PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
26550961-0	2016	Involvement of CCL3/CCR5 Signaling in Dorsal Root Ganglion in Remifentanil-induced Hyperalgesia in Rats.	Remifentanil	62-74	C-C motif chemokine ligand 3	Rattus norvegicus	15-19
26550961-9	2016	Moreover, the expression of mRNAs and proteins of CCL3 and its receptor CCR5 in DRG were dramatically increased after remifentanil infusion as compared with the normal saline group.	Remifentanil	118-130	C-C motif chemokine ligand 3	Rattus norvegicus	50-54
26550961-0	2016	Involvement of CCL3/CCR5 Signaling in Dorsal Root Ganglion in Remifentanil-induced Hyperalgesia in Rats.	Remifentanil	62-74	C-C motif chemokine receptor 5	Rattus norvegicus	20-24
26550961-9	2016	Moreover, the expression of mRNAs and proteins of CCL3 and its receptor CCR5 in DRG were dramatically increased after remifentanil infusion as compared with the normal saline group.	Remifentanil	118-130	C-C motif chemokine receptor 5	Rattus norvegicus	72-76
26550961-12	2016	CONCLUSIONS: The results highlighted the fact that CCL3 and its receptor CCR5 in DRG might contribute to remifentanil-induced hyperalgesia.	Remifentanil	105-117	C-C motif chemokine ligand 3	Rattus norvegicus	51-55
26550961-3	2016	In this paper we explored whether CCL3 and CCR5, the mainly receptor of CCL3, play a role in the remifentanil-induced hyperalgesia in DRG by using a rat model with remifentanil administration.	Remifentanil	97-109	C-C motif chemokine ligand 3	Rattus norvegicus	34-38
26550961-12	2016	CONCLUSIONS: The results highlighted the fact that CCL3 and its receptor CCR5 in DRG might contribute to remifentanil-induced hyperalgesia.	Remifentanil	105-117	C-C motif chemokine receptor 5	Rattus norvegicus	73-77
26550961-3	2016	In this paper we explored whether CCL3 and CCR5, the mainly receptor of CCL3, play a role in the remifentanil-induced hyperalgesia in DRG by using a rat model with remifentanil administration.	Remifentanil	97-109	C-C motif chemokine receptor 5	Rattus norvegicus	43-47
26550961-3	2016	In this paper we explored whether CCL3 and CCR5, the mainly receptor of CCL3, play a role in the remifentanil-induced hyperalgesia in DRG by using a rat model with remifentanil administration.	Remifentanil	97-109	C-C motif chemokine ligand 3	Rattus norvegicus	72-76
26550961-3	2016	In this paper we explored whether CCL3 and CCR5, the mainly receptor of CCL3, play a role in the remifentanil-induced hyperalgesia in DRG by using a rat model with remifentanil administration.	Remifentanil	164-176	C-C motif chemokine ligand 3	Rattus norvegicus	34-38
26550961-3	2016	In this paper we explored whether CCL3 and CCR5, the mainly receptor of CCL3, play a role in the remifentanil-induced hyperalgesia in DRG by using a rat model with remifentanil administration.	Remifentanil	164-176	C-C motif chemokine receptor 5	Rattus norvegicus	43-47
26550961-5	2016	Real-time polymerase chain reaction and Western blot analysis were used to evaluate time course of CCL3 and CCR5 expression in DRG after remifentanil infusion.	Remifentanil	137-149	C-C motif chemokine ligand 3	Rattus norvegicus	99-103
26550961-5	2016	Real-time polymerase chain reaction and Western blot analysis were used to evaluate time course of CCL3 and CCR5 expression in DRG after remifentanil infusion.	Remifentanil	137-149	C-C motif chemokine receptor 5	Rattus norvegicus	108-112
27487636-0	2016	REMIFENTANIL VS FENTANYL DURING DAY CASE DENTAL SURGERY IN PEOPLE WITH SPECIAL NEEDS: A COMPARATIVE, PILOT STUDY OF THEIR EFFECT ON STRESS RESPONSE AND POSTOPERATIVE PAIN.	Remifentanil	0-12	early growth response 3	Homo sapiens	101-106
26724371-0	2016	Up-regulation of CXCL1 and CXCR2 contributes to remifentanil-induced hypernociception via modulating spinal NMDA receptor expression and phosphorylation in rats.	Remifentanil	48-60	C-X-C motif chemokine ligand 1	Rattus norvegicus	17-22
26724371-0	2016	Up-regulation of CXCL1 and CXCR2 contributes to remifentanil-induced hypernociception via modulating spinal NMDA receptor expression and phosphorylation in rats.	Remifentanil	48-60	C-X-C motif chemokine receptor 2	Rattus norvegicus	27-32
26724371-9	2016	Furthermore, spinal CXCL1and CXCR2 mRNA and protein expressions were elevated after remifentanil exposure.	Remifentanil	84-96	C-X-C motif chemokine ligand 1	Rattus norvegicus	20-25
26724371-9	2016	Furthermore, spinal CXCL1and CXCR2 mRNA and protein expressions were elevated after remifentanil exposure.	Remifentanil	84-96	C-X-C motif chemokine receptor 2	Rattus norvegicus	29-34
26724371-10	2016	It was also found that remifentanil infusion could up-regulate NR2B-containing NMDA receptor expression and phosphorylation in spinal cord, which was markedly inhibited by SB225002.	Remifentanil	23-35	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	63-67
26397761-0	2016	Delay discounting of the mu-opioid receptor agonist remifentanil in rhesus monkeys.	Remifentanil	52-64	opioid receptor mu 1	Macaca mulatta	25-43
27249618-0	2016	Changes in cognitive function due to combined propofol and remifentanil treatment are associated with phosphorylation of Tau in the hippocampus, abnormal total water and calcium contents of the brain, and elevated serum S100beta levels.	Remifentanil	59-71	S100 calcium binding protein B	Rattus norvegicus	220-228
27249618-10	2016	RESULTS: Treatment with propofol and remifentanil markedly increased the latent period in the Morris water maze test, increased number the extent of Tau phosphorylation in the hippocampus, adversely modulated total water and calcium content in the brain, and elevated serum S100beta levels.	Remifentanil	37-49	S100 calcium binding protein B	Rattus norvegicus	274-282
26859874-1	2016	BACKGROUND: Ultralow doses of naloxone, an opioid and toll-like receptor 4 antagonist, blocked remifentanil-induced hyperalgesia and the associated increase in the minimum alveolar concentration (MAC), but not tolerance.	Remifentanil	95-107	toll-like receptor 4	Rattus norvegicus	54-74
26468894-0	2016	Remifentanil Preconditioning Reduces Postischemic Myocardial Infarction and Improves Left Ventricular Performance via Activation of the Janus Activated Kinase-2/Signal Transducers and Activators of Transcription-3 Signal Pathway and Subsequent Inhibition of Glycogen Synthase Kinase-3beta in Rats.	Remifentanil	0-12	Janus kinase 2	Rattus norvegicus	136-160
26468894-0	2016	Remifentanil Preconditioning Reduces Postischemic Myocardial Infarction and Improves Left Ventricular Performance via Activation of the Janus Activated Kinase-2/Signal Transducers and Activators of Transcription-3 Signal Pathway and Subsequent Inhibition of Glycogen Synthase Kinase-3beta in Rats.	Remifentanil	0-12	glycogen synthase kinase 3 beta	Rattus norvegicus	258-288
26468894-12	2016	Remifentanil preconditioning reduced postischemic myocardial infarction and hemodynamic dysfunction induced by myocardial ischemia reperfusion injury concomitant with increased phosphorylation of STAT3 at tyr-705 (p-STAT3) and glycogen synthase kinase-3beta but not Akt.	Remifentanil	0-12	signal transducer and activator of transcription 3	Rattus norvegicus	196-201
26468894-12	2016	Remifentanil preconditioning reduced postischemic myocardial infarction and hemodynamic dysfunction induced by myocardial ischemia reperfusion injury concomitant with increased phosphorylation of STAT3 at tyr-705 (p-STAT3) and glycogen synthase kinase-3beta but not Akt.	Remifentanil	0-12	signal transducer and activator of transcription 3	Rattus norvegicus	216-221
26468894-12	2016	Remifentanil preconditioning reduced postischemic myocardial infarction and hemodynamic dysfunction induced by myocardial ischemia reperfusion injury concomitant with increased phosphorylation of STAT3 at tyr-705 (p-STAT3) and glycogen synthase kinase-3beta but not Akt.	Remifentanil	0-12	glycogen synthase kinase 3 beta	Rattus norvegicus	227-257
26468894-3	2016	We hypothesized that remifentanil preconditioning confers cardioprotection via the JAK2/STAT3 and/or PI3K/Akt activation-mediated glycogen synthase kinase-3beta inhibition.	Remifentanil	21-33	Janus kinase 2	Rattus norvegicus	83-87
26468894-12	2016	Remifentanil preconditioning reduced postischemic myocardial infarction and hemodynamic dysfunction induced by myocardial ischemia reperfusion injury concomitant with increased phosphorylation of STAT3 at tyr-705 (p-STAT3) and glycogen synthase kinase-3beta but not Akt.	Remifentanil	0-12	AKT serine/threonine kinase 1	Rattus norvegicus	266-269
26468894-15	2016	Remifentanil preconditioning also attenuated posthypoxic cardiomyocyte injury and increased p-STAT3 and glycogen synthase kinase-3beta in isolated primary cardiomyocytes and H9C2 cells.	Remifentanil	0-12	signal transducer and activator of transcription 3	Rattus norvegicus	94-99
26468894-15	2016	Remifentanil preconditioning also attenuated posthypoxic cardiomyocyte injury and increased p-STAT3 and glycogen synthase kinase-3beta in isolated primary cardiomyocytes and H9C2 cells.	Remifentanil	0-12	glycogen synthase kinase 3 beta	Rattus norvegicus	104-134
26468894-16	2016	STAT3 gene knockdown with specific synthetic RNA cancelled remifentanil preconditioning cardioprotection, whereas glycogen synthase kinase-3beta gene knockdown, which per se did not affect STAT3 under hypoxia/reoxygenation condition, preserved remifentanil preconditioning cardioprotection regardless of STAT3 abrogation.	Remifentanil	59-71	signal transducer and activator of transcription 3	Rattus norvegicus	0-5
26468894-16	2016	STAT3 gene knockdown with specific synthetic RNA cancelled remifentanil preconditioning cardioprotection, whereas glycogen synthase kinase-3beta gene knockdown, which per se did not affect STAT3 under hypoxia/reoxygenation condition, preserved remifentanil preconditioning cardioprotection regardless of STAT3 abrogation.	Remifentanil	244-256	glycogen synthase kinase 3 beta	Rattus norvegicus	114-144
26468894-17	2016	CONCLUSIONS: Remifentanil preconditioning confers cardioprotection primarily via activation of JAK2/STAT3 signaling that can function independent of PI3K/Akt activation.	Remifentanil	13-25	Janus kinase 2	Rattus norvegicus	95-99
26468894-17	2016	CONCLUSIONS: Remifentanil preconditioning confers cardioprotection primarily via activation of JAK2/STAT3 signaling that can function independent of PI3K/Akt activation.	Remifentanil	13-25	signal transducer and activator of transcription 3	Rattus norvegicus	100-105
26468894-17	2016	CONCLUSIONS: Remifentanil preconditioning confers cardioprotection primarily via activation of JAK2/STAT3 signaling that can function independent of PI3K/Akt activation.	Remifentanil	13-25	AKT serine/threonine kinase 1	Rattus norvegicus	154-157
26468894-18	2016	Glycogen synthase kinase-3beta is a critical downstream effector of remifentanil preconditioning cardioprotection.	Remifentanil	68-80	glycogen synthase kinase 3 beta	Rattus norvegicus	0-30
