with ceftriaxone, a beta-lactam antibiotic that upregulates GLT-1 expression, could prevent development of hyperalgesia and allodynia following repeated morphine, reverse pain arising from central or peripheral neuropathy, and reduce glial activation in these models. Ceftriaxone 78-89 solute carrier family 1 member 2 Rattus norvegicus 133-138 20547213-10 2010 EAE and CCI each significantly reduced the expression of membrane-bound, dimerized GLT-1 protein in lumbar spinal cord, an effect normalized by ceftriaxone. Ceftriaxone 144-155 solute carrier family 1 member 2 Homo sapiens 83-88 20576749-26 2010 The hospital antibiotic policy resulted in ceftriaxone being the most heavily prescribed third-generation cephalosporin, which might be expected to select for cefotaximases such as CTX-M-15. Ceftriaxone 43-54 extended spectrum beta-lactamase CTX-M-15 Klebsiella pneumoniae 181-189 20471977-0 2010 In vitro treatments with ceftriaxone promote elimination of mutant glial fibrillary acidic protein and transcription down-regulation. Ceftriaxone 25-36 glial fibrillary acidic protein Homo sapiens 67-98 20471977-4 2010 Here we show that ceftriaxone is able to reduce the intracytoplasmic aggregates of mutant GFAP in a cellular model of Alexander disease. Ceftriaxone 18-29 glial fibrillary acidic protein Homo sapiens 90-94 20471977-6 2010 Ceftriaxone has also been shown to modulate the proteasome system, thus decreasing NF-kappaB activation and GFAP promoter transcriptional regulation, which further accounts for the down-modulation of GFAP protein levels. Ceftriaxone 0-11 glial fibrillary acidic protein Homo sapiens 200-204 20663216-0 2010 Ceftriaxone-induced up-regulation of cortical and striatal GLT1 in the R6/2 model of Huntington"s disease. Ceftriaxone 0-11 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 59-63 20663216-2 2010 At 7 weeks of age, R6/2 mice, which model an aggressive form of juvenile HD, show a glutamate-uptake deficit in striatum that can be reversed by treatment with ceftriaxone, a beta-lactam antibiotic that increases GLT1 expression. Ceftriaxone 160-171 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 213-217 20663216-4 2010 Here, we tested whether ceftriaxone can reverse the decline in GLT1 expression that occurs in older R6/2s. Ceftriaxone 24-35 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 63-67 20663216-7 2010 Despite a significant GLT1 reduction in saline-treated R6/2 mice relative to WT at 13, but not 9, weeks of age, ceftriaxone treatment increased cortical and striatal GLT1 expression relative to saline in all tested mice. Ceftriaxone 112-123 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 166-170 20663216-8 2010 CONCLUSIONS: The ability of ceftriaxone to up-regulate GLT1 in R6/2 mice at an age when GLT1 expression is significantly reduced suggests that the mechanism for increasing GLT1 expression is still functional. Ceftriaxone 28-39 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 55-59 20663216-8 2010 CONCLUSIONS: The ability of ceftriaxone to up-regulate GLT1 in R6/2 mice at an age when GLT1 expression is significantly reduced suggests that the mechanism for increasing GLT1 expression is still functional. Ceftriaxone 28-39 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 88-92 20663216-8 2010 CONCLUSIONS: The ability of ceftriaxone to up-regulate GLT1 in R6/2 mice at an age when GLT1 expression is significantly reduced suggests that the mechanism for increasing GLT1 expression is still functional. Ceftriaxone 28-39 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 88-92 20682036-10 2010 Remarkably, homozygous FVL mice were strongly protected against death due to pneumococcal pneumonia when treated with ceftriaxone, which was associated with more pronounced FXIII depletion; this protective effect was not observed in the absence of antibiotic therapy. Ceftriaxone 118-129 coagulation factor V Homo sapiens 23-26 20211890-1 2010 Using 98 clinical methicillin-susceptible Staphylococcus aureus isolates of known beta-lactamase (Bla) type, we found a pronounced inoculum effect for cephalexin (mostly Bla type A and C strains), a mild inoculum effect for cephalothin (especially types B and C), and no inoculum effects for ceftriaxone and cefuroxime. Ceftriaxone 292-303 beta-lactamase Staphylococcus aureus 98-101 20004063-2 2010 Identification of beta-lactam antibiotics as pharmaceuticals which activate GLT-1 transporters prompted us to hypothesize that repeated beta-lactam antibiotic (ceftriaxone) administration blocks development of tolerance to morphine antinociception through GLT-1 activation. Ceftriaxone 160-171 solute carrier family 1 member 2 Rattus norvegicus 76-81 20004063-2 2010 Identification of beta-lactam antibiotics as pharmaceuticals which activate GLT-1 transporters prompted us to hypothesize that repeated beta-lactam antibiotic (ceftriaxone) administration blocks development of tolerance to morphine antinociception through GLT-1 activation. Ceftriaxone 160-171 solute carrier family 1 member 2 Rattus norvegicus 256-261 20045054-4 2010 Early treatment with ceftriaxone prior to the onset of epilepsy increased expression of astrocyte glutamate transporters, decreased extracellular glutamate levels, neuronal death, and seizure frequency, and improved survival in Tsc1(GFAP)CKO mice. Ceftriaxone 21-32 TSC complex subunit 1 Mus musculus 228-232 20045054-4 2010 Early treatment with ceftriaxone prior to the onset of epilepsy increased expression of astrocyte glutamate transporters, decreased extracellular glutamate levels, neuronal death, and seizure frequency, and improved survival in Tsc1(GFAP)CKO mice. Ceftriaxone 21-32 glial fibrillary acidic protein Mus musculus 233-237 20022427-6 2010 To further determine whether the above anti-nociceptive effects of Cef are a result of the up-regulation of spinal GLT-1 expression and its function, we further observed the effects of intrathecal administration of Cef in the same model. Ceftriaxone 67-70 solute carrier family 1 member 2 Rattus norvegicus 115-120 20022427-7 2010 It was found that intrathecal administration of Cef led to the specific up-regulation of GLT-1 expression and glutamate uptake ((3)H-glutamate) in the spinal dorsal horn, and similar anti-nociceptive effects to those of intraperitoneal administration of Cef. Ceftriaxone 48-51 solute carrier family 1 member 2 Rattus norvegicus 89-94 20022427-8 2010 The above effects of intrathecal Cef administration were all significantly inhibited by intrathecal administration of GLT-1 antisense oligodeoxynucleotides (As-ODNs). Ceftriaxone 33-36 solute carrier family 1 member 2 Rattus norvegicus 118-123 19717140-6 2010 We also examined the affect of ceftriaxone (previously shown to increase GLT-1) and N-acetylcysteine treatment on the expression of GLT-1 and xCT. Ceftriaxone 31-42 solute carrier family 1 member 2 Homo sapiens 132-137 19717140-6 2010 We also examined the affect of ceftriaxone (previously shown to increase GLT-1) and N-acetylcysteine treatment on the expression of GLT-1 and xCT. Ceftriaxone 31-42 solute carrier family 7 member 11 Homo sapiens 142-145 19717140-9 2010 Ceftriaxone restored GLT-1 and xCT levels and prevented cue- and cocaine-induced reinstatement of drug seeking. Ceftriaxone 0-11 solute carrier family 1 member 2 Homo sapiens 21-26 19717140-9 2010 Ceftriaxone restored GLT-1 and xCT levels and prevented cue- and cocaine-induced reinstatement of drug seeking. Ceftriaxone 0-11 solute carrier family 7 member 11 Homo sapiens 31-34 20423712-3 2010 Therefore, an attempt was made to explore its neuroprotective potential in cerebral ischemia/reperfusion injury using ceftriaxone, a GLT-1 modulator. Ceftriaxone 118-129 solute carrier family 1 member 2 Homo sapiens 133-138 20423712-7 2010 Furthermore, inhibition of ceftriaxone-mediated increased glutamine synthetase activity by dihydrokainate (DHK), a GLT-1 specific inhibitor, confirms the specific effect of ceftriaxone on GLT-1 activity. Ceftriaxone 27-38 glutamate-ammonia ligase Homo sapiens 58-78 20423712-7 2010 Furthermore, inhibition of ceftriaxone-mediated increased glutamine synthetase activity by dihydrokainate (DHK), a GLT-1 specific inhibitor, confirms the specific effect of ceftriaxone on GLT-1 activity. Ceftriaxone 27-38 solute carrier family 1 member 2 Homo sapiens 115-120 20423712-7 2010 Furthermore, inhibition of ceftriaxone-mediated increased glutamine synthetase activity by dihydrokainate (DHK), a GLT-1 specific inhibitor, confirms the specific effect of ceftriaxone on GLT-1 activity. Ceftriaxone 27-38 solute carrier family 1 member 2 Homo sapiens 188-193 20423712-7 2010 Furthermore, inhibition of ceftriaxone-mediated increased glutamine synthetase activity by dihydrokainate (DHK), a GLT-1 specific inhibitor, confirms the specific effect of ceftriaxone on GLT-1 activity. Ceftriaxone 173-184 glutamate-ammonia ligase Homo sapiens 58-78 20423712-7 2010 Furthermore, inhibition of ceftriaxone-mediated increased glutamine synthetase activity by dihydrokainate (DHK), a GLT-1 specific inhibitor, confirms the specific effect of ceftriaxone on GLT-1 activity. Ceftriaxone 173-184 solute carrier family 1 member 2 Homo sapiens 115-120 20423712-7 2010 Furthermore, inhibition of ceftriaxone-mediated increased glutamine synthetase activity by dihydrokainate (DHK), a GLT-1 specific inhibitor, confirms the specific effect of ceftriaxone on GLT-1 activity. Ceftriaxone 173-184 solute carrier family 1 member 2 Homo sapiens 188-193 20423712-8 2010 In addition, ceftriaxone also induced a significant (P<0.01) increase in [(3)H]-glutamate uptake, mediated by GLT-1 in glial enriched preparation, as evidenced by use of DHK and DL-threo-beta-benzyloxyaspartate (DL-TBOA). Ceftriaxone 13-24 solute carrier family 1 member 2 Homo sapiens 113-118 20350284-10 2010 It was also found that activities of antioxidant enzymes such as catalase were significantly increased (p<0.001) along with decreased (p<0.001) in lipid peroxidation (malonaldialdehyde) level in CSF of vancoplus treated group as compared to infected as well as ceftriaxone resistance group and come back to normal level. Ceftriaxone 267-278 catalase Mus musculus 65-73 20194529-7 2010 At the concentration of 20 microM, several drugs, including cefazolin, cefotaxime, ceftriaxone, and ketoprofen, significantly inhibited [(3)H]PGE(2) uptake into MRP4-expressing membrane vesicles. Ceftriaxone 83-94 ATP-binding cassette, sub-family C (CFTR/MRP), member 4 Mus musculus 161-165 20072121-2 2010 Recently, it has been shown that ceftriaxone (CEF)-induced GLT-1 upregulation is associated with an impairment of the prepulse inhibition (PPI) of the startle reflex, a simple form of information processing that is reduced in schizophrenia, and determines a strong reduction in hippocampal metabotropic glutamate receptor (mGluR)2/3-dependent long-term depression. Ceftriaxone 33-44 solute carrier family 1 member 2 Rattus norvegicus 59-64 20072121-2 2010 Recently, it has been shown that ceftriaxone (CEF)-induced GLT-1 upregulation is associated with an impairment of the prepulse inhibition (PPI) of the startle reflex, a simple form of information processing that is reduced in schizophrenia, and determines a strong reduction in hippocampal metabotropic glutamate receptor (mGluR)2/3-dependent long-term depression. Ceftriaxone 33-44 glutamate metabotropic receptor 2 Rattus norvegicus 290-330 20072121-2 2010 Recently, it has been shown that ceftriaxone (CEF)-induced GLT-1 upregulation is associated with an impairment of the prepulse inhibition (PPI) of the startle reflex, a simple form of information processing that is reduced in schizophrenia, and determines a strong reduction in hippocampal metabotropic glutamate receptor (mGluR)2/3-dependent long-term depression. Ceftriaxone 46-49 solute carrier family 1 member 2 Rattus norvegicus 59-64 20072121-2 2010 Recently, it has been shown that ceftriaxone (CEF)-induced GLT-1 upregulation is associated with an impairment of the prepulse inhibition (PPI) of the startle reflex, a simple form of information processing that is reduced in schizophrenia, and determines a strong reduction in hippocampal metabotropic glutamate receptor (mGluR)2/3-dependent long-term depression. Ceftriaxone 46-49 glutamate metabotropic receptor 2 Rattus norvegicus 290-330 20072121-4 2010 We showed that administration of LY379268 (1 mg/kg) prevented PPI alterations associated with GLT-1 upregulation, suggesting that