26468894-3	2016	We hypothesized that remifentanil preconditioning confers cardioprotection via the JAK2/STAT3 and/or PI3K/Akt activation-mediated glycogen synthase kinase-3beta inhibition.	Remifentanil	21-33	signal transducer and activator of transcription 3	Rattus norvegicus	88-93
26468894-3	2016	We hypothesized that remifentanil preconditioning confers cardioprotection via the JAK2/STAT3 and/or PI3K/Akt activation-mediated glycogen synthase kinase-3beta inhibition.	Remifentanil	21-33	AKT serine/threonine kinase 1	Rattus norvegicus	106-109
26468894-3	2016	We hypothesized that remifentanil preconditioning confers cardioprotection via the JAK2/STAT3 and/or PI3K/Akt activation-mediated glycogen synthase kinase-3beta inhibition.	Remifentanil	21-33	glycogen synthase kinase 3 beta	Rattus norvegicus	130-160
26442411-14	2015	Remifentanil was increased up to 1 mug x kg(-1) x min(-1).	Remifentanil	0-12	CD59 molecule (CD59 blood group)	Homo sapiens	50-56
26647795-10	2015	Remifentanil administration significantly decreased concentrations of malondialdehyde, and increased catalase and superoxide dismutase enzyme activities (p<0.05).	Remifentanil	0-12	catalase	Rattus norvegicus	101-109
25919765-0	2015	Remifentanil Ameliorates Liver Ischemia-Reperfusion Injury Through Inhibition of Interleukin-18 Signaling.	Remifentanil	0-12	interleukin 18	Rattus norvegicus	81-95
25919765-10	2015	Although remifentanil pretreatment significantly decreased I/R-induced IL-18 expression, it further upregulated IL-18BP levels in liver tissues.	Remifentanil	9-21	interleukin 18	Rattus norvegicus	71-76
25919765-10	2015	Although remifentanil pretreatment significantly decreased I/R-induced IL-18 expression, it further upregulated IL-18BP levels in liver tissues.	Remifentanil	9-21	interleukin 18 binding protein	Rattus norvegicus	112-119
25919765-11	2015	The I/R-induced increases of hepatic interferon-gamma, tumor necrosis factor-alpha and IL-1beta expression, and neutrophil infiltration were also significantly reduced by remifentanil.	Remifentanil	171-183	tumor necrosis factor	Rattus norvegicus	29-82
25919765-11	2015	The I/R-induced increases of hepatic interferon-gamma, tumor necrosis factor-alpha and IL-1beta expression, and neutrophil infiltration were also significantly reduced by remifentanil.	Remifentanil	171-183	interleukin 1 beta	Rattus norvegicus	87-95
25919765-12	2015	Naloxone inhibited the remifentanil-induced downregulation of IL-18, but not the elevation of IL-18BP, and significantly attenuated its protective effects on liver I/R injury.	Remifentanil	23-35	interleukin 18	Rattus norvegicus	62-67
25919765-14	2015	Modulating the hepatic IL-18/IL-18BP balance and inhibiting IL-18 signaling mediate, at least in part, the hepatoprotective effects of remifentanil.	Remifentanil	135-147	interleukin 18	Rattus norvegicus	23-28
26550187-0	2015	Involvement of AQP 1 in the cardio-protective effect of remifentanil post-conditioning in ischemia/reperfusion rats.	Remifentanil	56-68	aquaporin 1	Rattus norvegicus	15-20
26550187-1	2015	BACKGROUND: our research aim to study the role of AQP1 in the cardioprotective effect of remifentanil post-conditioning for myocardial ischemia/reperfusion injury.	Remifentanil	89-101	aquaporin 1	Rattus norvegicus	50-54
26550187-13	2015	CONCLUSION: Cardioprotective effect of remifentanil post-conditioning may initiate through inhibiting the function of AQP1.	Remifentanil	39-51	aquaporin 1	Rattus norvegicus	118-122
26777139-0	2016	Impaired hippocampal synaptic plasticity and NR2A/2B expression ratio in remifentanil withdrawal rats.	Remifentanil	73-85	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	45-51
26777139-9	2016	In electrophysiology test, remifentanil group rats showed a trend for a rightward shift of input/output relationship and significant deficits in maintenance of STP and LTP.	Remifentanil	27-39	thyroid hormone receptor interactor 10	Rattus norvegicus	160-163
26777139-11	2016	In the whole-cell patch-clamp recording, after elimination from remifentanil incubation, mEPSC frequency was down regulated in hippocampal CA1 neurons, indicating that basal synaptic transmission were affected by remifentanil withdrawal.	Remifentanil	64-76	carbonic anhydrase 1	Rattus norvegicus	139-142
26777139-11	2016	In the whole-cell patch-clamp recording, after elimination from remifentanil incubation, mEPSC frequency was down regulated in hippocampal CA1 neurons, indicating that basal synaptic transmission were affected by remifentanil withdrawal.	Remifentanil	213-225	carbonic anhydrase 1	Rattus norvegicus	139-142
26368667-10	2015	The inhibition of iNOS reverted the protective effect of propofol on the BHR induced by remifentanil (non-sensitized: +47.11+-7.70%; passively sensitized: +70.51+-11.39%; P<0.05 vs. control).	Remifentanil	88-100	nitric oxide synthase 2	Equus caballus	18-22
25819118-0	2015	Neuron-restrictive silencer factor in periaqueductal gray contributes to remifentanil-induced postoperative hyperalgesia via repression of the mu-opioid receptor.	Remifentanil	73-85	RE1 silencing transcription factor	Homo sapiens	0-34
26571899-1	2015	OBJECTIVE: To explore the impacts on EC50 in the remifentanil inhibition of tracheal intubation response by the transcutaneous electrical acupoint stimulation (TEAS) at Hegu (LI 4) and Neiguan (PC 6).	Remifentanil	49-61	lipase family member N	Homo sapiens	175-179
26571899-1	2015	OBJECTIVE: To explore the impacts on EC50 in the remifentanil inhibition of tracheal intubation response by the transcutaneous electrical acupoint stimulation (TEAS) at Hegu (LI 4) and Neiguan (PC 6).	Remifentanil	49-61	proprotein convertase subtilisin/kexin type 5	Homo sapiens	194-198
26283875-11	2015	During hypoxic-reoxygenation condition, remifentanil preconditioning induced the expression of BMP-2, osteocalcin, Akt, type I collagen, osterix, TGF-beta1, HIF-1alpha, and RUNX2 in osteoblasts.	Remifentanil	40-52	bone morphogenetic protein 2	Homo sapiens	95-100
26283875-11	2015	During hypoxic-reoxygenation condition, remifentanil preconditioning induced the expression of BMP-2, osteocalcin, Akt, type I collagen, osterix, TGF-beta1, HIF-1alpha, and RUNX2 in osteoblasts.	Remifentanil	40-52	bone gamma-carboxyglutamate protein	Homo sapiens	102-113
26283875-11	2015	During hypoxic-reoxygenation condition, remifentanil preconditioning induced the expression of BMP-2, osteocalcin, Akt, type I collagen, osterix, TGF-beta1, HIF-1alpha, and RUNX2 in osteoblasts.	Remifentanil	40-52	AKT serine/threonine kinase 1	Homo sapiens	115-118
26283875-11	2015	During hypoxic-reoxygenation condition, remifentanil preconditioning induced the expression of BMP-2, osteocalcin, Akt, type I collagen, osterix, TGF-beta1, HIF-1alpha, and RUNX2 in osteoblasts.	Remifentanil	40-52	Sp7 transcription factor	Homo sapiens	137-144
26283875-11	2015	During hypoxic-reoxygenation condition, remifentanil preconditioning induced the expression of BMP-2, osteocalcin, Akt, type I collagen, osterix, TGF-beta1, HIF-1alpha, and RUNX2 in osteoblasts.	Remifentanil	40-52	transforming growth factor beta 1	Homo sapiens	146-155
26283875-11	2015	During hypoxic-reoxygenation condition, remifentanil preconditioning induced the expression of BMP-2, osteocalcin, Akt, type I collagen, osterix, TGF-beta1, HIF-1alpha, and RUNX2 in osteoblasts.	Remifentanil	40-52	hypoxia inducible factor 1 subunit alpha	Homo sapiens	157-167
26283875-11	2015	During hypoxic-reoxygenation condition, remifentanil preconditioning induced the expression of BMP-2, osteocalcin, Akt, type I collagen, osterix, TGF-beta1, HIF-1alpha, and RUNX2 in osteoblasts.	Remifentanil	40-52	RUNX family transcription factor 2	Homo sapiens	173-178
26149148-1	2015	OBJECTIVE: To investigate the influence of sex on the cough-preventing effect of target-controlled infusion(TCI)of remifentanil during anesthetic emergence.	Remifentanil	115-127	latexin	Homo sapiens	108-111
25819118-0	2015	Neuron-restrictive silencer factor in periaqueductal gray contributes to remifentanil-induced postoperative hyperalgesia via repression of the mu-opioid receptor.	Remifentanil	73-85	opioid receptor mu 1	Homo sapiens	143-161
25819118-1	2015	BACKGROUND: The ultra-short-acting mu-opioid receptor (MOR) agonist remifentanil induces postoperative hyperalgesia both in preclinical and clinical research studies.	Remifentanil	68-80	opioid receptor mu 1	Homo sapiens	35-53
25819118-1	2015	BACKGROUND: The ultra-short-acting mu-opioid receptor (MOR) agonist remifentanil induces postoperative hyperalgesia both in preclinical and clinical research studies.	Remifentanil	68-80	opioid receptor mu 1	Homo sapiens	55-58
25819118-7	2015	RESULTS: NRSF expression levels were enhanced after intraoperative infusion of remifentanil, resulting in repression of MOR expression in the periaqueductal gray (PAG).	Remifentanil	79-91	RE1 silencing transcription factor	Homo sapiens	9-13
25819118-7	2015	RESULTS: NRSF expression levels were enhanced after intraoperative infusion of remifentanil, resulting in repression of MOR expression in the periaqueductal gray (PAG).	Remifentanil	79-91	opioid receptor mu 1	Homo sapiens	120-123
25819118-8	2015	NRSF blockade with an NRSF antisense oligonucleotide significantly enhanced the expression levels of MOR and alleviated mechanical allodynia and thermal hyperalgesia induced by intraoperative infusion of remifentanil.	Remifentanil	204-216	RE1 silencing transcription factor	Homo sapiens	0-4
25819118-8	2015	NRSF blockade with an NRSF antisense oligonucleotide significantly enhanced the expression levels of MOR and alleviated mechanical allodynia and thermal hyperalgesia induced by intraoperative infusion of remifentanil.	Remifentanil	204-216	RE1 silencing transcription factor	Homo sapiens	22-26
25819118-8	2015	NRSF blockade with an NRSF antisense oligonucleotide significantly enhanced the expression levels of MOR and alleviated mechanical allodynia and thermal hyperalgesia induced by intraoperative infusion of remifentanil.	Remifentanil	204-216	opioid receptor mu 1	Homo sapiens	101-104
25819118-9	2015	CONCLUSION: NRSF functions as a negative regulator of MOR in PAG and contributes to remifentanil-induced postoperative hyperalgesia.	Remifentanil	84-96	RE1 silencing transcription factor	Homo sapiens	12-16
25819118-9	2015	CONCLUSION: NRSF functions as a negative regulator of MOR in PAG and contributes to remifentanil-induced postoperative hyperalgesia.	Remifentanil	84-96	opioid receptor mu 1	Homo sapiens	54-57
25501899-0	2015	Spinal peroxynitrite contributes to remifentanil-induced postoperative hyperalgesia via enhancement of divalent metal transporter 1 without iron-responsive element-mediated iron accumulation in rats.	Remifentanil	36-48	RoBo-1	Rattus norvegicus	103-131
25659616-7	2015	RESULTS: In cultured cardiomyocytes, remifentanil incubation significantly increased the phosphorylation of ERK1/2 and this effect was blocked by both NAL and 8-SPT (P < 0.01 and P < 0.05, respectively).	Remifentanil	37-49	mitogen activated protein kinase 3	Rattus norvegicus	108-114
25501899-5	2015	This study aims to determine whether peroxynitrite contributes to remifentanil-induced postoperative hyperalgesia via DMT1-mediated iron accumulation.	Remifentanil	66-78	RoBo-1	Rattus norvegicus	118-122
25501899-13	2015	CONCLUSIONS: Our study identifies that spinal peroxynitrite activates DMT1(-)IRE, leading to abnormal iron accumulation in remifentanil-induced postoperative hyperalgesia, while providing the rationale for the development of molecular hydrogen and "iron-targeted" therapies.	Remifentanil	123-135	RoBo-1	Rattus norvegicus	70-74
25697071-1	2015	Patients suffering from Alzheimer"s disease, Parkinson"s disease and dementia with Lewy bodies can be treated well with the cholinesterase inhibitors rivastigmine or donepezil, and because of the increasing number of these patients undergoing surgery in general anaesthesia we find it urgent to draw attention to possible complications such as severe bradycardia or third-degree heart block when propofol and remifentanil are being used.	Remifentanil	409-421	butyrylcholinesterase	Homo sapiens	124-138
26419105-3	2015	By using desflurane under continuous infusion of remifentanil 0.2-0.5 mug x kg(-1) x min(-1), BIS values were maintained between 40 and 60 during the surgery.	Remifentanil	49-61	CD59 molecule (CD59 blood group)	Homo sapiens	85-91
26080847-4	2015	Remifentanil infusion rate was 0.2 microg kg-1  min-1, while the propofol infusion rate was adjusted to maintain BIS values within the range of 30-50.	Remifentanil	0-12	CD59 molecule (CD59 blood group)	Homo sapiens	48-53
25867330-0	2015	Phosphorylation of the GluN1 subunit in dorsal horn neurons by remifentanil: a mechanism for opioid-induced hyperalgesia.	Remifentanil	63-75	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	23-28
25867330-3	2015	However, the effect of remifentanil on the levels of the GluN1 subunit of the NMDAR in dorsal horn neurons (DHNs) has not been reported.	Remifentanil	23-35	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	57-62
25867330-4	2015	We investigated the effect of remifentanil, along with ketamine (NMDAR antagonist) and naloxone (mu-opioid receptor antagonist), on GluN1 mRNA levels and the amount of phosphorylated GluN1 in primary cultures of embryonic rat DHNs.	Remifentanil	30-42	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	132-137
25233045-0	2015	Effect-site concentration and plasma concentration of remifentanil during TCI are not the same.	Remifentanil	54-66	latexin	Homo sapiens	74-77
25932115-6	2015	The depression of the increased levels of proinflammatory cytokines and p-NR2B after remifentanil treatment may contribute to the anti-hyperalgesia effects of PHA-543613and PNU-120596 via alpha7-nAChRs.	Remifentanil	85-97	glutamate ionotropic receptor NMDA type subunit 2B	Homo sapiens	74-78
25670917-2	2015	The chemically related opioid remifentanil with its different pharmacokinetics and binding affinities for delta- and kappa-opioid receptors might be more effective in attenuating these responses.	Remifentanil	30-42	opioid receptor kappa 1	Homo sapiens	106-139
26121800-1	2015	BACKGROUND: Using an algorithm by which the effect-site concentration of propofol (esTEC) necessary for BIS level set from information input from BIS monitor and TCI pump is estimated, the effect of remifentanil on esTEC was investigated.	Remifentanil	199-211	latexin	Homo sapiens	162-165
26401735-8	2015	Endotracheal intubation was performed after the target concentrations of propofol and remifentanil reached 4 mug mL-1 and 4 ng mL-1, respectively.	Remifentanil	86-98	L1 cell adhesion molecule	Mus musculus	113-123
26401735-8	2015	Endotracheal intubation was performed after the target concentrations of propofol and remifentanil reached 4 mug mL-1 and 4 ng mL-1, respectively.	Remifentanil	86-98	L1 cell adhesion molecule	Mus musculus	113-117
25498394-8	2015	RESULTS: We found that membrane trafficking of DOR, NR1 and NR2B subunits in the spinal cord increased after remifentanil administration and surgery.	Remifentanil	109-121	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	52-55
25498394-8	2015	RESULTS: We found that membrane trafficking of DOR, NR1 and NR2B subunits in the spinal cord increased after remifentanil administration and surgery.	Remifentanil	109-121	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	60-64
25241067-9	2014	Here, we found that the analgesic effect of remifentanil was followed by long-term hyperalgesia lasting at least postoperative 7 days, which was accompanied with increase in NR2B expression and trafficking from cytoplasm to surface and MnSOD nitration in dorsal horn.	Remifentanil	44-56	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	174-178
26681083-0	2015	Maternal and neonatal effects of remifentanil in women undergoing cesarean section in relation to ABCB1 and OPRM1 polymorphisms.	Remifentanil	33-45	ATP binding cassette subfamily B member 1	Homo sapiens	98-103
26681083-0	2015	Maternal and neonatal effects of remifentanil in women undergoing cesarean section in relation to ABCB1 and OPRM1 polymorphisms.	Remifentanil	33-45	opioid receptor mu 1	Homo sapiens	108-113
26681083-1	2015	The aim of our study was to evaluate possible effect of ABCB1, and OPRM1 polymorphisms on the efficacy and safety of remifentanil in women undergoing elective cesarean section under general anesthesia.	Remifentanil	117-129	ATP binding cassette subfamily B member 1	Homo sapiens	56-61
26681083-1	2015	The aim of our study was to evaluate possible effect of ABCB1, and OPRM1 polymorphisms on the efficacy and safety of remifentanil in women undergoing elective cesarean section under general anesthesia.	Remifentanil	117-129	opioid receptor mu 1	Homo sapiens	67-72
26681083-8	2015	Decreased stabilizing effects of remifentanil on maternal hemodynamics has been observed in ABCB1 wild type mothers, while the adaptation of the neonates was clinically worse in OPRM1 wild type, and ABCB1 variant allele carriers.	Remifentanil	33-45	ATP binding cassette subfamily B member 1	Homo sapiens	92-97
25241067-9	2014	Here, we found that the analgesic effect of remifentanil was followed by long-term hyperalgesia lasting at least postoperative 7 days, which was accompanied with increase in NR2B expression and trafficking from cytoplasm to surface and MnSOD nitration in dorsal horn.	Remifentanil	44-56	superoxide dismutase 2	Rattus norvegicus	236-241
25241067-13	2014	In conclusion, HRS (10 ml/kg) might reverse remifentanil-induced hyperalgesia, through regulating NR2B-containing NMDAR trafficking to control MnSOD nitration and enhance MnSOD activity.	Remifentanil	44-56	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	98-102
25241067-13	2014	In conclusion, HRS (10 ml/kg) might reverse remifentanil-induced hyperalgesia, through regulating NR2B-containing NMDAR trafficking to control MnSOD nitration and enhance MnSOD activity.	Remifentanil	44-56	superoxide dismutase 2	Rattus norvegicus	143-148
24564266-8	2014	NCA remifentanil and fentanyl offer similarly effective pain control after pediatric cardiac surgery, but remifentanil has fewer side effects than fentanyl, indicating the suitability of remifentanil for use in NCA systems.	Remifentanil	4-16	CEA cell adhesion molecule 6	Homo sapiens	0-3
24748477-5	2014	Remifentanil also attenuated the concentrations of proinflammatory cytokines tumor necrosis factor alpha, interleukin-1beta, and interleukin-6 in BALF, as well as effectively repressed the activation of nuclear factor-kappaB (NF-kappaB), which has been associated with the inhibition of IkappaBalpha degradation.These results suggest that remifentanil may be a suitable treatment for LPS-induced ALI.	Remifentanil	0-12	tumor necrosis factor	Rattus norvegicus	77-104
24748477-5	2014	Remifentanil also attenuated the concentrations of proinflammatory cytokines tumor necrosis factor alpha, interleukin-1beta, and interleukin-6 in BALF, as well as effectively repressed the activation of nuclear factor-kappaB (NF-kappaB), which has been associated with the inhibition of IkappaBalpha degradation.These results suggest that remifentanil may be a suitable treatment for LPS-induced ALI.	Remifentanil	0-12	interleukin 1 beta	Rattus norvegicus	106-123
24748477-5	2014	Remifentanil also attenuated the concentrations of proinflammatory cytokines tumor necrosis factor alpha, interleukin-1beta, and interleukin-6 in BALF, as well as effectively repressed the activation of nuclear factor-kappaB (NF-kappaB), which has been associated with the inhibition of IkappaBalpha degradation.These results suggest that remifentanil may be a suitable treatment for LPS-induced ALI.	Remifentanil	0-12	interleukin 6	Rattus norvegicus	129-142
24748477-5	2014	Remifentanil also attenuated the concentrations of proinflammatory cytokines tumor necrosis factor alpha, interleukin-1beta, and interleukin-6 in BALF, as well as effectively repressed the activation of nuclear factor-kappaB (NF-kappaB), which has been associated with the inhibition of IkappaBalpha degradation.These results suggest that remifentanil may be a suitable treatment for LPS-induced ALI.	Remifentanil	0-12	NFKB inhibitor alpha	Rattus norvegicus	287-299
24590579-4	2014	Therefore, this study focuses on the interaction of morphine and fentanyl-type opioids (alfentanil, remifentanil and sufentanil) with 5-HT3A receptors.	Remifentanil	100-112	5-hydroxytryptamine receptor 3A	Homo sapiens	134-140
25126703-0	2014	Glycogen synthase kinase-3beta inhibition prevents remifentanil-induced postoperative hyperalgesia via regulating the expression and function of AMPA receptors.	Remifentanil	51-63	glycogen synthase kinase 3 beta	Rattus norvegicus	0-30
25126703-2	2014	We previously reported that activation of glycogen synthase kinase-3beta (GSK-3beta) contributes to remifentanil-induced hyperalgesia via regulating N-methyl-D-aspartate receptor plasticity in the spinal dorsal horn.	Remifentanil	100-112	glycogen synthase kinase 3 beta	Rattus norvegicus	42-72
25126703-2	2014	We previously reported that activation of glycogen synthase kinase-3beta (GSK-3beta) contributes to remifentanil-induced hyperalgesia via regulating N-methyl-D-aspartate receptor plasticity in the spinal dorsal horn.	Remifentanil	100-112	glycogen synthase kinase 3 beta	Rattus norvegicus	74-83
25126703-3	2014	In this study, we demonstrated that GSK-3beta inhibition prevented remifentanil-induced postoperative hyperalgesia via regulating alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) expression and function in the spinal dorsal horn.	Remifentanil	67-79	glycogen synthase kinase 3 beta	Rattus norvegicus	36-45
25126703-7	2014	RESULTS: Membrane AMPAR subunit GluR1 was upregulated in the spinal cord in remifentanil-induced postoperative hyperalgesia rats (275 +- 36.54 [mean +- SD] vs 100 +- 9.53, P = 0.0009).	Remifentanil	76-88	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	32-37