CEF-induced PPI impairment was mGluR2/3 dependent. Ceftriaxone 130-133 solute carrier family 1 member 2 Rattus norvegicus 94-99 20072121-4 2010 We showed that administration of LY379268 (1 mg/kg) prevented PPI alterations associated with GLT-1 upregulation, suggesting that CEF-induced PPI impairment was mGluR2/3 dependent. Ceftriaxone 130-133 glutamate receptor, ionotropic, AMPA2 (alpha 2) Mus musculus 161-167 20072121-5 2010 In addition, we showed that CEF-induced GLT-1 upregulaton did not alter the expression of mGluR2/3, and also that it occurred at sites of mGluR2/3 expression. Ceftriaxone 28-31 solute carrier family 1 member 2 Rattus norvegicus 40-45 20072121-5 2010 In addition, we showed that CEF-induced GLT-1 upregulaton did not alter the expression of mGluR2/3, and also that it occurred at sites of mGluR2/3 expression. Ceftriaxone 28-31 glutamate receptor, ionotropic, AMPA2 (alpha 2) Mus musculus 138-144 19651762-3 2009 We show that up-regulation of the glutamate transporter GLT-1 by ceftriaxone severely impaired mGluR-dependent long-term depression (LTD), induced at rat mossy fibre (MF)-CA3 synapses by repetitive stimulation of afferent fibres. Ceftriaxone 65-76 solute carrier family 1 member 2 Rattus norvegicus 56-61 19694903-0 2009 Induction of Nrf2 and xCT are involved in the action of the neuroprotective antibiotic ceftriaxone in vitro. Ceftriaxone 87-98 NFE2 like bZIP transcription factor 2 Homo sapiens 13-17 19694903-0 2009 Induction of Nrf2 and xCT are involved in the action of the neuroprotective antibiotic ceftriaxone in vitro. Ceftriaxone 87-98 solute carrier family 7 member 11 Homo sapiens 22-25 19694903-5 2009 Ceftriaxone increased system x(c)(-) and glutathione levels independently of its effect on excitatory amino acid transporters by induction of the transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2), a known inducer of system x(c)(-), and the specific x(c)(-) subunit xCT. Ceftriaxone 0-11 NFE2 like bZIP transcription factor 2 Homo sapiens 167-171 19694903-5 2009 Ceftriaxone increased system x(c)(-) and glutathione levels independently of its effect on excitatory amino acid transporters by induction of the transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2), a known inducer of system x(c)(-), and the specific x(c)(-) subunit xCT. Ceftriaxone 0-11 NFE2 like bZIP transcription factor 2 Homo sapiens 173-216 19694903-5 2009 Ceftriaxone increased system x(c)(-) and glutathione levels independently of its effect on excitatory amino acid transporters by induction of the transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2), a known inducer of system x(c)(-), and the specific x(c)(-) subunit xCT. Ceftriaxone 0-11 solute carrier family 7 member 11 Homo sapiens 287-290 19694903-7 2009 Similar ceftriaxone-stimulated changes in Nrf2, system x(c)(-), and glutathione were observed in rat cortical and spinal astrocytes. Ceftriaxone 8-19 NFE2 like bZIP transcription factor 2 Rattus norvegicus 42-46 19694903-8 2009 In addition, ceftriaxone induced xCT mRNA expression in stem cell-derived human motor neurons. Ceftriaxone 13-24 solute carrier family 7 member 11 Homo sapiens 33-36 19694903-9 2009 We conclude that ceftriaxone-mediated neuroprotection might relate more strongly to activation of the antioxidant defense system including Nrf2 and system x(c)(-) than to excitatory amino acid transporter induction. Ceftriaxone 17-28 NFE2 like bZIP transcription factor 2 Homo sapiens 139-143 20067122-0 2009 [Post antibiotic, post beta-lactamase inhibitor and post antibiotic sub-MIC effect of ceftriaxone/tazobactam on beta-lactamase-producing Escherichia coli in vitro]. Ceftriaxone 86-97 beta-lactamase Escherichia coli 112-126 20067122-1 2009 OBJECTIVE: To study post antibiotic effect (PAE), post beta-lactamase inhibitor effect (PLIE) and post antibiotic sub-MIC effect (PASME) of ceftriaxone/tazobactam on beta-lactamase-producing Escherichia coli in vitro. Ceftriaxone 140-151 beta-lactamase Escherichia coli 166-180 20067122-2 2009 METHODS: The minimal inhibitory concentration (MIC) of ceftriaxone/tazobactam against 4 types of beta-lactamase producing E. coli strains, was measured by two-fold agar dilution method. Ceftriaxone 55-66 beta-lactamase Escherichia coli 97-111 19651762-3 2009 We show that up-regulation of the glutamate transporter GLT-1 by ceftriaxone severely impaired mGluR-dependent long-term depression (LTD), induced at rat mossy fibre (MF)-CA3 synapses by repetitive stimulation of afferent fibres. Ceftriaxone 65-76 carbonic anhydrase 3 Rattus norvegicus 171-174 19651762-7 2009 Furthermore, ceftriaxone-induced GLT-1 up-regulation significantly reduced the magnitude of LTP at MF-CA3 synapses but not at Schaffer collateral-CA1 synapses. Ceftriaxone 13-24 solute carrier family 1 member 2 Rattus norvegicus 33-38 19651762-7 2009 Furthermore, ceftriaxone-induced GLT-1 up-regulation significantly reduced the magnitude of LTP at MF-CA3 synapses but not at Schaffer collateral-CA1 synapses. Ceftriaxone 13-24 carbonic anhydrase 3 Rattus norvegicus 102-105 19806886-5 2009 Co-administration of ceftriaxone sodium with morphine attenuated morphine tolerance and up-regulated GLT-1 expression, and the MWT remained at high level after 6 days. Ceftriaxone 21-39 solute carrier family 1 member 2 Rattus norvegicus 101-106 19625514-6 2009 Immunoblotting confirmed that the ceftriaxone-induced blockade of cocaine relapse was associated with an increase in GLT1 expression in both PFC and NAcc. Ceftriaxone 34-45 solute carrier family 1 member 2 Rattus norvegicus 117-121 18985735-2 2009 To do this, we studied PPI in rats treated with ceftriaxone (200 mg/kg/day for 8 days), an antibiotic that selectively enhances GLT-1 expression and activity. Ceftriaxone 48-59 solute carrier family 1 member 2 Rattus norvegicus 128-133 19442074-0 2009 Ceftriaxone-vancomycin drug toxicity reduction by VRP 1020 in Mus musculus mice. Ceftriaxone 0-11 TBC1 domain family, member 8 Mus musculus 50-53 19442074-5 2009 Ceftriaxone or vancomycin administration significantly increased malonaldialdehyde levels (p < 0.001) but significant decreased in superoxide dismutase (p<0.01) and catalase (p<0.001) activities. Ceftriaxone 0-11 catalase Mus musculus 171-179 18985735-3 2009 We showed that ceftriaxone-induced GLT-1 upregulation is associated with impaired PPI of the startle, that this effect is reversed by dihydrokainate, a GLT-1 antagonist, that GLT-1 expression correlates negatively with PPI, and that PPI normalizes when GLT-1a levels return to baseline. Ceftriaxone 15-26 solute carrier family 1 member 2 Rattus norvegicus 35-40 18985735-3 2009 We showed that ceftriaxone-induced GLT-1 upregulation is associated with impaired PPI of the startle, that this effect is reversed by dihydrokainate, a GLT-1 antagonist, that GLT-1 expression correlates negatively with PPI, and that PPI normalizes when GLT-1a levels return to baseline. Ceftriaxone 15-26 solute carrier family 1 member 2 Rattus norvegicus 152-157 18985735-3 2009 We showed that ceftriaxone-induced GLT-1 upregulation is associated with impaired PPI of the startle, that this effect is reversed by dihydrokainate, a GLT-1 antagonist, that GLT-1 expression correlates negatively with PPI, and that PPI normalizes when GLT-1a levels return to baseline. Ceftriaxone 15-26 solute carrier family 1 member 2 Rattus norvegicus 152-157 19023027-6 2009 Corroborating the involvement of enhanced glutamate uptake, wild-type mice treated for 1 wk with ceftriaxone, an EAAT2 expression activator, showed a 49-70% reduction in VMR to CRD. Ceftriaxone 97-108 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 113-118 19008722-1 2008 OBJECTIVE: Ceftriaxone has been reported to reduce neuronal damage in amyotrophic lateral sclerosis and in an in-vitro model of neuronal ischaemia through increased expression and activity of the glutamate transporter, GLT1. Ceftriaxone 11-22 solute carrier family 1 member 3 Rattus norvegicus 196-217 19023027-7 2009 Moreover, systemic pretreatment with the selective EAAT2 transporter blocker dihydrokainate reversed the ceftriaxone-blunted nociceptive response to CRD. Ceftriaxone 105-116 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 51-56 19008722-1 2008 OBJECTIVE: Ceftriaxone has been reported to reduce neuronal damage in amyotrophic lateral sclerosis and in an in-vitro model of neuronal ischaemia through increased expression and activity of the glutamate transporter, GLT1. Ceftriaxone 11-22 solute carrier family 1 member 2 Rattus norvegicus 219-223 19008722-10 2008 Ceftriaxone did not increase GLT1 expression, but increased GLT1 activity (P < 0.05). Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 60-64 18773080-2 2008 In order to identify pathways to dampen excitotoxic inflammatory CNS damage, we assessed the effects of a beta-lactam antibiotic, ceftriaxone, reported to enhance expression of glial EAAT2, in "Myelin Oligodendrocyte Glycoprotein" (MOG)-induced EAE. Ceftriaxone 130-141 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 183-188 18779351-9 2008 The MICs and EC(50)s of both strains were significantly increased (P < 0.05) for ceftriaxone when comparing human and bovine serum albumin, whereas the EC(50)s were not significantly different for ertapenem. Ceftriaxone 84-95 albumin Homo sapiens 128-141 18703755-3 2008 Recently it was demonstrated that ceftriaxone increased expression of the glutamate transporter (GLT1) and its biochemical and functional activity in the brain of rodents. Ceftriaxone 34-45 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 97-101 18644397-5 2008 Therefore, we tested the hypothesis that a beta-lactam antibiotic (ceftriaxone), by increasing glutamate uptake, prevents tolerance to hypothermia induced by a kappa opioid receptor agonist (U-50,488H). Ceftriaxone 67-78 opioid receptor kappa 1 Homo sapiens 160-181 18644397-12 2008 These results identify a functional interaction between ceftriaxone and U50,488H in vivo and provide pharmacological evidence that a beta-lactam antibiotic abolishes tolerance to hypothermia induced by a kappa opioid receptor agonist. Ceftriaxone 56-67 opioid receptor kappa 1 Homo sapiens 204-225 18773080-2 2008 In order to identify pathways to dampen excitotoxic inflammatory CNS damage, we assessed the effects of a beta-lactam antibiotic, ceftriaxone, reported to enhance expression of glial EAAT2, in "Myelin Oligodendrocyte Glycoprotein" (MOG)-induced EAE. Ceftriaxone 130-141 myelin oligodendrocyte glycoprotein Mus musculus 194-229 18773080-2 2008 In order to identify pathways to dampen excitotoxic inflammatory CNS damage, we assessed the effects of a beta-lactam antibiotic, ceftriaxone, reported to enhance expression of glial EAAT2, in "Myelin Oligodendrocyte Glycoprotein" (MOG)-induced EAE. Ceftriaxone 130-141 myelin oligodendrocyte glycoprotein Mus musculus 232-235 18773080-3 2008 Ceftriaxone profoundly ameliorated the clinical course of murine MOG-induced EAE both under preventive and therapeutic regimens. Ceftriaxone 0-11 myelin oligodendrocyte glycoprotein Mus musculus 65-68 18773080-5 2008 Moreover, the clinical effect of ceftriaxone was preserved in the presence of the EAAT2-specific transport inhibitor, dihydrokainate, while dihydrokainate alone caused an aggravated EAE course. Ceftriaxone 33-44 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 82-87 18773080-7 2008 Ceftriaxone treatment indirectly hampered T cell proliferation and proinflammatory INFgamma and IL17 secretion through modulation of myelin-antigen presentation by antigen-presenting cells (APCs) e.g. dendritic cells (DCs) and reduced T cell migration into the CNS in vivo. Ceftriaxone 0-11 interleukin 17A Mus musculus 96-100 18592743-13 2008 A majority of enterotoxin-producing isolates were resistant to 2 of 10 antibiotics tested, ceftriaxone and clindamycin. Ceftriaxone 91-102 cpe Clostridium perfringens 14-25 18339814-4 2008 ATP-dependent uptake of several cephalosporins including cefoperazone, cefbuperazone, cefpiramide, and ceftriaxone, all of which are mainly excreted into bile, was confirmed in membrane vesicles from Sf9 cells transfected with rat Mrp2. Ceftriaxone 103-114 ATP binding cassette subfamily C member 2 Rattus norvegicus 231-235 17436229-7 2007 However, spirochetes grew from the tissue samples of one-third of the mice treated with anti-TNF-alpha simultaneously or 4 weeks after ceftriaxone. Ceftriaxone 135-146 tumor necrosis factor Mus musculus 93-102 