25126703-8	2014	Selective GSK-3beta inhibitors, LiCl and TDZD, treatment ameliorates remifentanil-induced postoperative hyperalgesia, and this was associated with the downregulated GluR1 subunit in the membrane fraction (254 +- 23.51 vs 119 +- 14.74, P = 0.0027; 254 +- 23.51 vs 124 +- 9.35, P = 0.0032).	Remifentanil	69-81	glycogen synthase kinase 3 beta	Rattus norvegicus	10-19
25126703-8	2014	Selective GSK-3beta inhibitors, LiCl and TDZD, treatment ameliorates remifentanil-induced postoperative hyperalgesia, and this was associated with the downregulated GluR1 subunit in the membrane fraction (254 +- 23.51 vs 119 +- 14.74, P = 0.0027; 254 +- 23.51 vs 124 +- 9.35, P = 0.0032).	Remifentanil	69-81	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	165-170
25126703-11	2014	CONCLUSIONS: These results indicate that amelioration of remifentanil-induced postoperative hyperalgesia by GSK-3beta inhibition is attributed to downregulated AMPAR GluR1 expression in the membrane fraction and inhibition of AMPAR function via altering pGluR1 and Rab5 expression in the spinal dorsal horn.	Remifentanil	57-69	glycogen synthase kinase 3 beta	Rattus norvegicus	108-117
25126703-11	2014	CONCLUSIONS: These results indicate that amelioration of remifentanil-induced postoperative hyperalgesia by GSK-3beta inhibition is attributed to downregulated AMPAR GluR1 expression in the membrane fraction and inhibition of AMPAR function via altering pGluR1 and Rab5 expression in the spinal dorsal horn.	Remifentanil	57-69	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	166-171
25269492-0	2014	[Changes of Mu-opioid receptor and neuron-restrictive silencer factor in periaquductal gray in mouse models of remifentanil-induced postoperative hyperalgesia].	Remifentanil	111-123	opioid receptor, mu 1	Mus musculus	12-30
25269492-0	2014	[Changes of Mu-opioid receptor and neuron-restrictive silencer factor in periaquductal gray in mouse models of remifentanil-induced postoperative hyperalgesia].	Remifentanil	111-123	RE1-silencing transcription factor	Mus musculus	35-69
25269492-1	2014	OBJECTIVE: To determine the changes of Mu-opioid receptor (Mor) and neuron-restrictive silencer factor (NRSF) in periaquductal gray (PAG) in mouse models of remifentanil-induced postoperative hyperalgesia.	Remifentanil	157-169	RE1-silencing transcription factor	Mus musculus	68-102
25269492-1	2014	OBJECTIVE: To determine the changes of Mu-opioid receptor (Mor) and neuron-restrictive silencer factor (NRSF) in periaquductal gray (PAG) in mouse models of remifentanil-induced postoperative hyperalgesia.	Remifentanil	157-169	RE1-silencing transcription factor	Mus musculus	104-108
25269492-8	2014	CONCLUSION: Intraoperative infusion of remifentanil induces postoperative hyperalgesia in mouse models, accompanied with decreased expressions of Mor and increased of NRSF level in PAG neurons, which may be involved in remifentanil induced hyperalgesia.	Remifentanil	39-51	opioid receptor, mu 1	Mus musculus	146-149
25269492-8	2014	CONCLUSION: Intraoperative infusion of remifentanil induces postoperative hyperalgesia in mouse models, accompanied with decreased expressions of Mor and increased of NRSF level in PAG neurons, which may be involved in remifentanil induced hyperalgesia.	Remifentanil	39-51	RE1-silencing transcription factor	Mus musculus	167-171
25269492-8	2014	CONCLUSION: Intraoperative infusion of remifentanil induces postoperative hyperalgesia in mouse models, accompanied with decreased expressions of Mor and increased of NRSF level in PAG neurons, which may be involved in remifentanil induced hyperalgesia.	Remifentanil	219-231	RE1-silencing transcription factor	Mus musculus	167-171
25135729-0	2014	Effect of electro-acupuncture stimulation of Ximen (PC4) and Neiguan (PC6) on remifentanil-induced breakthrough pain following thoracal esophagectomy.	Remifentanil	78-90	keratin 6B	Homo sapiens	52-55
25135729-0	2014	Effect of electro-acupuncture stimulation of Ximen (PC4) and Neiguan (PC6) on remifentanil-induced breakthrough pain following thoracal esophagectomy.	Remifentanil	78-90	proprotein convertase subtilisin/kexin type 5	Homo sapiens	70-73
25135729-20	2014	It was concluded that intraoperative ipsilateral EAS at PC4 and PC6 provides effective postoperative analgesia for patients undergoing radical esophagectomy with remifentanil anesthesia and significantly decrease requirement for parental narcotics.	Remifentanil	162-174	proprotein convertase subtilisin/kexin type 5	Homo sapiens	64-67
24951883-9	2014	RESULTS: We found that NR1 membrane trafficking in DRG increased, possibly due to GSK-3beta activation after remifentanil infusion.	Remifentanil	109-121	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	23-26
24769228-6	2014	Correlated with the pain behavior changes, Western blotting revealed that there was a significant increase in the expression of Cdk5 and its activator p35/p25, and further the kinase activity of Cdk5 in spinal dorsal horn after intraoperative infusion of remifentanil.	Remifentanil	255-267	cyclin-dependent kinase 5	Rattus norvegicus	128-132
24769228-2	2014	Our previous study showed that tyrosine phosphorylation of NMDAR subunit 2B (NR2B) at Tyr1472 in spinal dorsal horn contributes to the postoperative hyperalgesia induced by remifentanil.	Remifentanil	173-185	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	59-75
24769228-2	2014	Our previous study showed that tyrosine phosphorylation of NMDAR subunit 2B (NR2B) at Tyr1472 in spinal dorsal horn contributes to the postoperative hyperalgesia induced by remifentanil.	Remifentanil	173-185	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	77-81
24951883-9	2014	RESULTS: We found that NR1 membrane trafficking in DRG increased, possibly due to GSK-3beta activation after remifentanil infusion.	Remifentanil	109-121	glycogen synthase kinase 3 beta	Rattus norvegicus	82-91
24769228-4	2014	In the present study, a rat model of postoperative pain was used to investigate the role of Cdk5 in spinal dorsal horn in remifentanil-induced hyperalgesia and the intervention of pretreatment with Cdk5 inhibitor roscovitine.	Remifentanil	122-134	cyclin-dependent kinase 5	Rattus norvegicus	92-96
24781573-11	2014	remifentanil was ineffective on necrotic death, whereas it significantly reduced caspase-3 activity and cortical cleaved caspase-3 levels.	Remifentanil	0-12	caspase 3	Mus musculus	81-90
24197291-9	2014	Compared with TEA, both high-dose and low-dose remifentanil significantly suppressed increases in ACTH, ADH, and cortisol during pneumoperitoneum.	Remifentanil	47-59	proopiomelanocortin	Homo sapiens	98-102
24197291-9	2014	Compared with TEA, both high-dose and low-dose remifentanil significantly suppressed increases in ACTH, ADH, and cortisol during pneumoperitoneum.	Remifentanil	47-59	arginine vasopressin	Homo sapiens	104-107
25006366-12	2014	RESULTS: The logistic regression model showed that the probability of preventing rocuronium-induced withdrawal movement was as follows: exp (-3.49 + 2.07 x remifentanil concentration) / (1 + exp [-3.49 + 2.07 x remifentanil concentration]).	Remifentanil	156-168	muscleblind like splicing regulator 1	Homo sapiens	136-139
25006366-12	2014	RESULTS: The logistic regression model showed that the probability of preventing rocuronium-induced withdrawal movement was as follows: exp (-3.49 + 2.07 x remifentanil concentration) / (1 + exp [-3.49 + 2.07 x remifentanil concentration]).	Remifentanil	211-223	muscleblind like splicing regulator 1	Homo sapiens	136-139
24769228-6	2014	Correlated with the pain behavior changes, Western blotting revealed that there was a significant increase in the expression of Cdk5 and its activator p35/p25, and further the kinase activity of Cdk5 in spinal dorsal horn after intraoperative infusion of remifentanil.	Remifentanil	255-267	cyclin-dependent kinase 5 regulatory subunit 1	Rattus norvegicus	151-154
24769228-6	2014	Correlated with the pain behavior changes, Western blotting revealed that there was a significant increase in the expression of Cdk5 and its activator p35/p25, and further the kinase activity of Cdk5 in spinal dorsal horn after intraoperative infusion of remifentanil.	Remifentanil	255-267	lipocalin 2	Rattus norvegicus	155-158
24769228-6	2014	Correlated with the pain behavior changes, Western blotting revealed that there was a significant increase in the expression of Cdk5 and its activator p35/p25, and further the kinase activity of Cdk5 in spinal dorsal horn after intraoperative infusion of remifentanil.	Remifentanil	255-267	cyclin-dependent kinase 5	Rattus norvegicus	195-199
24769228-9	2014	These results suggested that Cdk5 may contribute to remifentanil-induced postoperative hyperalgesia via regulating the phosphorylation of NMDAR and mGluR5 in spinal dorsal horn.	Remifentanil	52-64	cyclin-dependent kinase 5	Rattus norvegicus	29-33
24769228-9	2014	These results suggested that Cdk5 may contribute to remifentanil-induced postoperative hyperalgesia via regulating the phosphorylation of NMDAR and mGluR5 in spinal dorsal horn.	Remifentanil	52-64	glutamate receptor, ionotropic, kainate 1	Mus musculus	148-154
24769228-10	2014	These findings provide experimental evidence for the further application of Cdk5 inhibitor in preventing remifentanil-induced hyperalgesia.	Remifentanil	105-117	cyclin-dependent kinase 5	Rattus norvegicus	76-80
24781573-11	2014	remifentanil was ineffective on necrotic death, whereas it significantly reduced caspase-3 activity and cortical cleaved caspase-3 levels.	Remifentanil	0-12	caspase 3	Mus musculus	121-130
24781573-13	2014	remifentanil inhibited cortical Bax protein expression, caspase-9 activity, and preserved mitochondrial integrity, whereas it had no effect on caspase-8 activity.	Remifentanil	0-12	BCL2-associated X protein	Mus musculus	32-35
24781573-13	2014	remifentanil inhibited cortical Bax protein expression, caspase-9 activity, and preserved mitochondrial integrity, whereas it had no effect on caspase-8 activity.	Remifentanil	0-12	caspase 9	Mus musculus	56-65
25487930-3	2014	In remifentanil group remifentanil was infused intravenously with micro pump in 0.05-0.1 microg kg-1 min-1.	Remifentanil	3-15	CD59 molecule (CD59 blood group)	Homo sapiens	101-106
24651236-0	2014	Changes in plasma orexin-A levels in sevoflurane-remifentanil anesthesia in young and elderly patients undergoing elective lumbar surgery.	Remifentanil	49-61	hypocretin neuropeptide precursor	Homo sapiens	18-24
24651239-9	2014	CONCLUSIONS: The activation of glia, the production of proinflammatory cytokines, and the expression of CB2 and p-NR2B in the spinal dorsal horn increase significantly during the process of remifentanil-induced hyperalgesia.	Remifentanil	190-202	cannabinoid receptor 2	Rattus norvegicus	104-107
24651239-9	2014	CONCLUSIONS: The activation of glia, the production of proinflammatory cytokines, and the expression of CB2 and p-NR2B in the spinal dorsal horn increase significantly during the process of remifentanil-induced hyperalgesia.	Remifentanil	190-202	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	114-118
24724445-7	2014	Remifentanil might directly increase SOD, independent of sympathetic nervous system.	Remifentanil	0-12	superoxide dismutase 1	Homo sapiens	37-40
24783622-12	2014	CONCLUSIONS: Remifentanil infusion at 0.02 microg x kg(-1) x min(-1) can safely be used without any serious adverse events, while it may not be enough for postoperative analgesia.	Remifentanil	13-25	CD59 molecule (CD59 blood group)	Homo sapiens	61-67
25487930-3	2014	In remifentanil group remifentanil was infused intravenously with micro pump in 0.05-0.1 microg kg-1 min-1.	Remifentanil	22-34	CD59 molecule (CD59 blood group)	Homo sapiens	101-106
24071376-12	2014	Continuous infusion of nicardipine attenuated the increase in NAG, which is a marker of renal tubular injury, during hypotensive anesthesia with desflurane and remifentanil.	Remifentanil	160-172	N-acetyl-alpha-glucosaminidase	Homo sapiens	62-65
25500932-0	2014	Association between single nucleotide polymorphisms in the OPRM1 gene and intraoperative remifentanil consumption in northern Chinese women.	Remifentanil	89-101	opioid receptor mu 1	Homo sapiens	59-64
25500932-2	2014	In this study, we assessed the association between SNPs in the OPRM1 gene and intraoperative remifentanil consumption as well as perioperative side effects during gynecological hysteroscopic surgery in women from Northern China.	Remifentanil	93-105	opioid receptor mu 1	Homo sapiens	63-68
25500932-12	2014	CONCLUSIONS: SNP rs558025 in the OPRM1 gene was associated with intraoperative remifentanil consumption during gynecological hysteroscopic surgery in our subjects.	Remifentanil	79-91	opioid receptor mu 1	Homo sapiens	33-38
23990403-0	2013	The role of glycogen synthase kinase-3beta in glioma cell apoptosis induced by remifentanil.	Remifentanil	79-91	glycogen synthase kinase 3 beta	Homo sapiens	12-42
23990403-5	2013	The purpose of this study was to assess whether remifentanil can induce the apoptosis of C6 cells through GSK-3beta activation.	Remifentanil	48-60	glycogen synthase kinase 3 beta	Homo sapiens	106-115
23990403-11	2013	The measurement of GSK-3beta activation showed that remifentanil increased the cellular level of GSK-3beta.	Remifentanil	52-64	glycogen synthase kinase 3 beta	Homo sapiens	19-28
23990403-11	2013	The measurement of GSK-3beta activation showed that remifentanil increased the cellular level of GSK-3beta.	Remifentanil	52-64	glycogen synthase kinase 3 beta	Homo sapiens	97-106
23990403-13	2013	These results suggest that remifentanil is able to induce C6 cell apoptosis through GSK-3beta activation, which provides a basis for its potential use in the treatment of malignant gliomas.	Remifentanil	27-39	glycogen synthase kinase 3 beta	Homo sapiens	84-93
23609459-9	2013	In addition, remifentanil postconditioning enhanced the expression of anti-apoptotic gene Bcl-2 while suppressed the expression of pro-apoptotic gene Bax in hippocampal CA1 region.	Remifentanil	13-25	BCL2, apoptosis regulator	Rattus norvegicus	90-95
24190484-0	2013	Remifentanil preconditioning alleviating brain damage of cerebral ischemia reperfusion rats by regulating the JNK signal pathway and TNF-alpha/TNFR1 signal pathway.	Remifentanil	0-12	mitogen-activated protein kinase 8	Rattus norvegicus	110-113
24190484-0	2013	Remifentanil preconditioning alleviating brain damage of cerebral ischemia reperfusion rats by regulating the JNK signal pathway and TNF-alpha/TNFR1 signal pathway.	Remifentanil	0-12	tumor necrosis factor	Rattus norvegicus	133-142
24190484-0	2013	Remifentanil preconditioning alleviating brain damage of cerebral ischemia reperfusion rats by regulating the JNK signal pathway and TNF-alpha/TNFR1 signal pathway.	Remifentanil	0-12	TNF receptor superfamily member 1A	Rattus norvegicus	143-148
24190484-4	2013	Results showed that Remifentanil pretreatment significantly decreased the CD4(+) and increased the CD8(+) in cerebral tissues.	Remifentanil	20-32	Cd4 molecule	Rattus norvegicus	74-77
24190484-5	2013	Additionally, CD4(+)/CD8(+) in CIR + Remifentanil group was markedly lower than that in CIR group.	Remifentanil	37-49	Cd4 molecule	Rattus norvegicus	14-17
24190484-6	2013	TNF-alpha and TNFR1 in CIR + Remifentanil group rats was found to be significant lower than that in CIR group rats.	Remifentanil	29-41	tumor necrosis factor	Rattus norvegicus	0-9
24190484-6	2013	TNF-alpha and TNFR1 in CIR + Remifentanil group rats was found to be significant lower than that in CIR group rats.	Remifentanil	29-41	TNF receptor superfamily member 1A	Rattus norvegicus	14-19
24190484-7	2013	The expression levels of Cyt-c, caspase-3, caspase-9 and pJNK proteins in brain of CIR + Remifentanil group rats were found to significantly decreased compared to CIR group rats.	Remifentanil	89-101	caspase 3	Rattus norvegicus	32-41
24190484-7	2013	The expression levels of Cyt-c, caspase-3, caspase-9 and pJNK proteins in brain of CIR + Remifentanil group rats were found to significantly decreased compared to CIR group rats.	Remifentanil	89-101	caspase 9	Rattus norvegicus	43-52
24190484-8	2013	In addition, decreased ROS level indirectly inhibit JNK activation and cell death in CIR rat receiving Remifentanil preconditioning.	Remifentanil	103-115	mitogen-activated protein kinase 8	Rattus norvegicus	52-55
24190484-10	2013	The inhibitory effects of Remifentanil preconditioning on the brain damage are achieved probably through blocking the activation of TNF-alpha/TNFR1, JNK signal transduction pathways, which implies that Remifentanil preconditioning may be a potential and effective way for prevention of the ischemic/reperfusion injury through the suppression extrinsic apoptotic signal pathway induced by TNF-alpha/TNFR1, JNK signal pathways.	Remifentanil	26-38	tumor necrosis factor	Rattus norvegicus	132-141
24190484-10	2013	The inhibitory effects of Remifentanil preconditioning on the brain damage are achieved probably through blocking the activation of TNF-alpha/TNFR1, JNK signal transduction pathways, which implies that Remifentanil preconditioning may be a potential and effective way for prevention of the ischemic/reperfusion injury through the suppression extrinsic apoptotic signal pathway induced by TNF-alpha/TNFR1, JNK signal pathways.	Remifentanil	26-38	TNF receptor superfamily member 1A	Rattus norvegicus	142-147
24190484-10	2013	The inhibitory effects of Remifentanil preconditioning on the brain damage are achieved probably through blocking the activation of TNF-alpha/TNFR1, JNK signal transduction pathways, which implies that Remifentanil preconditioning may be a potential and effective way for prevention of the ischemic/reperfusion injury through the suppression extrinsic apoptotic signal pathway induced by TNF-alpha/TNFR1, JNK signal pathways.	Remifentanil	26-38	mitogen-activated protein kinase 8	Rattus norvegicus	149-152
24190484-10	2013	The inhibitory effects of Remifentanil preconditioning on the brain damage are achieved probably through blocking the activation of TNF-alpha/TNFR1, JNK signal transduction pathways, which implies that Remifentanil preconditioning may be a potential and effective way for prevention of the ischemic/reperfusion injury through the suppression extrinsic apoptotic signal pathway induced by TNF-alpha/TNFR1, JNK signal pathways.	Remifentanil	26-38	tumor necrosis factor	Rattus norvegicus	388-397
24190484-10	2013	The inhibitory effects of Remifentanil preconditioning on the brain damage are achieved probably through blocking the activation of TNF-alpha/TNFR1, JNK signal transduction pathways, which implies that Remifentanil preconditioning may be a potential and effective way for prevention of the ischemic/reperfusion injury through the suppression extrinsic apoptotic signal pathway induced by TNF-alpha/TNFR1, JNK signal pathways.	Remifentanil	26-38	TNF receptor superfamily member 1A	Rattus norvegicus	398-403
24190484-10	2013	The inhibitory effects of Remifentanil preconditioning on the brain damage are achieved probably through blocking the activation of TNF-alpha/TNFR1, JNK signal transduction pathways, which implies that Remifentanil preconditioning may be a potential and effective way for prevention of the ischemic/reperfusion injury through the suppression extrinsic apoptotic signal pathway induced by TNF-alpha/TNFR1, JNK signal pathways.	Remifentanil	26-38	mitogen-activated protein kinase 8	Rattus norvegicus	405-408
24190484-10	2013	The inhibitory effects of Remifentanil preconditioning on the brain damage are achieved probably through blocking the activation of TNF-alpha/TNFR1, JNK signal transduction pathways, which implies that Remifentanil preconditioning may be a potential and effective way for prevention of the ischemic/reperfusion injury through the suppression extrinsic apoptotic signal pathway induced by TNF-alpha/TNFR1, JNK signal pathways.	Remifentanil	202-214	tumor necrosis factor	Rattus norvegicus	132-141
24190484-10	2013	The inhibitory effects of Remifentanil preconditioning on the brain damage are achieved probably through blocking the activation of TNF-alpha/TNFR1, JNK signal transduction pathways, which implies that Remifentanil preconditioning may be a potential and effective way for prevention of the ischemic/reperfusion injury through the suppression extrinsic apoptotic signal pathway induced by TNF-alpha/TNFR1, JNK signal pathways.	Remifentanil	202-214	TNF receptor superfamily member 1A	Rattus norvegicus	142-147
24190484-10	2013	The inhibitory effects of Remifentanil preconditioning on the brain damage are achieved probably through blocking the activation of TNF-alpha/TNFR1, JNK signal transduction pathways, which implies that Remifentanil preconditioning may be a potential and effective way for prevention of the ischemic/reperfusion injury through the suppression extrinsic apoptotic signal pathway induced by TNF-alpha/TNFR1, JNK signal pathways.	Remifentanil	202-214	mitogen-activated protein kinase 8	Rattus norvegicus	149-152
24190484-10	2013	The inhibitory effects of Remifentanil preconditioning on the brain damage are achieved probably through blocking the activation of TNF-alpha/TNFR1, JNK signal transduction pathways, which implies that Remifentanil preconditioning may be a potential and effective way for prevention of the ischemic/reperfusion injury through the suppression extrinsic apoptotic signal pathway induced by TNF-alpha/TNFR1, JNK signal pathways.	Remifentanil	202-214	tumor necrosis factor	Rattus norvegicus	388-397