18326497-9 2008 The specific NF-kappaB binding site at the -272 position of the EAAT2 promoter was responsible for ceftriaxone-mediated EAAT2 induction. Ceftriaxone 99-110 nuclear factor kappa B subunit 1 Homo sapiens 13-22 18326497-9 2008 The specific NF-kappaB binding site at the -272 position of the EAAT2 promoter was responsible for ceftriaxone-mediated EAAT2 induction. Ceftriaxone 99-110 solute carrier family 1 member 2 Homo sapiens 64-69 18326497-9 2008 The specific NF-kappaB binding site at the -272 position of the EAAT2 promoter was responsible for ceftriaxone-mediated EAAT2 induction. Ceftriaxone 99-110 solute carrier family 1 member 2 Homo sapiens 120-125 18326497-10 2008 In addition, ceftriaxone increased glutamate uptake, a primary function of EAAT2, and EAAT2 small interference RNA completely inhibited ceftriaxone-induced glutamate uptake activity in PHFA. Ceftriaxone 13-24 solute carrier family 1 member 2 Homo sapiens 75-80 18326497-10 2008 In addition, ceftriaxone increased glutamate uptake, a primary function of EAAT2, and EAAT2 small interference RNA completely inhibited ceftriaxone-induced glutamate uptake activity in PHFA. Ceftriaxone 136-147 solute carrier family 1 member 2 Homo sapiens 86-91 18326497-11 2008 Taken together, our data indicate that ceftriaxone is a potent modulator of glutamate transport in PHFA through NF-kappaB-mediated EAAT2 promoter activation. Ceftriaxone 39-50 nuclear factor kappa B subunit 1 Homo sapiens 112-121 18326497-11 2008 Taken together, our data indicate that ceftriaxone is a potent modulator of glutamate transport in PHFA through NF-kappaB-mediated EAAT2 promoter activation. Ceftriaxone 39-50 solute carrier family 1 member 2 Homo sapiens 131-136 18304843-6 2008 Considering previous reports on upregulation of the expression of Glial Glutamate Transporter on ceftriaxone administration, the therapeutic potential of ceftriaxone in ameliorating hypobaric hypoxia induced memory impairment was investigated in male Sprague Dawley rats. Ceftriaxone 97-108 solute carrier family 1 member 3 Rattus norvegicus 66-93 18304843-12 2008 The therapeutic potential of ceftriaxone in providing neuroprotection in excitotoxic conditions by increasing Glial Glutamate Transporter expression and thereby enhancing glutamate uptake from the synapse has also been explored. Ceftriaxone 29-40 solute carrier family 1 member 3 Rattus norvegicus 110-137 18353560-3 2008 To test this hypothesis, we administered ceftriaxone, a beta-lactam antibiotic known to elevate GLT1 expression (200 mg/kg, i.p., for 5 days), to symptomatic R6/2 mice, a widely studied transgenic model of HD. Ceftriaxone 41-52 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 96-100 18353560-5 2008 Assessment of GLT1 expression in striatum confirmed a ceftriaxone-induced increase relative to vehicle. Ceftriaxone 54-65 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 14-18 18353560-10 2008 The glutamate uptake deficit, moreover, is present in symptomatic HD mice and reversal of this deficit by up-regulating the functional expression of GLT1 with ceftriaxone attenuates the HD phenotype. Ceftriaxone 159-170 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 149-153 18154526-5 2008 CTX-M-type ESBLs exhibit powerful activity against cefotaxime and ceftriaxone but generally not against ceftazidime, which has important implications for laboratory detection. Ceftriaxone 66-77 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 0-3 18048959-1 2007 In this study, we determined the in vitro inhibitory effects of ceftriaxone sodium, imipenem and ornidazole on hydratase and esterase activities of human erythrocyte carbonic anhydrase-I and II isozymes (CA I and II). Ceftriaxone 64-82 carbonic anhydrase 1 Homo sapiens 166-186 18048959-1 2007 In this study, we determined the in vitro inhibitory effects of ceftriaxone sodium, imipenem and ornidazole on hydratase and esterase activities of human erythrocyte carbonic anhydrase-I and II isozymes (CA I and II). Ceftriaxone 64-82 carbonic anhydrase 1 Homo sapiens 204-215 18048959-7 2007 The obtained IC50 values (inhibitor concentrations which cause 50% inhibition of in vitro enzyme activity) for esterase activity were 1.900, 0.008, 0.318 mM for hCA-I and 2.542, 0.0258, 0.343 mM for hCA-II for ceftriaxone sodium, imipenem and ornidazole, respectively. Ceftriaxone 210-228 cytochrome P450 family 24 subfamily A member 1 Homo sapiens 161-172 18048959-8 2007 IC50 values for CO2-hydratase activity were 0.864, 0.00354, 0.131 mM for hCA-I and 1.118, 0.0214, 0.263 mM for hCA-II for ceftriaxone sodium, imipenem and ornidazole, respectively. Ceftriaxone 122-140 cytochrome P450 family 24 subfamily A member 1 Homo sapiens 73-84 18048959-8 2007 IC50 values for CO2-hydratase activity were 0.864, 0.00354, 0.131 mM for hCA-I and 1.118, 0.0214, 0.263 mM for hCA-II for ceftriaxone sodium, imipenem and ornidazole, respectively. Ceftriaxone 122-140 carbonic anhydrase 2 Homo sapiens 111-117 18048959-9 2007 In conclusion, ceftriaxone sodium, imipenem and ornidazole showed inhibitory effects on human erythrocte carbonic anhydrase-I and II isozyme activities under in vitro conditions. Ceftriaxone 15-33 carbonic anhydrase 1 Homo sapiens 105-125 17491002-0 2007 In vitro efficacy of ceftriaxone/sulbactam against Escherichia coli isolates producing CTX-M-15 extended-spectrum beta-lactamase. Ceftriaxone 21-32 hypothetical protein Escherichia coli 87-95 17520506-5 2007 After changing the antibiotics to ceftriaxon and metronidazole, acute cholangitis being suspected, the fever subsided immediately and the CRP level decreased. Ceftriaxone 34-44 C-reactive protein Homo sapiens 138-141 18326497-4 2008 Ceftriaxone, one of the beta-lactam antibiotics, is a stimulator of EAAT2 expression with neuroprotective effects in both in vitro and in vivo models based in part on its ability to inhibit neuronal cell death by glutamate excitotoxicity. Ceftriaxone 0-11 solute carrier family 1 member 2 Homo sapiens 68-73 18326497-6 2008 We investigated the mechanism by which ceftriaxone enhances EAAT2 expression in primary human fetal astrocytes (PHFA). Ceftriaxone 39-50 solute carrier family 1 member 2 Homo sapiens 60-65 18326497-7 2008 Ceftriaxone elevated EAAT2 transcription in PHFA through the nuclear factor-kappaB (NF-kappaB) signaling pathway. Ceftriaxone 0-11 solute carrier family 1 member 2 Homo sapiens 21-26 18326497-7 2008 Ceftriaxone elevated EAAT2 transcription in PHFA through the nuclear factor-kappaB (NF-kappaB) signaling pathway. Ceftriaxone 0-11 nuclear factor kappa B subunit 1 Homo sapiens 61-82 18326497-7 2008 Ceftriaxone elevated EAAT2 transcription in PHFA through the nuclear factor-kappaB (NF-kappaB) signaling pathway. Ceftriaxone 0-11 nuclear factor kappa B subunit 1 Homo sapiens 84-93 18342307-1 2008 Ceftriaxone (a beta-lactam antibiotic) has recently been identified as having the rare ability to increase the expression and functional activity of the glutamate transporter subtype 1 (GLT-1) in rat spinal cord cultures. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 153-191 17613033-0 2007 Preparation and evaluation of mucin-gelatin mucoadhesive microspheres for rectal delivery of ceftriaxone sodium. Ceftriaxone 93-111 solute carrier family 13 member 2 Rattus norvegicus 30-35 17613033-5 2007 The results obtained from this study may indicate that ceftriaxone sodium could be successfully delivered rectally when embedded in microspheres formulated with either type A gelatin alone or its admixtures with porcine mucin; hence providing a therapeutically viable alternative route for the delivery of this acid-labile third generation cephalosporin. Ceftriaxone 55-73 solute carrier family 13 member 2 Rattus norvegicus 220-225 17436229-10 2007 CONCLUSIONS: This report shows that, after ceftriaxone treatment for 5 days, a portion of B. burgdorferi-infected mice still have live spirochetes in their body, which are activated by anti-TNF-alpha treatment. Ceftriaxone 43-54 tumor necrosis factor Mus musculus 190-199 17442809-7 2007 Upregulation of GLT-1 expression in astrocytes with ceftriaxone protected CA1 neurons from forebrain ischemia. Ceftriaxone 52-63 solute carrier family 1 member 2 Rattus norvegicus 16-21 17363173-3 2007 Nature 433:73-77] reported that beta-lactam antibiotics (including ceftriaxone, which easily crosses the blood-brain barrier) increase glutamate transporter 1 (GLT-1) expression and reduce cell death resulting from oxygen-glucose deprivation (OGD) in dissociated embryonic cortical cultures. Ceftriaxone 67-78 solute carrier family 1 member 2 Rattus norvegicus 135-158 17363173-3 2007 Nature 433:73-77] reported that beta-lactam antibiotics (including ceftriaxone, which easily crosses the blood-brain barrier) increase glutamate transporter 1 (GLT-1) expression and reduce cell death resulting from oxygen-glucose deprivation (OGD) in dissociated embryonic cortical cultures. Ceftriaxone 67-78 solute carrier family 1 member 2 Rattus norvegicus 160-165 17363173-6 2007 Whole-cell patch clamp recording of glutamate-induced N-methyl-d-aspartate (NMDA) currents from CA1 pyramidal neurons showed a larger potentiation of these currents after application of 15 microM dl-threo-beta-benzyloxyaspartic acid (TBOA; a potent blocker of glutamate transporters) in ceftriaxone-injected animals than in untreated animals, indicating increased glutamate transporter activity. Ceftriaxone 287-298 carbonic anhydrase 1 Rattus norvegicus 96-99 17442809-7 2007 Upregulation of GLT-1 expression in astrocytes with ceftriaxone protected CA1 neurons from forebrain ischemia. Ceftriaxone 52-63 carbonic anhydrase 1 Rattus norvegicus 74-77 17371739-13 2007 CONCLUSIONS: Previous use of ceftriaxone and ciprofloxacin are independent risk factors for the development of VAPA. Ceftriaxone 29-40 VAMP associated protein A Homo sapiens 111-115 15750057-4 2005 All the isolates demonstrated resistance to ceftriaxone and ceftazidime due to the production of an extended-spectrum beta-lactamase (ESBL). Ceftriaxone 44-55 beta-lactamase Salmonella enterica 118-132 15907788-2 2005 reported that beta-lactam antibiotics, including penicillin and ceftriaxone, are potential therapeutic drugs to treat some neurological disorders, e.g., amyotrophic lateral sclerosis (ALS), by modulating the expression of glutamate transporter GLT1 via gene activation. Ceftriaxone 64-75 solute carrier family 1 member 2 Homo sapiens 244-248 15990986-10 2005 The prevalence of ESBL-producers increased significantly during therapy in OASIS II among 193 ceftriaxone/metronidazole recipients (from 4 [2.1%] to 18 [9.3%]) (p<0.001), whereas no ertapenem recipient was colonized with an ESBL-producer at the end of therapy in either study. Ceftriaxone 94-105 cAMP responsive element binding protein 3 like 1 Homo sapiens 75-80 17122424-2 2007 Recently, beta-lactam antibiotics, like ceftriaxone (CTX), were reported to induce the upregulation of GLT-1. Ceftriaxone 40-51 solute carrier family 1 member 2 Homo sapiens 103-108 15967622-4 2005 In the case of ceftriaxone the situation is even more complicated, three overlapping processes coexist with pK1 2.37 (COOH), pK2 3.03 (aminothiazole) and pK3 4.21 (hydroxytriazinone). Ceftriaxone 15-26 pyruvate kinase L/R Homo sapiens 108-111 15967622-4 2005 In the case of ceftriaxone the situation is even more complicated, three overlapping processes coexist with pK1 2.37 (COOH), pK2 3.03 (aminothiazole) and pK3 4.21 (hydroxytriazinone). Ceftriaxone 15-26 prokineticin 2 Homo sapiens 125-128 15967622-4 2005 In the case of ceftriaxone the situation is even more complicated, three overlapping processes coexist with pK1 2.37 (COOH), pK2 3.03 (aminothiazole) and pK3 4.21 (hydroxytriazinone). Ceftriaxone 15-26 pyruvate kinase M1/2 Homo sapiens 154-157 16315580-4 2005 The parenteral agent ceftriaxone is the drug of choice for severe acute and chronic infections, due to good penetration into CSF, convenient single daily dosage regimen and proven high efficacy in clinical trials involving a wide variety of disseminated infections. Ceftriaxone 21-32 colony stimulating factor 2 Homo sapiens 125-128 15772139-0 2005 Ceftriaxone pharmacokinetics in interleukin-10-treated murine pneumococcal pneumonia. Ceftriaxone 0-11 interleukin 10 Mus musculus 32-46 15772139-1 2005 OBJECTIVES: Anti-inflammatory therapy with interleukin-10 (IL-10) was previously reported to reduce pulmonary inflammation and to prevent septicaemia in murine