24190484-10	2013	The inhibitory effects of Remifentanil preconditioning on the brain damage are achieved probably through blocking the activation of TNF-alpha/TNFR1, JNK signal transduction pathways, which implies that Remifentanil preconditioning may be a potential and effective way for prevention of the ischemic/reperfusion injury through the suppression extrinsic apoptotic signal pathway induced by TNF-alpha/TNFR1, JNK signal pathways.	Remifentanil	202-214	TNF receptor superfamily member 1A	Rattus norvegicus	398-403
24190484-10	2013	The inhibitory effects of Remifentanil preconditioning on the brain damage are achieved probably through blocking the activation of TNF-alpha/TNFR1, JNK signal transduction pathways, which implies that Remifentanil preconditioning may be a potential and effective way for prevention of the ischemic/reperfusion injury through the suppression extrinsic apoptotic signal pathway induced by TNF-alpha/TNFR1, JNK signal pathways.	Remifentanil	202-214	mitogen-activated protein kinase 8	Rattus norvegicus	405-408
23609459-9	2013	In addition, remifentanil postconditioning enhanced the expression of anti-apoptotic gene Bcl-2 while suppressed the expression of pro-apoptotic gene Bax in hippocampal CA1 region.	Remifentanil	13-25	BCL2 associated X, apoptosis regulator	Rattus norvegicus	150-153
23609459-9	2013	In addition, remifentanil postconditioning enhanced the expression of anti-apoptotic gene Bcl-2 while suppressed the expression of pro-apoptotic gene Bax in hippocampal CA1 region.	Remifentanil	13-25	carbonic anhydrase 1	Rattus norvegicus	169-172
23636304-2	2013	OBJECTIVE: This experiment examined the effects of delayed reinforcement on choice between food and the mu-opioid receptor agonist remifentanil.	Remifentanil	131-143	opioid receptor mu 1	Macaca mulatta	104-122
24147079-0	2013	Inhibition of glycogen synthase kinase-3beta prevents remifentanil-induced hyperalgesia via regulating the expression and function of spinal N-methyl-D-aspartate receptors in vivo and vitro.	Remifentanil	54-66	glycogen synthase kinase 3 beta	Rattus norvegicus	14-44
24147079-3	2013	Recently, we found that glycogen synthase kinase-3beta (GSK-3beta) modulated NMDA receptor trafficking in a rat model of remifentanil-induced postoperative hyperalgesia.	Remifentanil	121-133	glycogen synthase kinase 3 beta	Rattus norvegicus	24-54
24147079-3	2013	Recently, we found that glycogen synthase kinase-3beta (GSK-3beta) modulated NMDA receptor trafficking in a rat model of remifentanil-induced postoperative hyperalgesia.	Remifentanil	121-133	glycogen synthase kinase 3 beta	Rattus norvegicus	56-65
24147079-4	2013	In the current study, it was demonstrated that GSK-3beta inhibition prevented remifentanil-induced hyperalgesia via regulating the expression and function of spinal NMDA receptors in vivo and in vitro.	Remifentanil	78-90	glycogen synthase kinase 3 beta	Rattus norvegicus	47-56
24147079-8	2013	We found that remifentanil infusion at 1 mug kg(-1) min(-1) and 2 mug kg(-1) min(-1) caused mechanical and thermal hyperalgesia, up-regulated NMDA receptor subunits NR1 and NR2B expression in both membrane fraction and total lysate of the spinal cord dorsal horn and increased GSK-3beta activity in spinal cord dorsal horn.	Remifentanil	14-26	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	165-168
24147079-8	2013	We found that remifentanil infusion at 1 mug kg(-1) min(-1) and 2 mug kg(-1) min(-1) caused mechanical and thermal hyperalgesia, up-regulated NMDA receptor subunits NR1 and NR2B expression in both membrane fraction and total lysate of the spinal cord dorsal horn and increased GSK-3beta activity in spinal cord dorsal horn.	Remifentanil	14-26	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	173-177
24147079-8	2013	We found that remifentanil infusion at 1 mug kg(-1) min(-1) and 2 mug kg(-1) min(-1) caused mechanical and thermal hyperalgesia, up-regulated NMDA receptor subunits NR1 and NR2B expression in both membrane fraction and total lysate of the spinal cord dorsal horn and increased GSK-3beta activity in spinal cord dorsal horn.	Remifentanil	14-26	glycogen synthase kinase 3 beta	Rattus norvegicus	277-286
24147079-9	2013	GSK-3beta inhibitor TDZD-8 significantly attenuated remifentanil-induced mechanical and thermal hyperalgesia from 2 h to 48 h after infusion, and this was associated with reversal of up-regulated NR1 and NR2B subunits in both membrane fraction and total lysate.	Remifentanil	52-64	glycogen synthase kinase 3 beta	Rattus norvegicus	0-9
24147079-9	2013	GSK-3beta inhibitor TDZD-8 significantly attenuated remifentanil-induced mechanical and thermal hyperalgesia from 2 h to 48 h after infusion, and this was associated with reversal of up-regulated NR1 and NR2B subunits in both membrane fraction and total lysate.	Remifentanil	52-64	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	196-199
24147079-9	2013	GSK-3beta inhibitor TDZD-8 significantly attenuated remifentanil-induced mechanical and thermal hyperalgesia from 2 h to 48 h after infusion, and this was associated with reversal of up-regulated NR1 and NR2B subunits in both membrane fraction and total lysate.	Remifentanil	52-64	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	204-208
24147079-11	2013	These results suggest that inhibition of GSK-3beta can significantly ameliorate remifentanil-induced hyperalgesia via modulating the expression and function of NMDA receptors, which present useful insights into the mechanistic action of GSK-3beta inhibitor as potential anti-hyperalgesic agents for treating OIH.	Remifentanil	80-92	glycogen synthase kinase 3 beta	Rattus norvegicus	41-50
24147079-11	2013	These results suggest that inhibition of GSK-3beta can significantly ameliorate remifentanil-induced hyperalgesia via modulating the expression and function of NMDA receptors, which present useful insights into the mechanistic action of GSK-3beta inhibitor as potential anti-hyperalgesic agents for treating OIH.	Remifentanil	80-92	glycogen synthase kinase 3 beta	Rattus norvegicus	237-246
23792280-4	2013	For this purpose, we first examined the pharmacological properties of both remifentanil and morphine at the MOP receptor, endogenously expressed in the human neuroblastoma SH-SY5Y cell line, to regulate adenylyl cyclase and the MAP kinase ERK1/2 pathway, their potency to promote MOP receptor phosphorylation, arrestin 3-CFP (cyan fluorescent protein) recruitment and receptor trafficking during acute and sustained exposure.	Remifentanil	75-87	mitogen-activated protein kinase 3	Homo sapiens	239-245
23792280-4	2013	For this purpose, we first examined the pharmacological properties of both remifentanil and morphine at the MOP receptor, endogenously expressed in the human neuroblastoma SH-SY5Y cell line, to regulate adenylyl cyclase and the MAP kinase ERK1/2 pathway, their potency to promote MOP receptor phosphorylation, arrestin 3-CFP (cyan fluorescent protein) recruitment and receptor trafficking during acute and sustained exposure.	Remifentanil	75-87	arrestin 3	Homo sapiens	310-320
23792280-4	2013	For this purpose, we first examined the pharmacological properties of both remifentanil and morphine at the MOP receptor, endogenously expressed in the human neuroblastoma SH-SY5Y cell line, to regulate adenylyl cyclase and the MAP kinase ERK1/2 pathway, their potency to promote MOP receptor phosphorylation, arrestin 3-CFP (cyan fluorescent protein) recruitment and receptor trafficking during acute and sustained exposure.	Remifentanil	75-87	complement factor properdin	Homo sapiens	321-324
23792280-5	2013	In the second part of this work, we studied the effects of a prior exposure of remifentanil on morphine-induced inhibition of cAMP accumulation, activation of ERK1/2 and analgesia.	Remifentanil	79-91	mitogen-activated protein kinase 3	Homo sapiens	159-165
23607370-13	2013	The systemic inflammatory response triggered by intestinal IRI was significantly attenuated in mice pretreated with remifentanil (159 vs 805 pg/ml of IL-6 after saline pretreatment, with 92 pg/ml in the sham groups).	Remifentanil	116-128	interleukin 6	Mus musculus	150-154
23869185-0	2013	The effect of intraoperative use of high-dose remifentanil on postoperative insulin resistance and muscle protein catabolism: a randomized controlled study.	Remifentanil	46-58	insulin	Homo sapiens	76-83
23869185-1	2013	OBJECTIVE: We investigated the effect of the intraoperative use of a high dose remifentanil on insulin resistance and muscle protein catabolism.	Remifentanil	79-91	insulin	Homo sapiens	95-102
23869185-11	2013	CONCLUSION: Use of high-dose remifentanil as intraoperative analgesia during elective gastrectomy reduced postoperative insulin resistance, although it did not reduce postoperative muscle protein catabolism.	Remifentanil	29-41	insulin	Homo sapiens	120-127
23608616-12	2013	Remifentanil preconditioning inhibited I/R-induced increases in tumor necrosis factor alpha, intercellular adhesion molecule 1, and nuclear factor kappaB p65 levels in liver tissues.	Remifentanil	0-12	tumor necrosis factor	Rattus norvegicus	64-91
23608616-12	2013	Remifentanil preconditioning inhibited I/R-induced increases in tumor necrosis factor alpha, intercellular adhesion molecule 1, and nuclear factor kappaB p65 levels in liver tissues.	Remifentanil	0-12	intercellular adhesion molecule 1	Rattus norvegicus	93-126
23608616-12	2013	Remifentanil preconditioning inhibited I/R-induced increases in tumor necrosis factor alpha, intercellular adhesion molecule 1, and nuclear factor kappaB p65 levels in liver tissues.	Remifentanil	0-12	synaptotagmin 1	Rattus norvegicus	154-157
23503369-0	2013	Modeling the influence of the A118G polymorphism in the OPRM1 gene and of noxious stimulation on the synergistic relation between propofol and remifentanil: sedation and analgesia in endoscopic procedures.	Remifentanil	143-155	opioid receptor mu 1	Homo sapiens	56-61
23503369-1	2013	BACKGROUND: The presence of the A118G single nucleotide polymorphism in the OPRM1 gene as well as noxious stimulation might affect the requirements of remifentanil for patients undergoing ultrasonographic endoscopy under sedation-analgesia with propofol and remifentanil.	Remifentanil	151-163	opioid receptor mu 1	Homo sapiens	76-81
23503369-1	2013	BACKGROUND: The presence of the A118G single nucleotide polymorphism in the OPRM1 gene as well as noxious stimulation might affect the requirements of remifentanil for patients undergoing ultrasonographic endoscopy under sedation-analgesia with propofol and remifentanil.	Remifentanil	258-270	opioid receptor mu 1	Homo sapiens	76-81
23052952-4	2013	The aim of this study is to evaluate the safety and efficacy of sedation with remifentanil target-controlled infusion (Remi-TCI) in patients with spontaneous ventilation undergoing FFB in ICU.	Remifentanil	78-90	latexin	Homo sapiens	124-127
23697200-3	2013	Anesthesia was induced with midazolam (5 mg) and remifentanil (0.1.ag x kg-1 x min-1) and the trachea was intubated following administration of rocuronium.	Remifentanil	49-61	CD59 molecule (CD59 blood group)	Homo sapiens	79-84
23241726-0	2013	Intraoperative infusion of 0.6-0.9 microg kg(-1) min(-1) remifentanil induces acute tolerance in young children after laparoscopic ureteroneocystostomy.	Remifentanil	57-69	CD59 molecule (CD59 blood group)	Homo sapiens	49-55
23267003-0	2013	Glycogen synthase kinase-3beta contributes to remifentanil-induced postoperative hyperalgesia via regulating N-methyl-D-aspartate receptor trafficking.	Remifentanil	46-58	glycogen synthase kinase 3 beta	Rattus norvegicus	0-30
23267003-4	2013	We designed the present study to examine the hypothesis that glycogen synthase kinase (GSK)-3beta could contribute to remifentanil-induced postoperative hyperalgesia via regulating NMDA receptor trafficking in the spinal cord.	Remifentanil	118-130	glycogen synthase kinase 3 beta	Rattus norvegicus	61-97
23267003-9	2013	Moreover, remifentanil infusion increased the expression of GSK-3beta mRNA and protein as well as the GSK-3beta activity in the spinal cord.	Remifentanil	10-22	glycogen synthase kinase 3 beta	Rattus norvegicus	60-69
23267003-9	2013	Moreover, remifentanil infusion increased the expression of GSK-3beta mRNA and protein as well as the GSK-3beta activity in the spinal cord.	Remifentanil	10-22	glycogen synthase kinase 3 beta	Rattus norvegicus	102-111
23267003-10	2013	More importantly, intraoperative infusion of remifentanil increased NMDA receptor subunits (NR1 and NR2B) trafficking from the intracellular pool to surface pool in the spinal cord, which was significantly attenuated by TDZD-8.	Remifentanil	45-57	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	92-95
23267003-10	2013	More importantly, intraoperative infusion of remifentanil increased NMDA receptor subunits (NR1 and NR2B) trafficking from the intracellular pool to surface pool in the spinal cord, which was significantly attenuated by TDZD-8.	Remifentanil	45-57	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	100-104
23267003-11	2013	CONCLUSION: The above results suggest that activation of GSK-3beta contributes to remifentanil-induced postoperative hyperalgesia via regulating NMDA receptor subunits (NR1 and NR2B) trafficking in the spinal cord.	Remifentanil	82-94	glycogen synthase kinase 3 beta	Rattus norvegicus	57-66
23267003-11	2013	CONCLUSION: The above results suggest that activation of GSK-3beta contributes to remifentanil-induced postoperative hyperalgesia via regulating NMDA receptor subunits (NR1 and NR2B) trafficking in the spinal cord.	Remifentanil	82-94	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	169-172
23267003-11	2013	CONCLUSION: The above results suggest that activation of GSK-3beta contributes to remifentanil-induced postoperative hyperalgesia via regulating NMDA receptor subunits (NR1 and NR2B) trafficking in the spinal cord.	Remifentanil	82-94	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	177-181
23267003-12	2013	Inhibition of GSK-3beta may be an effective novel option for the treatment of remifentanil-induced postoperative hyperalgesia.	Remifentanil	78-90	glycogen synthase kinase 3 beta	Rattus norvegicus	14-23
23480345-7	2013	In particular, remifentanil decreased activation of intracellular signaling pathways, including p38 and ERK1/2, and expression of pro-inflammatory cytokines, including TNF-alpha, IL-6 and IL-8.	Remifentanil	15-27	mitogen-activated protein kinase 1	Homo sapiens	96-99
23480345-7	2013	In particular, remifentanil decreased activation of intracellular signaling pathways, including p38 and ERK1/2, and expression of pro-inflammatory cytokines, including TNF-alpha, IL-6 and IL-8.	Remifentanil	15-27	mitogen-activated protein kinase 3	Homo sapiens	104-110
23480345-7	2013	In particular, remifentanil decreased activation of intracellular signaling pathways, including p38 and ERK1/2, and expression of pro-inflammatory cytokines, including TNF-alpha, IL-6 and IL-8.	Remifentanil	15-27	tumor necrosis factor	Homo sapiens	168-177
23480345-7	2013	In particular, remifentanil decreased activation of intracellular signaling pathways, including p38 and ERK1/2, and expression of pro-inflammatory cytokines, including TNF-alpha, IL-6 and IL-8.	Remifentanil	15-27	interleukin 6	Homo sapiens	179-183
23480345-7	2013	In particular, remifentanil decreased activation of intracellular signaling pathways, including p38 and ERK1/2, and expression of pro-inflammatory cytokines, including TNF-alpha, IL-6 and IL-8.	Remifentanil	15-27	C-X-C motif chemokine ligand 8	Homo sapiens	188-192
23480345-8	2013	Especially the decreased activation of cytokines and MAPKs was significantly reverted by a kappa-opioid receptor antagonist on remifentanil with LPS.	Remifentanil	127-139	opioid receptor kappa 1	Homo sapiens	91-112
23480345-9	2013	These results demonstrate that remifentanil can attenuate human neutrophils activations induced by LPS and a kappa-opioid receptor be probably involved in these anti-inflammatory effects mediated by remifentanil.	Remifentanil	199-211	opioid receptor kappa 1	Homo sapiens	109-130
23402298-4	2013	The genotyping was combined with an analysis of plasma levels of the opioid peptide beta-endorphin in 80 well-defined patients with chronic low back pain scheduled for spinal fusion surgery, and with differential sensitivity to the opioid analgesic remifentanil.	Remifentanil	249-261	proopiomelanocortin	Homo sapiens	84-98
22967972-1	2012	OBJECTIVE: To evaluate the feasibility and efficacy of Narcotrend (NT) monitor in monitoring the depth of anesthesia in severely burned patients with target-controlled infusion (TCI) of remifentanil hydrochloride and propofol during perioperative period.	Remifentanil	186-212	latexin	Homo sapiens	178-181
22381051-9	2012	The level of IL-6 at the end of surgery was lower for sevoflurane (69.5 [35.9-121.0] pg/mL) than propofol-remifentanil (128.2 [92.8-163.8] pg/mL, p = 0.03), but this difference was not maintained 24 hours after surgery.	Remifentanil	106-118	interleukin 6	Homo sapiens	13-17
23382975-10	2013	The lower nadir SaO(2) and higher insulin growth factor binding protein-1 (IGFBP-1) were associated with higher analgesic sensitivity to remifentanil (SaO(2), P = 0.0440; IGFBP-1, P = 0.0013).	Remifentanil	137-149	insulin like growth factor binding protein 1	Homo sapiens	34-73
23382975-10	2013	The lower nadir SaO(2) and higher insulin growth factor binding protein-1 (IGFBP-1) were associated with higher analgesic sensitivity to remifentanil (SaO(2), P = 0.0440; IGFBP-1, P = 0.0013).	Remifentanil	137-149	insulin like growth factor binding protein 1	Homo sapiens	75-82
23382975-10	2013	The lower nadir SaO(2) and higher insulin growth factor binding protein-1 (IGFBP-1) were associated with higher analgesic sensitivity to remifentanil (SaO(2), P = 0.0440; IGFBP-1, P = 0.0013).	Remifentanil	137-149	insulin like growth factor binding protein 1	Homo sapiens	171-178
22895704-7	2012	Similar to our recent reports of morphine-TLR4/MD2 binding, here we provide a combination of in silico and biophysical data to support (+)-naloxone and remifentanil binding to TLR4/MD2.	Remifentanil	152-164	toll-like receptor 4	Rattus norvegicus	42-46
22895704-7	2012	Similar to our recent reports of morphine-TLR4/MD2 binding, here we provide a combination of in silico and biophysical data to support (+)-naloxone and remifentanil binding to TLR4/MD2.	Remifentanil	152-164	lymphocyte antigen 96	Rattus norvegicus	47-50
22895704-7	2012	Similar to our recent reports of morphine-TLR4/MD2 binding, here we provide a combination of in silico and biophysical data to support (+)-naloxone and remifentanil binding to TLR4/MD2.	Remifentanil	152-164	toll-like receptor 4	Rattus norvegicus	176-180
22895704-7	2012	Similar to our recent reports of morphine-TLR4/MD2 binding, here we provide a combination of in silico and biophysical data to support (+)-naloxone and remifentanil binding to TLR4/MD2.	Remifentanil	152-164	lymphocyte antigen 96	Rattus norvegicus	181-184
22991798-10	2012	CONCLUSIONS: We found that more than 0.5 microg x kg(-1) x min(-1) of remifentanil can blunt cardiovascular responses to tracheal intubation without severe cardiovascular depression.	Remifentanil	70-82	CD59 molecule (CD59 blood group)	Homo sapiens	59-65
22967972-5	2012	All patients received TCI of remifentanil hydrochloride and propofol to induce and maintain anesthesia.	Remifentanil	29-55	latexin	Homo sapiens	22-25
22967972-24	2012	CONCLUSIONS: Application of Narcotrend monitor in monitoring the depth of anesthesia in severely burned patients during perioperative period with TCI of remifentanil hydrochloride and propofol is beneficial to reducing dosage of narcotics and shortening duration of recovery from anesthesia, and it can accurately predict the level of consciousness of patients at the time of withdrawal of anesthesia.	Remifentanil	153-179	latexin	Homo sapiens	146-149
22251106-7	2012	Limiting maximal infusion rate during remifentanil TCI suppressed remifentanil-induced cough.	Remifentanil	38-50	latexin	Homo sapiens	51-54
22444868-9	2012	In DRG cultures, MOR agonists morphine, DAMGO, and remifentanil each increased MMP-9 expression in neurons, whereas the opioid receptor antagonist naloxone and the MOR-selective antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) suppressed morphine-induced MMP-9 expression.	Remifentanil	51-63	opioid receptor, mu 1	Mus musculus	17-20
22444868-9	2012	In DRG cultures, MOR agonists morphine, DAMGO, and remifentanil each increased MMP-9 expression in neurons, whereas the opioid receptor antagonist naloxone and the MOR-selective antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) suppressed morphine-induced MMP-9 expression.	Remifentanil	51-63	matrix metallopeptidase 9	Mus musculus	79-84
22444868-9	2012	In DRG cultures, MOR agonists morphine, DAMGO, and remifentanil each increased MMP-9 expression in neurons, whereas the opioid receptor antagonist naloxone and the MOR-selective antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) suppressed morphine-induced MMP-9 expression.	Remifentanil	51-63	matrix metallopeptidase 9	Mus musculus	264-269
21392805-7	2012	RESULTS: In normoglycemia, remifentanil-preconditioning improved the viability of cardiomyocytes (P < 0.01) and prevented the increase of caspase-3 activity and Ca(2+) overload after H/R injury (P < 0.05).	Remifentanil	27-39	caspase 3	Rattus norvegicus	141-150
21392805-8	2012	In addition, decrease in Akt, ERK1/2, and Bcl-2, and the increase in Bax by H/R was attenuated by remifentanil-preconditioning (P < 0.05).	Remifentanil	98-110	AKT serine/threonine kinase 1	Rattus norvegicus	25-28
21392805-8	2012	In addition, decrease in Akt, ERK1/2, and Bcl-2, and the increase in Bax by H/R was attenuated by remifentanil-preconditioning (P < 0.05).	Remifentanil	98-110	mitogen activated protein kinase 3	Rattus norvegicus	30-36
21392805-8	2012	In addition, decrease in Akt, ERK1/2, and Bcl-2, and the increase in Bax by H/R was attenuated by remifentanil-preconditioning (P < 0.05).	Remifentanil	98-110	BCL2, apoptosis regulator	Rattus norvegicus	42-47