pneumococcal pneumonia treated with ceftriaxone. Ceftriaxone 196-207 interleukin 10 Mus musculus 43-57 15772139-1 2005 OBJECTIVES: Anti-inflammatory therapy with interleukin-10 (IL-10) was previously reported to reduce pulmonary inflammation and to prevent septicaemia in murine pneumococcal pneumonia treated with ceftriaxone. Ceftriaxone 196-207 interleukin 10 Mus musculus 59-64 15772139-2 2005 In the present report, we investigated the influence of pulmonary infection and IL-10 administration on the pharmacokinetics of ceftriaxone. Ceftriaxone 128-139 interleukin 10 Mus musculus 80-85 15772139-10 2005 Co-administration of IL-10 with ceftriaxone in infected animals further retained ceftriaxone in the bloodstream and reduced its volume of distribution at steady state and the ratio of AUC(lung)/AUC(serum). Ceftriaxone 32-43 interleukin 10 Mus musculus 21-26 15772139-10 2005 Co-administration of IL-10 with ceftriaxone in infected animals further retained ceftriaxone in the bloodstream and reduced its volume of distribution at steady state and the ratio of AUC(lung)/AUC(serum). Ceftriaxone 81-92 interleukin 10 Mus musculus 21-26 15772139-12 2005 CONCLUSIONS: The results suggest that pulmonary infection, and therapy with IL-10, both affect the pharmacokinetics of ceftriaxone. Ceftriaxone 119-130 interleukin 10 Mus musculus 76-81 15772139-13 2005 Indeed, administration of IL-10 + ceftriaxone improved the survival rate of mice (P < 0.001 compared with therapy with ceftriaxone alone). Ceftriaxone 122-133 interleukin 10 Mus musculus 26-31 15273090-1 2004 The emergence in the United States of resistance to expanded-spectrum cephalosporin (e.g., ceftriaxone) within the salmonellae has been associated primarily with three large (>100-kb) plasmids (designated types A, B, and C) and one 10.1-kb plasmid (type D) that carry the blaCMY-2 gene. Ceftriaxone 91-102 CMY-2 beta-lactamase 2 Salmonella enterica subsp. enterica serovar Typhimurium 275-283 15813992-3 2005 In January"s edition of Nature, Rothstein et al (2005) reports that the most commonly used class of antibiotics (beta-lactam antibiotics) such as ceftriaxone promoted the expression of GLT1 and demonstrated a functional role in both in vitro and in vivo models of glutamate neurotoxicity. Ceftriaxone 146-157 solute carrier family 1 member 2 Homo sapiens 185-189 15635412-8 2005 When delivered to animals, the beta-lactam ceftriaxone increased both brain expression of GLT1 and its biochemical and functional activity. Ceftriaxone 43-54 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 90-94 16359197-1 2005 Multidrug-resistant Salmonella Newport with decreased susceptibility to ceftriaxone (MDR-AmpC) is becoming increasingly common in its food animal reservoirs and in humans. Ceftriaxone 72-83 ampC Salmonella enterica subsp. enterica serovar Newport 89-93 15364010-5 2004 With ceftriaxone therapy, none of the wild-type mice but 43% of the p50-deficient animals died. Ceftriaxone 5-16 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 68-71 15273090-2 2004 In the present study, the distribution of these four known blaCMY-2-carrying plasmids among 35 ceftriaxone-resistant Salmonella isolates obtained from 1998 to 2001 was examined. Ceftriaxone 95-106 CMY-2 beta-lactamase 2 Salmonella enterica subsp. enterica serovar Typhimurium 59-67 15222981-4 2004 Human lymphocytes cultured in the presence of ampicillin or ceftriaxone produced Hsp 60 and Hsp 27, estimated by immunoblotting in a time-dependent manner and the increased levels of Hsp 60 and Hsp 27 correlated with enhanced resistance of the lymphocytes to apoptosis, as determined by flow cytometry. Ceftriaxone 60-71 heat shock protein family D (Hsp60) member 1 Homo sapiens 81-87 15222981-4 2004 Human lymphocytes cultured in the presence of ampicillin or ceftriaxone produced Hsp 60 and Hsp 27, estimated by immunoblotting in a time-dependent manner and the increased levels of Hsp 60 and Hsp 27 correlated with enhanced resistance of the lymphocytes to apoptosis, as determined by flow cytometry. Ceftriaxone 60-71 heat shock protein family B (small) member 1 Homo sapiens 92-98 15222981-4 2004 Human lymphocytes cultured in the presence of ampicillin or ceftriaxone produced Hsp 60 and Hsp 27, estimated by immunoblotting in a time-dependent manner and the increased levels of Hsp 60 and Hsp 27 correlated with enhanced resistance of the lymphocytes to apoptosis, as determined by flow cytometry. Ceftriaxone 60-71 heat shock protein family D (Hsp60) member 1 Homo sapiens 183-189 15222981-4 2004 Human lymphocytes cultured in the presence of ampicillin or ceftriaxone produced Hsp 60 and Hsp 27, estimated by immunoblotting in a time-dependent manner and the increased levels of Hsp 60 and Hsp 27 correlated with enhanced resistance of the lymphocytes to apoptosis, as determined by flow cytometry. Ceftriaxone 60-71 heat shock protein family B (small) member 1 Homo sapiens 194-200 15359893-0 2004 [Successful treatment of beta-lactamase-negative ampicillin-resistant Haemophilus influenzae type b meningitis with high-dose ceftriaxone administration]. Ceftriaxone 126-137 beta-lactamase TEM-1 Haemophilus influenzae 25-39 15094275-3 2004 Ciprofloxacin resistance was associated with mutations in gyrA and parC, whereas the ampC gene (bla(CMY-2)), responsible for ceftriaxone resistance, was carried by a transposon-like mobile element. Ceftriaxone 125-136 beta-lactamase Salmonella enterica 85-89 15207270-0 2004 Increased mortality and spatial memory deficits in TNF-alpha-deficient mice in ceftriaxone-treated experimental pneumococcal meningitis. Ceftriaxone 79-90 tumor necrosis factor Mus musculus 51-60 15099589-2 2004 Using a modified patch-clamp technique in combination with an ultrafast system for solution exchange we investigated the functional interaction of gentamicin, penicillin G, tetracycline, erythromycin and ceftriaxone with nAChR transiently transfected into HEK293 cells as a potential molecular target. Ceftriaxone 204-215 cholinergic receptor nicotinic alpha 4 subunit Homo sapiens 221-226 12854084-0 2003 Anti-tumor necrosis factor antibody impairs the therapeutic effect of ceftriaxone in murine pneumococcal pneumonia. Ceftriaxone 70-81 tumor necrosis factor Mus musculus 5-26 15063500-0 2004 Plasmid-mediated florfenicol and ceftriaxone resistance encoded by the floR and bla(CMY-2) genes in Salmonella enterica serovars Typhimurium and Newport isolated in the United States. Ceftriaxone 33-44 FloR Salmonella enterica 71-75 15063500-0 2004 Plasmid-mediated florfenicol and ceftriaxone resistance encoded by the floR and bla(CMY-2) genes in Salmonella enterica serovars Typhimurium and Newport isolated in the United States. Ceftriaxone 33-44 beta-lactamase Escherichia coli 80-83 14586882-11 2003 Protein mass of multidrug resistance protein 2 and its function, assessed by the hepatic maximum secretory rate of ceftriaxone, did not show significant changes in ILs or NILs compared with sham-operated rats. Ceftriaxone 115-126 ATP binding cassette subfamily B member 4 Rattus norvegicus 16-46 14527353-11 2003 The group of PRSP was with significantly higher rates of non-susceptibility for ceftriaxone (18.4%), cefurxime (58.6%), cefaclor (53.4%), compared with the group of PEN-S (0.5%, 1.8% and 0.2%, respectively) and the rate of multi-drug resistance in the isolates of PRSP group (92.9%) was significantly higher than that of PEN-S group (59.2%). Ceftriaxone 80-91 HtrA serine peptidase 3 Homo sapiens 13-17 12854084-8 2003 These data suggest that treatment with anti-TNF impairs the therapeutic efficacy of CEF during pneumococcal pneumonia. Ceftriaxone 84-87 tumor necrosis factor Mus musculus 44-47 12507831-11 2003 Among Enterobacter spp., resistance (MIC>or=32 mg/l) to aztreonam, ceftazidime and ceftriaxone ranged from 12.3 to 21.2% over the 4 years, whereas resistance in Klebsiella (MIC>or=2 mg/l) ranged from 5.9 to 6.8%. Ceftriaxone 86-97 histocompatibility minor 13 Homo sapiens 19-22 12615876-4 2003 Detection of KPC-2 may be a problem for clinical laboratories because in this study it was associated with positive extended-spectrum beta-lactamase (ESBL) confirmation tests (clavulanate-potentiated activities of ceftriaxone, ceftazidime, cefepime and aztreonam). Ceftriaxone 214-225 carbapenem-hydrolyzing beta-lactamase KPC-2 Klebsiella pneumoniae 13-18 12696635-1 2003 PURPOSE: To investigate the in vitro effects of gentamicin sulfate, vancomycin hydrochloride, sodium cefazolin and ceftriaxone on glucose 6-phosphate dehydrogenase enzyme (G6PD) purified from sheep lenses. Ceftriaxone 115-126 glucose-6-phosphate 1-dehydrogenase Ovis aries 130-170 12696635-1 2003 PURPOSE: To investigate the in vitro effects of gentamicin sulfate, vancomycin hydrochloride, sodium cefazolin and ceftriaxone on glucose 6-phosphate dehydrogenase enzyme (G6PD) purified from sheep lenses. Ceftriaxone 115-126 glucose-6-phosphate 1-dehydrogenase Ovis aries 172-176 12574281-8 2003 All but 1 of 14 screen-positive AmpC nonproducers (and ESBL nonproducers) were susceptible to ceftriaxone and cefepime at the standard inoculum as were 6 of 6 isolates that were randomly selected and tested with a high inoculum. Ceftriaxone 94-105 beta-lactamase Klebsiella pneumoniae 32-36 12198614-5 2002 With ceftriaxone therapy, none of the wt but 27% of the TLR2(-/-) mice died (P<.04). Ceftriaxone 5-16 toll-like receptor 2 Mus musculus 56-60 12645197-0 2002 Ceftriaxone-resistant Salmonella enterica serovar Hadar: evidence for interspecies transfer of blaCMY-2 in a Taiwanese university hospital. Ceftriaxone 0-11 beta-lactamase Salmonella enterica 95-103 11929691-8 2002 Overall, ceftriaxone and aztreonam were the best substrates for the detection of the ESBL phenotype between both E. coli isolates and K. pneumoniae ESBL phenotypes; however, there was significant variation between countries in substrate preference. Ceftriaxone 9-20 EsbL Escherichia coli 85-89 12130979-8 2002 Higher levels of tumor necrosis factor-alpha were measured in serum (p =.027) and peritoneal fluid (p =.001) of CRO-treated mice. Ceftriaxone 112-115 tumor necrosis factor Mus musculus 17-44 12015689-2 2002 For the assessable recipients of cefazolin-probenecid (n=59) and ceftriaxone-placebo (n=57), clinical cure occurred at the end of treatment in 86% and 96% (P=.11), respectively, and was maintained at 1 month of follow-up in 96% and 91% (P=.55), respectively. Ceftriaxone 65-76 endonuclease, poly(U) specific Homo sapiens 156-161 11909604-7 2002 The inhibition constant (K(i)) values of cefoperazone, cefazolin, ceftriaxone and cephaloridine for human-OAT1 were much lower than those for human-OAT3 and human-OAT4, whereas the K(i) values of cephalothin and cefotaxime for human-OAT3 were much lower than those for human-OAT1 and human-OAT4. Ceftriaxone 66-77 solute carrier family 22 member 11 Homo sapiens 290-294 11909604-7 2002 The inhibition constant (K(i)) values of cefoperazone, cefazolin, ceftriaxone and cephaloridine for human-OAT1 were much lower than those for human-OAT3 and human-OAT4, whereas the K(i) values of cephalothin and cefotaxime for human-OAT3 were much lower than those for human-OAT1 and human-OAT4. Ceftriaxone 66-77 solute carrier family 22 member 6 Homo sapiens 106-110 11909604-7 2002 The inhibition constant (K(i)) values of cefoperazone, cefazolin, ceftriaxone and cephaloridine for human-OAT1 were much lower than those for human-OAT3 and human-OAT4, whereas the K(i) values of cephalothin and cefotaxime for human-OAT3 were much lower than those for human-OAT1 and human-OAT4. Ceftriaxone 66-77 solute carrier family 22 member 8 Homo sapiens 233-237 11909604-7 2002 The inhibition constant (K(i)) values of cefoperazone, cefazolin, ceftriaxone and cephaloridine for human-OAT1 were much lower than those for human-OAT3 and human-OAT4, whereas the K(i) values of cephalothin and cefotaxime for human-OAT3 were much lower than those for human-OAT1 and human-OAT4. Ceftriaxone 66-77 solute carrier family 22 member 6 Homo sapiens 275-279 11929691-8 2002 Overall, ceftriaxone and aztreonam were the best substrates for the detection of the ESBL phenotype between both E. coli isolates and K. pneumoniae ESBL phenotypes; however, there was significant variation between countries in substrate preference. Ceftriaxone 9-20 EsbL Escherichia coli 148-152 11953180-12 2002 The beta-lactamase from K. pneumoniae 99595 had stronger activity against ceftazidime, ceftaxime, and ceftriaxone than that from K. pneumoniae 99607. Ceftriaxone 102-113 beta-lactamase Klebsiella pneumoniae 4-18 11850164-8 2002 For M. catarrhalis, beta-lactamase-negative isolates had MICs < or =0.12-0.25 mg/l for ampicillin and < or =0.03-0.12 mg/l for ceftriaxone. Ceftriaxone 133-144 beta-lactamase TEM-1 Haemophilus influenzae 20-34 11850164-9 2002 In contrast, beta-lactamase production resulted in MICs of < or = 0.12->16 mg/l for ampicillin and < or = 0.03-4 mg/l for ceftriaxone. Ceftriaxone 131-142 beta-lactamase TEM-1 Haemophilus influenzae 13-27 11709304-9 2001 For PRP-1 the best FME for the combination AMZ-CRO was 1.22 with drug concentrations of 1.68 mg/liter for AMZ and 0.17 mg/liter for CRO; the best FME for the combination VAN-CRO was 1.75 with VAN at 0.57 mg/liter and CRO at 0.17 mg/liter. Ceftriaxone 47-50 prion protein Homo sapiens 4-7 11709304-10 2001 For PRP-2 the best FME obtained for the combination AMZ-CRO was 1.05 with drug concentrations of 11.28 mg/liter for AMZ and 0.64 mg/liter for CRO; the best FME obtained for the combination VAN-CRO was 1.35 with VAN at 0.25 mg/liter and CRO at 1.49 mg/liter. Ceftriaxone 56-59 prion protein Homo sapiens 4-7 11709361-1 2001 Twenty-one Salmonella and 54 Escherichia coli isolates, recovered from food animals and retail ground meats, that exhibited decreased susceptibilities to ceftiofur and ceftriaxone were shown to possess a bla(CMY) gene. Ceftriaxone 168-179 beta-lactamase Escherichia coli 204-207 11709361-2 2001 The bla(CMY-4) gene was identified in an E. coli isolate recovered from retail chicken and was further shown to be responsible for resistance to cephalothin, ampicillin, and amoxicillin-clavulanic acid and elevated MICs of ceftriaxone, cefoxitin, and ceftiofur. Ceftriaxone 223-234 beta-lactamase Escherichia coli 4-7 11709304-10 2001 For PRP-2 the best FME obtained for the combination AMZ-CRO was 1.05 with drug concentrations of 11.28 mg/liter for AMZ and 0.64 mg/liter for CRO; the best FME obtained for the combination VAN-CRO was 1.35 with VAN at 0.25 mg/liter and CRO at 1.49 mg/liter. Ceftriaxone 142-145 prion protein Homo sapiens 4-7 11760173-3 2001 All 3 children responded to antibiotic regimens consisting of cefotaxime for 10 d, ceftriaxone for 3 weeks and ceftriaxone plus clindamycin for 4 weeks, respectively. Ceftriaxone 83-94 paired box 5 Homo sapiens 0-5 11320450-2 2001 The highest percentage of ESBL phenotype (defined as a minimum inhibitory concentration [MIC] > or =2 microg/mL for ceftazidime, ceftriaxone, or aztreonam) was detected among K. pneumoniae strains from Latin America (45%), followed by those from the Western Pacific region (25%), Europe (23%), the United States (8%), and Canada (5%). Ceftriaxone 132-143 CTX-M-15 Klebsiella pneumoniae 26-30 11393590-5 2001 Prostacyclin production and t-PA release were inhibited only by ceftriaxone at high concentrations. Ceftriaxone 64-75 plasminogen activator, tissue type Homo sapiens 28-32 11760173-3 2001 All 3 children responded to antibiotic regimens consisting of cefotaxime for 10 d, ceftriaxone for 3 weeks and ceftriaxone plus clindamycin for 4 weeks, respectively. Ceftriaxone 111-122 paired box 5 Homo sapiens 0-5 10747826-5 2000 Ceftriaxone was the most active agent against the penicillin-susceptible strain (CD50 = 2 mg/kg), but showed a 30-fold decrease in potency against the resistant strain. Ceftriaxone 0-11 intercellular adhesion molecule 5, telencephalin Mus musculus 81-85 11135779-0 2000 Emergence of domestically acquired ceftriaxone-resistant Salmonella infections associated with AmpC beta-lactamase. Ceftriaxone 35-46 beta lactamase DHA-1 Citrobacter freundii 95-99 11135779-14 2000 Most ceftriaxone-resistant Salmonella isolates had similar AmpC plasmid-mediated resistance. Ceftriaxone 5-16 beta lactamase DHA-1 Citrobacter freundii 59-63 10998137-7 2000 A part of these CD4+ T cell clones were cytotoxic, i.e., two selected ceftriaxone-specific T cell clones killed target cells after antigen stimulation. Ceftriaxone 70-81 CD4 molecule Homo sapiens 16-19 10929876-1 2000 In vitro activity of ceftiofur, a cephalosporin used in veterinary practice was compared using ceftriaxone-resistant (producing extended spectrum beta-lactamase (ESBL)) and -susceptible clinical isolates of Esherichia coli and Klebsiella pneumoniae. Ceftriaxone 95-106 beta-lactamase Klebsiella pneumoniae 146-160 10103209-1 1999 DNA sequencing data showed that five clinical isolates of Escherichia coli with reduced susceptibility to ceftazidime, ceftriaxone, and cefotaxime contain an ampC gene that is preceded by a strong promoter. Ceftriaxone 119-130 beta-lactamase Escherichia coli 158-162 10950626-6 2000 Several broad-spectrum beta-lactams ("fourth-generation" cephalosporins, carbapenems) are expected to be used with increasing frequency as a result of the emerging high rates of specific beta-lactamases that compromise the use of ceftriaxone, ceftazidime, and many beta-lactamase inhibition/ penicillin combinations. Ceftriaxone 230-241 beta-lactamase Staphylococcus aureus 187-201 10449953-7 1999 Enhanced cytokine levels, particularly of IL-5, were found in the supernatant of the LTT stimulated with ceftriaxone and metronidazole. Ceftriaxone 105-116 interleukin 5 Homo sapiens 42-46 9359724-6 1997 TNF-alpha was significantly reduced in animals treated with IL-10, dexamethasone, or both compared with levels in rabbits receiving ceftriaxone alone. Ceftriaxone 132-143 tumor necrosis factor Oryctolagus cuniculus 0-9 9635511-4 1998 However, the increase in NAG level was markedly less when isepamicin was administered in combination with ceftriaxone (p<0.01). Ceftriaxone 106-117 O-GlcNAcase Rattus norvegicus 25-28 9359724-6 1997 TNF-alpha was significantly reduced in animals treated with IL-10, dexamethasone, or both compared with levels in rabbits receiving ceftriaxone alone. Ceftriaxone 132-143 interleukin-10 Oryctolagus cuniculus 60-65 9044022-6 1997 In three of the four strains exposure to antibiotics resulted in considerably lower cytokine levels (ANOVA, P < 0.001), and TNF-alpha levels were significantly lower after exposure to penicillin or ceftriaxone than after chloramphenicol treatment. Ceftriaxone 201-212 tumor necrosis factor Homo sapiens 127-136 9276386-10 1997 Eighty-six blood isolates of E. coli and Klebsiella species were screened for ESBL expression by the double-disk and three-dimensional tests, both with ceftriaxone. Ceftriaxone 152-163 EsbL Klebsiella oxytoca 78-82 9300809-6 1997 Towards cefotaxime and ceftriaxone (third-generation cephalosporins), the S. fonticola enzyme exhibited catalytic efficiencies much higher than those of MEN-1 and extended-spectrum TEM derivative beta-lactamases. Ceftriaxone 23-34 menin 1 Homo sapiens 153-158 9263362-5 1997 In addition, IB-1 strains were associated with PPNG and displayed higher minimum inhibitory concentrations (MICs) for ceftriaxone, cefuroxime, and ciprofloxacin. Ceftriaxone 118-129 mitogen-activated protein kinase 8 interacting protein 1 Homo sapiens 13-17 9209783-8 1997 Two and 5 h after initiation of therapy, CSF TNF-alpha activities were lower with rifabutin 5 mg/kg/h than with ceftriaxone (medians 2 vs. 141 U/ml, p = 0.005 at 2 h; median 51 vs. 120 U/ml 5 h after initiation of therapy, p = 0.04). Ceftriaxone 112-123 tumor necrosis factor Oryctolagus cuniculus 45-54 9356840-7 1997 CONCLUSION: Ceftriaxone is a safe and effective option for the treatment of SBP. Ceftriaxone 12-23 selenium binding protein 1 Homo sapiens 76-79 9447470-1 1997 The stability and compatibility of anakinra (recombinant human interleukin-1 receptor antagonist) with ceftriaxone sodium in 0.9% sodium chloride or 5% dextrose injection was determined during a 4-h period at ambient room temperature and light. Ceftriaxone 103-121 interleukin 1 receptor antagonist Homo sapiens 63-96 8067731-1 1994 The kinetics of tumor necrosis factor (TNF) levels in serum during therapy with cell wall-active agents (ceftriaxone, imipenem) and gentamicin were investigated in rabbits with experimental endocarditis caused by an isogenic pair of Klebsiella pneumoniae strains: a TEM-3 beta-lactamase-producing strain (KpR) or its susceptible variant (KpS). Ceftriaxone 105-116 tumor necrosis factor Oryctolagus cuniculus 39-42 14688917-8 1996 It was concluded that children with complicated UTI could be treated alternatively by once daily ceftriaxone. Ceftriaxone 97-108 alpha-1-microglobulin/bikunin precursor Homo sapiens 48-51 8591944-2 1995 beta-Lactamases with pIs of 5.4 and 8.1 were detected by hydrolysis of ampicillin and ceftriaxone respectively among cefotaxime resistant serovars of Salmonella spp. Ceftriaxone 86-97 histocompatibility minor 13 Homo sapiens 161-164 8559623-4 1995 In contrast highly PRSP strains were resistant to most oral antimicrobials customarily used for AOM with one-third of strains highly resistant (MIC > or = 2.0 micrograms/ml) to ceftriaxone. Ceftriaxone 180-191 HtrA serine peptidase 3 Homo sapiens 19-23 8913478-0 1996 In vivo activities of ceftriaxone and vancomycin against Borrelia spp. Ceftriaxone 22-33 sphingosine-1-phosphate phosphatase 1 Mus musculus 66-69 8858476-8 1996 The effect of beta-lactamase synthesis was inhibited by the combination of amoxycillin with clavulanate, and by cefuroxime and ceftriaxone. Ceftriaxone 127-138 beta-lactamase Staphylococcus aureus 14-28 7560986-8 1995 Many strains are also resistant to newer cephalosporins like cefotaxime and ceftriaxone (MIC > or = 2 mg L-1). Ceftriaxone 76-87 immunoglobulin kappa variable 1-16 Homo sapiens 108-111 8067731-5 1994 The peak in the serum TNF levels occurred 4 h after the first antibiotic injection and with ceftriaxone was significantly higher (P < 0.05) against KpS (1.99 +/- 0.52 ng/ml) than against KpR (1.40 +/- 0.17 ng/ml). Ceftriaxone 92-103 tumor necrosis factor Oryctolagus cuniculus 22-25 8011012-3 1994 The influence of cefodizime (CAS 69739-16-8), a new broad spectrum cephalosporin with immunostimulatory effects, and ceftriaxone on the production of GM-CSF and IL-8 in HBEC primary cultures was investigated. Ceftriaxone 117-128 colony stimulating factor 2 Homo sapiens 150-156 8031041-9 1994 The 24-h urinary excretion of beta-galactosidase was significantly reduced in animals treated with the combination tobramycin-ceftriaxone compared with the administration of tobramycin alone at 40 and 60 mg/kg/12 h after 5 and 10 days (P < 0.05). Ceftriaxone 126-137 galactosidase, beta 1 Rattus norvegicus 30-48 2384579-3 1990 Ceftriaxone was tested with two sources of albumin (aqueous solution and diluted serum). Ceftriaxone 0-11 albumin Homo sapiens 43-50 8377450-9 1993 For persisting or increased fever or CRP elevation, 9 patients were treated with ceftriaxone and teicoplanin successfully. Ceftriaxone 81-92 C-reactive protein Homo sapiens 37-40 8060183-1 1993 Ceftriaxone (rocefin), a 3rd generation cephalosporin with prolonged action, was highly efficient (ED50 0.12 to 0.38 mg/mouse) against experimental plague in albino mice infected either by Fra+ or Fra- strains of the plague microbe. Ceftriaxone 0-11 rabaptin, RAB GTPase binding effector protein 2 Mus musculus 189-192 8060183-1 1993 Ceftriaxone (rocefin), a 3rd generation cephalosporin with prolonged action, was highly efficient (ED50 0.12 to 0.38 mg/mouse) against experimental plague in albino mice infected either by Fra+ or Fra- strains of the plague microbe. Ceftriaxone 0-11 rabaptin, RAB GTPase binding effector protein 2 Mus musculus 197-200 8060183-1 1993 Ceftriaxone (rocefin), a 3rd generation cephalosporin with prolonged action, was highly efficient (ED50 0.12 to 0.38 mg/mouse) against experimental plague in albino mice infected either by Fra+ or Fra- strains of the plague microbe. Ceftriaxone 13-20 rabaptin, RAB GTPase binding effector protein 2 Mus musculus 189-192 8060183-1 1993 Ceftriaxone (rocefin), a 3rd generation cephalosporin with prolonged action, was highly efficient (ED50 0.12 to 0.38 mg/mouse) against experimental plague in albino mice infected either by Fra+ or Fra- strains of the plague microbe. Ceftriaxone 13-20 rabaptin, RAB GTPase binding effector protein 2 Mus musculus 197-200 2403378-0 1990 Ceftriaxone binding to human serum albumin. Ceftriaxone 0-11 albumin Homo sapiens 29-42 2403378-8 1990 CEF free fraction (fp) in isolated human serum albumin (CEF fp = 7.7%) was increased by drugs which bind to Site I: sulfisoxazole (CEF fp = 68.1%), warfarin (CEF fp = 56.0%) and furosemide (CEF fp = 55.0%). Ceftriaxone 0-3 albumin Homo sapiens 41-54 2403378-10 1990 CEF appeared to bind to Site I (the warfarin site) on human serum albumin, and was displaced by PROB and DIAZ via a mechanism which did not involve direct competition at a common binding site. Ceftriaxone 0-3 albumin Homo sapiens 60-73 2384579-0 1990 High-performance liquid chromatographic determination of the binding of ceftriaxone to human serum albumin solution and albumin from diluted human serum. Ceftriaxone 72-83 albumin Homo sapiens 99-106 2384579-1 1990 The binding of ceftriaxone to human serum albumin has been studied by high-performance liquid chromatography. Ceftriaxone 15-26 albumin Homo sapiens 36-49 2195457-5 1990 In case of synergy, sonicated extracts have been prepared and examined by isoelectrofocusing with the detection of beta-lactamase activity by ceftriaxone and nitrocefin. Ceftriaxone 142-153 beta-lactamase Klebsiella pneumoniae 115-129 2292206-1 1990 A total of 33 patients with bacterial meningitis were treated with single daily doses of ceftriaxone (CTR 100 mg/kg/day i.v.) Ceftriaxone 89-100 calcitonin receptor Homo sapiens 102-105 2289997-6 1990 For ceftazidime and ceftriaxone similar changes of t1/2 and Vd are observed. Ceftriaxone 20-31 interleukin 1 receptor like 1 Homo sapiens 51-62 2091255-2 1990 Review of recent data from the USA and Europe indicates that delayed CSF sterilization occurs significantly more often with ampicillin/chloramphenicol and cefuroxime than with ceftriaxone and cefotaxime. Ceftriaxone 176-187 colony stimulating factor 2 Homo sapiens 69-72 33822092-0 2021 Dual azithromycin/ceftriaxone therapy for gonorrhoea in PrEP cohorts results in levels of macrolide consumption that exceed resistance thresholds by up to 7-fold. Ceftriaxone 18-29 prolyl endopeptidase Homo sapiens 56-60 2287905-5 1990 Both cephalosporins significantly reduced the incidence of UTI (ceftriaxone 11.9%, cephradine 17.6% compared to controls 47.2%; p less than 0.0005). Ceftriaxone 64-75 alpha-1-microglobulin/bikunin precursor Homo sapiens 59-62 33232732-8 2021 The first pattern (amoxicillin-clavulanate, ceftriaxone) is characterised by high rate of UAP in every department, the second (cloxacillin, rifampin) by high rate of SAP in every department and the third (broad-spectrum beta-lactams) by heterogeneous distribution of SAP/UAP among departments. Ceftriaxone 44-55 SH2 domain containing 1A Homo sapiens 166-169 33232732-8 2021 The first pattern (amoxicillin-clavulanate, ceftriaxone) is characterised by high rate of UAP in every department, the second (cloxacillin, rifampin) by high rate of SAP in every department and the third (broad-spectrum beta-lactams) by heterogeneous distribution of SAP/UAP among departments. Ceftriaxone 44-55 SH2 domain containing 1A Homo sapiens 267-270 34802899-8 2021 To test whether glutamate neurotoxicity plays a role in Niemann-Pick disease, type C1 progression, we treated NPC1 deficient mice with ceftriaxone and riluzole. Ceftriaxone 135-146 NPC intracellular cholesterol transporter 1 Mus musculus 110-114 34975778-5 2021 bla PRC-1 confers resistance to many beta-lactam antibiotics, including penicillins (penicillin G, amoxicillin, and amoxicillin-clavulanic acid) and cephalosporins (cefazolin, ceftriaxone, and cefotaxime). Ceftriaxone 176-187 protein regulator of cytokinesis 1 Homo sapiens 4-9 34409650-12 2021 Treatment with VPA or CEF enhanced the expression levels of GLT-1, GLAST, EAAC1, and GS, whereas the glutaminase expression level was reduced. Ceftriaxone 22-25 solute carrier family 1 member 2 Rattus norvegicus 60-65 34409650-12 2021 Treatment with VPA or CEF enhanced the expression levels of GLT-1, GLAST, EAAC1, and GS, whereas the glutaminase expression level was reduced. Ceftriaxone 22-25 solute carrier family 1 member 3 Rattus norvegicus 67-72 34409650-12 2021 Treatment with VPA or CEF enhanced the expression levels of GLT-1, GLAST, EAAC1, and GS, whereas the glutaminase expression level was reduced. Ceftriaxone 22-25 solute carrier family 1 member 1 Rattus norvegicus 74-79 34409650-12 2021 Treatment with VPA or CEF enhanced the expression levels of GLT-1, GLAST, EAAC1, and GS, whereas the glutaminase expression level was reduced. Ceftriaxone 22-25 glutaminase Rattus norvegicus 101-112 34938384-8 2021 Finally, ceftriaxone treatment increased the expression of the tight junction proteins zona occludens-1(ZO-1) and occludin in the colon, decreased the expression of the inflammation-related proteins TLR4, MyD88, and NF-kappaB in the colon, and decreased the serum concentration of the proinflammatory cytokines interleukin-1beta (IL-1beta), IL-6, and tumour necrosis factor-alpha (TNF-alpha). Ceftriaxone 9-20 tight junction protein 1 Mus musculus 104-108 34938384-8 2021 Finally, ceftriaxone treatment increased the expression of the tight junction proteins zona occludens-1(ZO-1) and occludin in the colon, decreased the expression of the inflammation-related proteins TLR4, MyD88, and NF-kappaB in the colon, and decreased the serum concentration of the proinflammatory cytokines interleukin-1beta (IL-1beta), IL-6, and tumour necrosis factor-alpha (TNF-alpha). Ceftriaxone 9-20 occludin Mus musculus 114-122 34938384-8 2021 Finally, ceftriaxone treatment increased the expression of the tight junction proteins zona occludens-1(ZO-1) and occludin in the colon, decreased the expression of the inflammation-related proteins TLR4, MyD88, and NF-kappaB in the colon, and decreased the serum concentration of the proinflammatory cytokines interleukin-1beta (IL-1beta), IL-6, and tumour necrosis factor-alpha (TNF-alpha). Ceftriaxone 9-20 toll-like receptor 4 Mus musculus 199-203 34938384-8 2021 Finally, ceftriaxone treatment increased the expression of the tight junction proteins zona occludens-1(ZO-1) and occludin in the colon, decreased the expression of the inflammation-related proteins TLR4, MyD88, and NF-kappaB in the colon, and decreased the serum concentration of the proinflammatory cytokines interleukin-1beta (IL-1beta), IL-6, and tumour necrosis factor-alpha (TNF-alpha). Ceftriaxone 9-20 myeloid differentiation primary response gene 88 Mus musculus 205-210 34938384-8 2021 Finally, ceftriaxone treatment increased the expression of the tight junction proteins zona occludens-1(ZO-1) and occludin in the colon, decreased the expression of the inflammation-related proteins TLR4, MyD88, and NF-kappaB in the colon, and decreased the serum concentration of the proinflammatory cytokines interleukin-1beta (IL-1beta), IL-6, and tumour necrosis factor-alpha (TNF-alpha). Ceftriaxone 9-20 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 216-225 34938384-8 2021 Finally, ceftriaxone treatment increased the expression of the tight junction proteins zona occludens-1(ZO-1) and occludin in the colon, decreased the expression of the inflammation-related proteins TLR4, MyD88, and NF-kappaB in the colon, and decreased the serum concentration of the proinflammatory cytokines interleukin-1beta (IL-1beta), IL-6, and tumour necrosis factor-alpha (TNF-alpha). Ceftriaxone 9-20 interleukin 1 beta Mus musculus 311-328 34938384-8 2021 Finally, ceftriaxone treatment increased the expression of the tight junction proteins zona occludens-1(ZO-1) and occludin in the colon, decreased the expression of the inflammation-related proteins TLR4, MyD88, and NF-kappaB in the colon, and decreased the serum concentration of the proinflammatory cytokines interleukin-1beta (IL-1beta), IL-6, and tumour necrosis factor-alpha (TNF-alpha). Ceftriaxone 9-20 interleukin 1 alpha Mus musculus 330-338 34938384-8 2021 Finally, ceftriaxone treatment increased the expression of the tight junction proteins zona occludens-1(ZO-1) and occludin in the colon, decreased the expression of the inflammation-related proteins TLR4, MyD88, and NF-kappaB in the colon, and decreased the serum concentration of the proinflammatory cytokines interleukin-1beta (IL-1beta), IL-6, and tumour necrosis factor-alpha (TNF-alpha). Ceftriaxone 9-20 interleukin 6 Mus musculus 341-345 34938384-8 2021 Finally, ceftriaxone treatment increased the expression of the tight junction proteins zona occludens-1(ZO-1) and occludin in the colon, decreased the expression of the inflammation-related proteins TLR4, MyD88, and NF-kappaB in the colon, and decreased the serum concentration of the proinflammatory cytokines interleukin-1beta (IL-1beta), IL-6, and tumour necrosis factor-alpha (TNF-alpha). Ceftriaxone 9-20 tumor necrosis factor Mus musculus 381-390 34802899-9 2021 Ceftriaxone is a beta-lactam antibiotic that is known to upregulate the expression of Slc1a2, an alternative glial glutamate transporter. Ceftriaxone 0-11 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 86-92 34802899-10 2021 Although ceftriaxone increased Slc1a2 expression, we did not observe a treatment effect in NPC1 mutant mice. Ceftriaxone 9-20 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 31-37 34153453-0 2021 Ceftriaxone regulates glutamate production and vesicular assembly in presynaptic terminals through GLT-1 in APP/PS1 mice. Ceftriaxone 0-11 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 99-104 34694535-0 2022 Effect of P-glycoprotein Inhibition on the Penetration of Ceftriaxone Across the Blood-Brain Barrier. Ceftriaxone 58-69 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 10-24 34694535-2 2022 Therefore, the present study aimed to investigate the effect of P-gp inhibition on the transport of ceftriaxone (CFX) across the BBB. Ceftriaxone 100-111 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 64-68 34694535-2 2022 Therefore, the present study aimed to investigate the effect of P-gp inhibition on the transport of ceftriaxone (CFX) across the BBB. Ceftriaxone 113-116 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 64-68 34612516-0 2022 Combination therapy of iPSC-derived conditioned medium with ceftriaxone alleviates bacteria-induced lung injury by targeting the NLRP3 inflammasome. Ceftriaxone 60-71 NLR family, pyrin domain containing 3 Rattus norvegicus 129-134 34387696-10 2021 The structures, including one of Artemis with the cephalosporin ceftriaxone, will help enable the rational development of selective SNM1 nuclease inhibitors. Ceftriaxone 64-75 DNA cross-link repair 1A Homo sapiens 132-136 34521349-11 2021 RESULTS: Compared with the TBI + vehicle group, the TBI + ceftriaxone 250 mg/kg group showed significantly lower ICP, improved motor dysfunction, reduced body weight loss, decreased infarct volume and neuronal apoptosis, decreased TBI-induced microglial activation and TNF-alpha expression in microglia, and increased GLT-1 expression in neurons and microglia. Ceftriaxone 58-69 tumor necrosis factor Rattus norvegicus 269-278 34521349-11 2021 RESULTS: Compared with the TBI + vehicle group, the TBI + ceftriaxone 250 mg/kg group showed significantly lower ICP, improved motor dysfunction, reduced body weight loss, decreased infarct volume and neuronal apoptosis, decreased TBI-induced microglial activation and TNF-alpha expression in microglia, and increased GLT-1 expression in neurons and microglia. Ceftriaxone 58-69 solute carrier family 1 member 2 Rattus norvegicus 318-323 34521349-13 2021 CONCLUSIONS: The intraperitoneal injection of ceftriaxone with 250 mg/kg/day for three days may attenuate TBI by increasing GLT-1 expression and reducing neuroinflammation and neuronal apoptosis, thereby resulting in an improvement in functional outcomes, and this neuroprotective effect is not related to its antibacterial effects. Ceftriaxone 46-57 solute carrier family 1 member 2 Rattus norvegicus 124-129 34363739-10 2021 Our results showed that hippocampal microinjection of ceftriaxone, as an activator of GLT-1, reduced some signs of morphine withdrawal, such as activity, diarrhea, head tremor, freezing, and ptosis. Ceftriaxone 54-65 solute carrier family 1 member 2 Rattus norvegicus 86-91 34880840-8 2021 Whole-genome analysis showed that serotype Typhimurium and its monophasic variant was the most prevalent in ceftriaxone-resistant isolates (37/53), which comprised ST34 (33/53), ST19 (2/53), and ST99 (2/53), and they were close related in the phylogenetic tree. Ceftriaxone 108-119 cyclin dependent kinase 2 associated protein 1 Homo sapiens 178-182 34130941-8 2021 Multivariable analysis identified exposure to ceftriaxone as an independent factor (OR 4.14, p = 0.018) associated with new vanA VREfm isolates. Ceftriaxone 46-57 Vancomycin Teicoplanin A-type resistance protein VanA / D-alanine--D-alanine ligase Enterococcus faecium 124-128 34130941-11 2021 CONCLUSION: Ceftriaxone use was associated with an increased risk of CTS patients acquiring vanA VREfm during an acute outbreak. Ceftriaxone 12-23 Vancomycin Teicoplanin A-type resistance protein VanA / D-alanine--D-alanine ligase Enterococcus faecium 92-96 34658774-0 2021 Neuroprotective Effects of Ceftriaxone Involve the Reduction of Abeta Burden and Neuroinflammatory Response in a Mouse Model of Alzheimer"s Disease. Ceftriaxone 27-38 amyloid beta (A4) precursor protein Mus musculus 64-69 34489258-3 2021 Platelet counts slowly trended down after starting ceftriaxone reaching 5 K/muL on day 12 of treatment. Ceftriaxone 51-62 tripartite motif containing 37 Homo sapiens 76-79 34153453-3 2021 Ceftriaxone has been reported to improve cognitive deficits in AD mice by increasing GLT-1 expression, glutamate transformation to glutamine, and glutamine efflux from astrocytes. Ceftriaxone 0-11 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 85-90 34153453-9 2021 Ceftriaxone treatment significantly increased SNAT1 expression and glutaminase activity in neurons in APP/PS1 mice. Ceftriaxone 0-11 solute carrier family 38, member 1 Mus musculus 46-51 34153453-9 2021 Ceftriaxone treatment significantly increased SNAT1 expression and glutaminase activity in neurons in APP/PS1 mice. Ceftriaxone 0-11 glutaminase Mus musculus 67-78 34153453-9 2021 Ceftriaxone treatment significantly increased SNAT1 expression and glutaminase activity in neurons in APP/PS1 mice. Ceftriaxone 0-11 presenilin 1 Mus musculus 106-109 34153453-10 2021 Similarly, VGLUT1/2 levels were increased in the presynaptic terminals of APP/PS1 mice treated with ceftriaxone. Ceftriaxone 100-111 solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 7 Mus musculus 11-19 34153453-10 2021 Similarly, VGLUT1/2 levels were increased in the presynaptic terminals of APP/PS1 mice treated with ceftriaxone. Ceftriaxone 100-111 presenilin 1 Mus musculus 78-81 34153453-11 2021 The deletion of one GLT-1 allele in APP/PS1 mice prevented the ceftriaxone-induced upregulation of SNAT1 and VGLUT1/2 expression, indicating that GLT-1 played an important role in ceftriaxone effect. Ceftriaxone 63-74 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 20-25 34153453-11 2021 The deletion of one GLT-1 allele in APP/PS1 mice prevented the ceftriaxone-induced upregulation of SNAT1 and VGLUT1/2 expression, indicating that GLT-1 played an important role in ceftriaxone effect. Ceftriaxone 63-74 solute carrier family 38, member 1 Mus musculus 99-104 34153453-11 2021 The deletion of one GLT-1 allele in APP/PS1 mice prevented the ceftriaxone-induced upregulation of SNAT1 and VGLUT1/2 expression, indicating that GLT-1 played an important role in ceftriaxone effect. Ceftriaxone 63-74 solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 7 Mus musculus 109-117 34153453-11 2021 The deletion of one GLT-1 allele in APP/PS1 mice prevented the ceftriaxone-induced upregulation of SNAT1 and VGLUT1/2 expression, indicating that GLT-1 played an important role in ceftriaxone effect. Ceftriaxone 63-74 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 146-151 34153453-11 2021 The deletion of one GLT-1 allele in APP/PS1 mice prevented the ceftriaxone-induced upregulation of SNAT1 and VGLUT1/2 expression, indicating that GLT-1 played an important role in ceftriaxone effect. Ceftriaxone 180-191 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 20-25 34153453-11 2021 The deletion of one GLT-1 allele in APP/PS1 mice prevented the ceftriaxone-induced upregulation of SNAT1 and VGLUT1/2 expression, indicating that GLT-1 played an important role in ceftriaxone effect. Ceftriaxone 180-191 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 146-151 34153453-12 2021 Based on the role of SNAT1, glutaminase, and VGLUT1/2 in the glutamate-glutamine cycle in neurons, the present results suggested that ceftriaxone improved the production and vesicular assembly of glutamate as a neurotransmitter in presynaptic terminals by acting on GLT-1 in APP/PS1 mice. Ceftriaxone 134-145 solute carrier family 38, member 1 Mus musculus 21-26 34153453-12 2021 Based on the role of SNAT1, glutaminase, and VGLUT1/2 in the glutamate-glutamine cycle in neurons, the present results suggested that ceftriaxone improved the production and vesicular assembly of glutamate as a neurotransmitter in presynaptic terminals by acting on GLT-1 in APP/PS1 mice. Ceftriaxone 134-145 glutaminase Mus musculus 28-39 34153453-12 2021 Based on the role of SNAT1, glutaminase, and VGLUT1/2 in the glutamate-glutamine cycle in neurons, the present results suggested that ceftriaxone improved the production and vesicular assembly of glutamate as a neurotransmitter in presynaptic terminals by acting on GLT-1 in APP/PS1 mice. Ceftriaxone 134-145 solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 7 Mus musculus 45-53 34153453-12 2021 Based on the role of SNAT1, glutaminase, and VGLUT1/2 in the glutamate-glutamine cycle in neurons, the present results suggested that ceftriaxone improved the production and vesicular assembly of glutamate as a neurotransmitter in presynaptic terminals by acting on GLT-1 in APP/PS1 mice. Ceftriaxone 134-145 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 266-271 34153453-12 2021 Based on the role of SNAT1, glutaminase, and VGLUT1/2 in the glutamate-glutamine cycle in neurons, the present results suggested that ceftriaxone improved the production and vesicular assembly of glutamate as a neurotransmitter in presynaptic terminals by acting on GLT-1 in APP/PS1 mice. Ceftriaxone 134-145 presenilin 1 Mus musculus 279-282 34445137-4 2021 This study investigated the consequences of ceftriaxone (CTX), an enhancer of glutamate transporter 1 expression, treatment on long-term synaptic potentiation (LTP) in the hippocampus of young rats. Ceftriaxone 44-55 solute carrier family 1 member 2 Rattus norvegicus 78-101 34189904-6 2021 Western blot and immunofluorescence revealed that incorporation of CL in a lipid bilayer ameliorated the docking of CEF-FK506-nilotinib-GSH-CL-liposomes at alpha-synuclein (alpha-syn), indicating a better targeting capability of the liposomes to degenerated neurons. Ceftriaxone 116-119 synuclein alpha Homo sapiens 156-171 34189904-6 2021 Western blot and immunofluorescence revealed that incorporation of CL in a lipid bilayer ameliorated the docking of CEF-FK506-nilotinib-GSH-CL-liposomes at alpha-synuclein (alpha-syn), indicating a better targeting capability of the liposomes to degenerated neurons. Ceftriaxone 116-119 synuclein alpha Homo sapiens 173-182 34349613-9 2021 The mucus SIgA and serum IL-10 levels were increased, and serum levels of LPS, IL-1beta, and TNF-alpha were decreased in the 60- and 90-mg omega-3 PUFA groups when compared with those in the ceftriaxone sodium-treated group. Ceftriaxone 191-209 interleukin 10 Mus musculus 25-30 34349613-9 2021 The mucus SIgA and serum IL-10 levels were increased, and serum levels of LPS, IL-1beta, and TNF-alpha were decreased in the 60- and 90-mg omega-3 PUFA groups when compared with those in the ceftriaxone sodium-treated group. Ceftriaxone 191-209 interleukin 1 alpha Mus musculus 79-87 34349613-9 2021 The mucus SIgA and serum IL-10 levels were increased, and serum levels of LPS, IL-1beta, and TNF-alpha were decreased in the 60- and 90-mg omega-3 PUFA groups when compared with those in the ceftriaxone sodium-treated group. Ceftriaxone 191-209 tumor necrosis factor Mus musculus 93-102 34356479-7 2021 Azithromycin combinations with either linezolid, ceftriaxone, gentamicin, or cefotaxime provided synergy in 42.1%, 44.7%, 31.6% and 7.9% of the 38 MAC-MRSA isolates, respectively. Ceftriaxone 49-60 solute carrier family 9 member A6 Homo sapiens 151-155 2582432-6 1989 Ceftriaxone at 1.0 mM produced 10x modulation of VP-16 cytotoxicity, 8x for DOX, and 2x for VBL. Ceftriaxone 0-11 host cell factor C1 Homo sapiens 49-54 35501756-8 2022 After ASP implementation, the trend toward an increase of oxacillin-resistant Staphylococcus aureus, ceftriaxone-resistant Escherichia coli, and meropenem-resistant Pseudomonas aeruginosa was reversed. Ceftriaxone 101-112 assembly factor for spindle microtubules Homo sapiens 6-9 35484974-7 2022 The findings suggest that antibiotic exposure during pregnancy, specifically ceftriaxone sodium, will adversely affects the behavior of offspring rats due to the imbalance of gut microbiota, especially S24-7, via VEGF and various metabolic pathways. Ceftriaxone 77-95 vascular endothelial growth factor A Rattus norvegicus 213-217 35387587-5 2022 A significant association was seen between the presence of hlyA hemolysin and susceptibility to ceftriaxone and ciprofloxacin (P < 0.05). Ceftriaxone 96-107 hemolysin transport protein Escherichia coli 59-63 35091052-5 2022 ESBL non-CRE phenotypes were defined as nonsusceptible to ceftriaxone (MIC >=2 microg/ml) and susceptible to ertapenem (MIC <=0.5 microg/ml). Ceftriaxone 58-69 EsbL Escherichia coli 0-4 34719508-9 2022 Furthermore, the GLT-1 agonist ceftriaxone showed a protective effect on TH-positive neuron impairment. Ceftriaxone 31-42 solute carrier family 1 member 2 Rattus norvegicus 17-22 34719508-9 2022 Furthermore, the GLT-1 agonist ceftriaxone showed a protective effect on TH-positive neuron impairment. Ceftriaxone 31-42 tyrosine hydroxylase Rattus norvegicus 73-75 34356479-9 2021 In conclusion, azithromycin combinations with either linezolid, or ceftriaxone showed synergism in most of the MAC-resistant MRSA clinical isolates. Ceftriaxone 67-78 solute carrier family 9 member A6 Homo sapiens 125-129 35094207-2 2022 In the present study, not only did we evaluate the binding strength of ceftriaxone and ceftizoxime to bovine serum albumin (BSA), but we also investigated the kinetic and thermodynamic parameters including KD, KA, DeltaS, and DeltaH. Ceftriaxone 71-82 albumin Homo sapiens 109-122 35094207-9 2022 Finally, molecular docking confirmed that the preferable binding sites of ceftizoxime and ceftriaxone were site IIA and site IB of albumin, respectively. Ceftriaxone 90-101 albumin Homo sapiens 131-138 35449634-7 2022 We present a case of ceftriaxone-induced agranulocytosis which was completely reversible upon stoppage of drug and granulocyte colony-stimulating factor administration. Ceftriaxone 21-32 colony stimulating factor 3 Homo sapiens 115-152 35253107-8 2022 Total and unbound ceftriaxone was best described in a two-compartment model with total body weight, serum albumin concentrations, creatinine clearance (CrCL), and the presence of RRT included as significant predictors of pharmacokinetics. Ceftriaxone 18-29 albumin Homo sapiens 100-113 35051699-1 2022 The beta-lactam antibiotic ceftriaxone (CTX) is a glutamate transporter subtype 1 (GLT-1) enhancer that reduces cocaine reinforcing efficacy and relapse in rats, but pharmacokinetic liabilities limit translational utility. Ceftriaxone 27-38 solute carrier family 1 member 2 Rattus norvegicus 50-81 35051699-1 2022 The beta-lactam antibiotic ceftriaxone (CTX) is a glutamate transporter subtype 1 (GLT-1) enhancer that reduces cocaine reinforcing efficacy and relapse in rats, but pharmacokinetic liabilities limit translational utility. Ceftriaxone 27-38 solute carrier family 1 member 2 Rattus norvegicus 83-88 35132833-7 2022 Of these, 80 ceftriaxone-resistant and two ceftriaxone-intermediate Escherichia coli from inside ceftriaxone-halos were confirmed as ESBL-producers. Ceftriaxone 43-54 EsbL Escherichia coli 133-137 35132833-7 2022 Of these, 80 ceftriaxone-resistant and two ceftriaxone-intermediate Escherichia coli from inside ceftriaxone-halos were confirmed as ESBL-producers. Ceftriaxone 97-108 EsbL Escherichia coli 133-137 35052960-2 2022 In this case series, 11 men with CBP (including patients with urological comorbidities) due to multi-resistant E. coli were treated with once-daily ceftriaxone intravenously for 6 weeks. Ceftriaxone 148-159 CREB binding protein Homo sapiens 33-36 2692515-4 1989 The beta-lactamase efficiently hydrolyzed cefotaxime and ceftriaxone but only moderately hydrolyzed ceftazidime and was inhibited by clavulanate and sulbactam (1 microM) and by anti-TEM-1 and anti-TEM-2 sera. Ceftriaxone 57-68 hypothetical protein Escherichia coli 182-187 2809257-3 1989 Administration of ceftriaxone 6 h after infection provoked rapid bacterial lysis associated with greatly increased concentrations of bacteria-free endotoxin (lipooligosaccharide) and tumor necrosis factor alpha (TNF) in the cerebrospinal fluid (CSF). Ceftriaxone 18-29 tumor necrosis factor Homo sapiens 183-210 2809257-3 1989 Administration of ceftriaxone 6 h after infection provoked rapid bacterial lysis associated with greatly increased concentrations of bacteria-free endotoxin (lipooligosaccharide) and tumor necrosis factor alpha (TNF) in the cerebrospinal fluid (CSF). Ceftriaxone 18-29 tumor necrosis factor Homo sapiens 212-215 2679370-9 1989 Killing kinetics showed that against some strains CP-65,207 is rapidly bactericidal at concentrations well below those required to achieve a similar degree of killing with cefotaxime, ceftazidime, and ceftriaxone. Ceftriaxone 201-212 hypothetical protein Pseudomonas aeruginosa 50-59 2779527-0 1989 Ceftriaxone binding to human serum albumin: competition with bilirubin. Ceftriaxone 0-11 albumin Homo sapiens 29-42 2779527-1 1989 Ceftriaxone, a cephalosporin, is bound reversibly to defatted human serum albumin from adults, with a first stoichiometric binding constant of 60,000 M-1, as found by equilibrium dialysis at pH 7.4, 37 degrees. Ceftriaxone 0-11 albumin Homo sapiens 68-81 3579254-2 1987 Ion pairing was used because ceftriaxone is a relatively polar compound which is poorly retained on C18 columns in standard reverse-phase high-performance liquid chromatography and which produces trailing peaks in the absence of ion-pairing agents. Ceftriaxone 29-40 Bardet-Biedl syndrome 9 Homo sapiens 100-103 3391863-3 1988 The CSF of all patients became sterile within 24-48 h. The CSF ceftriaxone concentrations 24 h after dosing were 10 to 100-fold higher than the MIC of the pathogenic bacteria early in therapy, and five to 50-fold higher at the end of therapy. Ceftriaxone 63-74 colony stimulating factor 2 Homo sapiens 4-7 3391863-3 1988 The CSF of all patients became sterile within 24-48 h. The CSF ceftriaxone concentrations 24 h after dosing were 10 to 100-fold higher than the MIC of the pathogenic bacteria early in therapy, and five to 50-fold higher at the end of therapy. Ceftriaxone 63-74 colony stimulating factor 2 Homo sapiens 59-62 3208543-4 1988 After the administration of 1 g of ceftriaxone during a constant intravenous infusion over a 30-min period, t 1/2 was 16.6 h, beta was 0.0418 +/- 0.0106 h-1, VD was 14.5 +/- 3.0 liters/1.73 m2 and Clp was 0.40 +/- 0.05 liters/h for the interdialysis period. Ceftriaxone 35-46 calmodulin like 3 Homo sapiens 197-200 3104483-2 1987 For E. cloacae, pre-incubation with ceftriaxone, cefoxitin, cefamandole, cefoperazone, or imipenem produced significantly larger amounts of beta-lactamase than did pre-incubation with moxalactam, clavulanate, ceftazidime, or aztreonam. Ceftriaxone 36-47 Beta lactamase Pseudomonas aeruginosa 140-154 3605877-6 1987 Some of the new cephalosporins of the third generation (cefotaxime and ceftriaxone) and cefuroxime have a good activity in vitro and a good passage to the CSF. Ceftriaxone 71-82 colony stimulating factor 2 Homo sapiens 155-158 3102630-1 1987 The interactions of imipenem, carbenicillin, cefotaxime, ceftriaxone, and azlocillin with the chromosomal beta-lactamase of Pseudomonas aeruginosa were compared. Ceftriaxone 57-68 Beta lactamase Pseudomonas aeruginosa 106-120 2811057-20 1989 Amongst the amino-thiazol-containing compounds cefotaxime, ceftriaxone, and cefodizime, increasing interaction with the PAH transporter was seen dependent of a second ionizable anionic group. Ceftriaxone 59-70 solute carrier family 22 member 6 Homo sapiens 120-135 6323376-1 1984 Ceftriaxone is a new cephalosporin with a broad spectrum of antibacterial activity and unique serum and CSF pharmacokinetics. Ceftriaxone 0-11 colony stimulating factor 2 Homo sapiens 104-107 3094173-3 1986 Ceftriaxone is a new, extended-spectrum cephalosporin with a long serum half-life and is many times more active than penicillin G against both beta-lactamase-positive and -negative strains of N. gonorrhoeae. Ceftriaxone 0-11 beta-lactamase Neisseria gonorrhoeae 143-157 3534698-4 1986 Indicating that the binding process is saturable, investigations performed with various isolated plasma proteins in physiologic concentrations show that ceftriaxone binds mainly to albumin, and marginally or not at all to alpha-1-acid glycoprotein, gammaglobulins, transferrin, haptoglobin, and lipoproteins. Ceftriaxone 153-164 transferrin Homo sapiens 265-276 3534698-4 1986 Indicating that the binding process is saturable, investigations performed with various isolated plasma proteins in physiologic concentrations show that ceftriaxone binds mainly to albumin, and marginally or not at all to alpha-1-acid glycoprotein, gammaglobulins, transferrin, haptoglobin, and lipoproteins. Ceftriaxone 153-164 haptoglobin Homo sapiens 278-289 3754551-0 1986 CSF exchange after the erroneous intrathecal injection of 800 mg ceftriaxone for pneumococcal meningitis. Ceftriaxone 65-76 colony stimulating factor 2 Homo sapiens 0-3 3906584-0 1985 Ceftriaxone: a beta-lactamase-stable, broad-spectrum cephalosporin with an extended half-life. Ceftriaxone 0-11 amyloid beta precursor protein Homo sapiens 13-19 6088747-8 1984 The quantitation of CSF diffusion of ceftriaxone was assessed by comparison of the areas under the CSF and plasma concentration-time curve. Ceftriaxone 37-48 colony stimulating factor 2 Homo sapiens 20-23 6088747-8 1984 The quantitation of CSF diffusion of ceftriaxone was assessed by comparison of the areas under the CSF and plasma concentration-time curve. Ceftriaxone 37-48 colony stimulating factor 2 Homo sapiens 99-102 6088747-9 1984 The mean ceftriaxone penetration into the CSF in neonates and infants with bacterial meningitis was 17%. Ceftriaxone 9-20 colony stimulating factor 2 Homo sapiens 42-45 6088747-11 1984 Mean ceftriaxone concentrations in the CSF in patients with bacterial meningitis were 2.8 mg/L after 24 hours, exceeding by many times the minimum inhibitory concentration of the common meningitis pathogens at this time. Ceftriaxone 5-16 colony stimulating factor 2 Homo sapiens 39-42 3757585-0 1986 Displacement effect of ceftriaxone on bilirubin bound to human serum albumin. Ceftriaxone 23-34 albumin Homo sapiens 63-76 3757585-1 1986 The effects of ceftriaxone, a "third-generation" cephalosporin, on bilirubin-serum albumin complexes were investigated. Ceftriaxone 15-26 albumin Homo sapiens 77-90 3987394-4 1985 Cefotaxime levels fall rapidly with a T 1/2 of 1.1 h, whereas ceftriaxone persists for 24 h with an unique T 1/2 of 8 h. Cefotaxime is eliminated by the kidneys and metabolized to desacetyl-cefotaxime resulting in a high total clearance. Ceftriaxone 62-73 interleukin 1 receptor like 1 Homo sapiens 107-117 19810169-4 1981 Both ceftazidime and ceftriaxone were highly active against beta-lactamase producing and non-beta-lactamase producing Haemophilus influenzae. Ceftriaxone 21-32 beta-lactamase TEM-1 Haemophilus influenzae 60-74 6322683-2 1984 In normal subjects, ceftriaxone was eliminated with a t1/2 beta of 5.2 h (range, 4.1 to 5.8). Ceftriaxone 20-31 CD5 molecule Homo sapiens 54-63 6298176-10 1983 When recultured 54 h after the last dose of ceftriaxone, both CSF and blood remained sterile in all treated animals. Ceftriaxone 44-55 colony stimulating factor 2 Homo sapiens 62-65 6280599-5 1982 Moxalactam and ceftriaxone produced the largest cerebrospinal fluid bactericidal titers against this beta-lactamase-producing strain of Haemophilus. Ceftriaxone 15-26 beta-lactamase TEM-1 Haemophilus influenzae 101-115 19810169-4 1981 Both ceftazidime and ceftriaxone were highly active against beta-lactamase producing and non-beta-lactamase producing Haemophilus influenzae. Ceftriaxone 21-32 beta-lactamase TEM-1 Haemophilus influenzae 93-107 33692138-5 2021 dDD had PPVs of >=96% for most organism-antibiotic pairs, including 100% (CI 96-100%) for Staphylococcus aureus and oxacillin and 99% (CI 93%-100%) for Enterobacterales and ceftriaxone. Ceftriaxone 173-184 vein Drosophila melanogaster 0-3 33836247-0 2021 Ceftriaxone reduces waterpipe tobacco smoke withdrawal-induced anxiety in rats via modulating the expression of TNF-alpha/NFkB, Nrf2, and GLT-1. Ceftriaxone 0-11 tumor necrosis factor Rattus norvegicus 112-121 33836247-0 2021 Ceftriaxone reduces waterpipe tobacco smoke withdrawal-induced anxiety in rats via modulating the expression of TNF-alpha/NFkB, Nrf2, and GLT-1. Ceftriaxone 0-11 RELA proto-oncogene, NF-kB subunit Rattus norvegicus 122-126 33836247-0 2021 Ceftriaxone reduces waterpipe tobacco smoke withdrawal-induced anxiety in rats via modulating the expression of TNF-alpha/NFkB, Nrf2, and GLT-1. Ceftriaxone 0-11 NFE2 like bZIP transcription factor 2 Rattus norvegicus 128-132 33836247-0 2021 Ceftriaxone reduces waterpipe tobacco smoke withdrawal-induced anxiety in rats via modulating the expression of TNF-alpha/NFkB, Nrf2, and GLT-1. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 138-143 33836247-10 2021 WTS exposure increased the relative mRNA levels for nuclear factor kB (NFkB), tumor necrosis factor-alpha (TNF-alpha), and brain-derived neurotrophic factor (BDNF) in the PFC, NAc and VTA, and ceftriaxone treatment reversed these effects. Ceftriaxone 193-204 brain-derived neurotrophic factor Rattus norvegicus 158-162 33986035-3 2021 The beta-lactam antibiotic ceftriaxone upregulates GLT-1 and attenuates cue- and cocaine-induced cocaine seeking without affecting motivation for natural rewards. Ceftriaxone 27-38 solute carrier family 1 member 2 Rattus norvegicus 51-56 33268669-5 2021 The spleen organ index of dams was significantly lower and the offspring serum interleukin-6 levels were significantly higher in ceftriaxone-treated mice compared with the control group. Ceftriaxone 129-140 interleukin 6 Mus musculus 79-92 33986035-5 2021 Thus, we aimed to develop novel molecules that retained the GLT-1 enhancing effects of ceftriaxone but displayed superior drug-like properties. Ceftriaxone 87-98 solute carrier family 1 member 2 Rattus norvegicus 60-65 33465464-3 2021 A number of studies have shown that ceftriaxone increases GLT-1 expression, the major glutamate transporter, and that treatment with this antibiotic reduces ethanol drinking. Ceftriaxone 36-47 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 58-63 33871467-3 2021 The authors present a case of a patient, working as a forester, who underwent left hip replacement arthroplasty having contracted a Borrelia burgdorferi infection in the past, and who was hospitalized 12 years before in the infectious ward due to suspected neuroborreliosis for which he was treated with Ceftriaxone 2 x 2.0 g intravenously for 4 weeks. Ceftriaxone 304-315 hedgehog interacting protein Homo sapiens 83-86 32476589-5 2021 The overall failure rate of ceftriaxone mono-therapy was observed in 75.6% (11.7% in high-risk non-neutropenic fever with a mean C-reactive protein level of 21.1 (+-23.2) mmol/L and 63.9% in low-risk non-neutropenic fever with a mean C-reactive protein level of 17.6 (+-53.9) mmol/L). Ceftriaxone 28-39 C-reactive protein Homo sapiens 129-147 33841104-1 2021 Pharmacological upregulation of glutamate transporter-1 (GLT-1), commonly achieved using the beta-lactam antibiotic ceftriaxone, represents a promising therapeutic strategy to accelerate glutamate uptake and prevent excitotoxic damage in neurological conditions. Ceftriaxone 116-127 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 32-55 33841104-1 2021 Pharmacological upregulation of glutamate transporter-1 (GLT-1), commonly achieved using the beta-lactam antibiotic ceftriaxone, represents a promising therapeutic strategy to accelerate glutamate uptake and prevent excitotoxic damage in neurological conditions. Ceftriaxone 116-127 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 57-62 33841104-5 2021 Here, we used two different compounds, ceftriaxone and LDN/OSU-0212320 (LDN), to upregulate GLT-1 in healthy wild-type mice. Ceftriaxone 39-50 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 92-97 33841104-7 2021 We found that while both ceftriaxone and LDN increased GLT-1 expression in multiple brain regions, they did not prevent activity-dependent slowing of glutamate clearance nor did they speed basal clearance rates, even in areas characterized by slow uptake (e.g., striatum). Ceftriaxone 25-36 solute carrier family 1 (glial high affinity glutamate transporter), member 2 Mus musculus 55-60