21392805-8	2012	In addition, decrease in Akt, ERK1/2, and Bcl-2, and the increase in Bax by H/R was attenuated by remifentanil-preconditioning (P < 0.05).	Remifentanil	98-110	BCL2 associated X, apoptosis regulator	Rattus norvegicus	69-72
21392805-14	2012	However, hyperglycemia mitigates H/R injury in NRVMs, and may reduce the protective effect of remifentanil-preconditioning that may be associated with the Akt pathways.	Remifentanil	94-106	AKT serine/threonine kinase 1	Rattus norvegicus	155-158
22240620-9	2012	The estimated EC(95) of remifentanil Ce was 3.38 (95% confidence interval 2.90-3.46) ng mL-1.	Remifentanil	24-36	L1 cell adhesion molecule	Mus musculus	88-92
22240620-12	2012	CONCLUSION: The estimated EC(95) of remifentanil Ce for smooth nasotracheal fibreoptic intubation with conscious sedation was 3.38 (95% CI 2.90-3.46) ng mL-1 when used in combination with midazolam and topical lidocaine.	Remifentanil	36-48	L1 cell adhesion molecule	Mus musculus	153-157
22207192-0	2012	Effects of surgery and/or remifentanil administration on the expression of pERK1/2, c-Fos and dynorphin in the dorsal root ganglia in mice.	Remifentanil	26-38	FBJ osteosarcoma oncogene	Mus musculus	84-89
22207192-4	2012	Surgery and/or remifentanil induced mechanical hypersensitivity, correlated with ERK1/2 phosphorylation and c-Fos expression in the DRG; changes were greater in the remifentanil + incision group and still present on day 14 (p < 0.01 vs. control).	Remifentanil	15-27	mitogen-activated protein kinase 3	Mus musculus	81-87
22207192-4	2012	Surgery and/or remifentanil induced mechanical hypersensitivity, correlated with ERK1/2 phosphorylation and c-Fos expression in the DRG; changes were greater in the remifentanil + incision group and still present on day 14 (p < 0.01 vs. control).	Remifentanil	15-27	FBJ osteosarcoma oncogene	Mus musculus	108-113
22207192-4	2012	Surgery and/or remifentanil induced mechanical hypersensitivity, correlated with ERK1/2 phosphorylation and c-Fos expression in the DRG; changes were greater in the remifentanil + incision group and still present on day 14 (p < 0.01 vs. control).	Remifentanil	165-177	mitogen-activated protein kinase 3	Mus musculus	81-87
22207192-4	2012	Surgery and/or remifentanil induced mechanical hypersensitivity, correlated with ERK1/2 phosphorylation and c-Fos expression in the DRG; changes were greater in the remifentanil + incision group and still present on day 14 (p < 0.01 vs. control).	Remifentanil	165-177	FBJ osteosarcoma oncogene	Mus musculus	108-113
22207192-5	2012	Intrathecal PD98059 (ERK1/2 inhibitor) partially reversed the mechanical hypersensitivity (44%, p < 0.05) observed in the remifentanil + incision group.	Remifentanil	125-137	mitogen-activated protein kinase 3	Mus musculus	21-27
22207192-9	2012	Surgery and/or remifentanil induce up-regulation of c-Fos and pERK in the DRG, approximately correlating with nociceptive behavior, also associated with an increased expression of prodynorphin/dynorphin.	Remifentanil	15-27	FBJ osteosarcoma oncogene	Mus musculus	52-57
22207192-9	2012	Surgery and/or remifentanil induce up-regulation of c-Fos and pERK in the DRG, approximately correlating with nociceptive behavior, also associated with an increased expression of prodynorphin/dynorphin.	Remifentanil	15-27	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	62-66
22301064-8	2012	Correlated with the pain behavior changes, Western blotting experiments also revealed that dexmedetomidine could decrease NR2B subunit phosphorylation (Tyr1472 site) in the dorsal horn, which was upregulated after remifentanil infusion.	Remifentanil	214-226	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	122-126
22490960-0	2012	[Changes of glycogen synthase kinase-3beta and its phosphorylation in spinal cord neurons in rats with incisional pain-remifentanil-induced hyperalgesia].	Remifentanil	119-131	glycogen synthase kinase 3 beta	Rattus norvegicus	12-42
22490960-1	2012	OBJECTIVE: To investigate the change in glycogen synthase kinase-3beta (GSK-3beta) in spinal cord neurons in rats with incisional pain (IP)-remifentanil-induced hyperalgesia.	Remifentanil	140-152	glycogen synthase kinase 3 beta	Rattus norvegicus	40-70
22490960-1	2012	OBJECTIVE: To investigate the change in glycogen synthase kinase-3beta (GSK-3beta) in spinal cord neurons in rats with incisional pain (IP)-remifentanil-induced hyperalgesia.	Remifentanil	140-152	glycogen synthase kinase 3 beta	Rattus norvegicus	72-81
22490960-10	2012	CONCLUSION: These data indicate that the increased GSK-3beta activity in rats spinal cord neurons is involved in remifentanil-induced hyperalgesia.	Remifentanil	113-125	glycogen synthase kinase 3 beta	Rattus norvegicus	51-60
22251106-7	2012	Limiting maximal infusion rate during remifentanil TCI suppressed remifentanil-induced cough.	Remifentanil	66-78	latexin	Homo sapiens	51-54
22015431-12	2012	The I/R insult enhanced the phosphorylation of ERK 1/2 and the expression of TNF-alpha, which were significantly reduced by remifentanil.	Remifentanil	124-136	mitogen activated protein kinase 3	Rattus norvegicus	47-54
22025495-3	2012	We also determined whether remifentanil-induced hyperalgesia is related to extracellular signal-regulated protein kinase 1/2 (ERK1/2) phosphorylation.	Remifentanil	27-39	mitogen activated protein kinase 3	Rattus norvegicus	126-132
22025495-11	2012	Significantly more phospho-ERK1/2-immunoreactive neurons in the superficial spinal dorsal horn were observed in the remifentanil 120-minute groups with hyperalgesia than in the 30-minute remifentanil groups without hyperalgesia, although U0126 did not suppress hyperalgesia.	Remifentanil	116-128	mitogen activated protein kinase 3	Rattus norvegicus	27-33
22025495-11	2012	Significantly more phospho-ERK1/2-immunoreactive neurons in the superficial spinal dorsal horn were observed in the remifentanil 120-minute groups with hyperalgesia than in the 30-minute remifentanil groups without hyperalgesia, although U0126 did not suppress hyperalgesia.	Remifentanil	187-199	mitogen activated protein kinase 3	Rattus norvegicus	27-33
22082683-0	2012	Selective 5-HT(1A)-R-agonist repinotan prevents remifentanil-induced ventilatory depression and prolongs antinociception.	Remifentanil	48-60	5-hydroxytryptamine receptor 1A	Rattus norvegicus	10-17
22015431-12	2012	The I/R insult enhanced the phosphorylation of ERK 1/2 and the expression of TNF-alpha, which were significantly reduced by remifentanil.	Remifentanil	124-136	tumor necrosis factor	Rattus norvegicus	77-86
22015431-14	2012	CONCLUSIONS: Remifentanil may be neuroprotective against focal I/R injury, possibly through the activation of delta-opioid receptors and attenuation of ERK 1/2 activity and TNF-alpha production, in the rat brain.	Remifentanil	13-25	mitogen activated protein kinase 3	Rattus norvegicus	152-159
22015431-14	2012	CONCLUSIONS: Remifentanil may be neuroprotective against focal I/R injury, possibly through the activation of delta-opioid receptors and attenuation of ERK 1/2 activity and TNF-alpha production, in the rat brain.	Remifentanil	13-25	tumor necrosis factor	Rattus norvegicus	173-182
21118844-8	2011	RESULTS: HR, K-ICG, and BIS were significantly decreased in the remifentanil 0 microg kg-1 min-1 group.	Remifentanil	64-76	CD59 molecule (CD59 blood group)	Homo sapiens	91-96
21802658-4	2011	In the present study, a single dose of the MOR agonist remifentanil was administered in detoxified alcohol-dependent patients and healthy control subjects to mimic the beta-endorphin-releasing properties of ethanol and to assess the effects of direct MOR stimulation on dopamine release in the mesolimbic reward system.	Remifentanil	55-67	opioid receptor mu 1	Homo sapiens	43-46
21802658-4	2011	In the present study, a single dose of the MOR agonist remifentanil was administered in detoxified alcohol-dependent patients and healthy control subjects to mimic the beta-endorphin-releasing properties of ethanol and to assess the effects of direct MOR stimulation on dopamine release in the mesolimbic reward system.	Remifentanil	55-67	proopiomelanocortin	Homo sapiens	168-182
21383616-0	2011	Remifentanil preconditioning reduces hepatic ischemia-reperfusion injury in rats via inducible nitric oxide synthase expression.	Remifentanil	0-12	nitric oxide synthase 2	Homo sapiens	95-116
21383616-8	2011	RESULTS: Remifentanil and L-arginine pretreatment reduced concentrations of serum aminotransferases and cytokines, decreased the concentrations of hepatic malondialdehyde and myeloperoxidase activity, and increased superoxide dismutase, nitric oxide, and inducible NOS expression in vivo.	Remifentanil	9-21	myeloperoxidase	Rattus norvegicus	175-190
21520591-0	2011	[Remifentanil prevents hyperglycemia and reduces insulin use during cardiopulmonary bypass in adult cardiac surgery].	Remifentanil	1-13	insulin	Homo sapiens	49-56
21520591-2	2011	METHODS: We retrospectively examined blood glucose monitored every 30 minutes during CPB and insulin dose in patients during CPB under remifentanil anesthesia (remifentanil group) and those under low dose fentanyl anesthesia (fentanyl group) in adult cardiac surgery.	Remifentanil	160-172	insulin	Homo sapiens	93-100
21520591-6	2011	Significantly less insulin was administered during CPB in remifentanil group than in fentanyl group.	Remifentanil	58-70	insulin	Homo sapiens	19-26
21520591-8	2011	CONCLUSIONS: Maximum blood glucose was lower and less insulin was administered during CPB in remifentanil group.	Remifentanil	93-105	insulin	Homo sapiens	54-61
23028840-12	2012	TNF-alpha exposure reduced respiration of complex-I, -II and -IV, an effect which was prevented by prior remifentanil incubation.	Remifentanil	105-117	tumor necrosis factor	Homo sapiens	0-9
23028840-13	2012	Furthermore, prior remifentanil incubation prevented TNF-alpha-induced IL-6 release of HepG2 cells, and attenuated fragmentation of pro-caspase-3 into cleaved active caspase 3 (an early marker of apoptosis).	Remifentanil	19-31	tumor necrosis factor	Homo sapiens	53-62
23028840-13	2012	Furthermore, prior remifentanil incubation prevented TNF-alpha-induced IL-6 release of HepG2 cells, and attenuated fragmentation of pro-caspase-3 into cleaved active caspase 3 (an early marker of apoptosis).	Remifentanil	19-31	interleukin 6	Homo sapiens	71-75
23028840-13	2012	Furthermore, prior remifentanil incubation prevented TNF-alpha-induced IL-6 release of HepG2 cells, and attenuated fragmentation of pro-caspase-3 into cleaved active caspase 3 (an early marker of apoptosis).	Remifentanil	19-31	caspase 3	Homo sapiens	132-145
23028840-13	2012	Furthermore, prior remifentanil incubation prevented TNF-alpha-induced IL-6 release of HepG2 cells, and attenuated fragmentation of pro-caspase-3 into cleaved active caspase 3 (an early marker of apoptosis).	Remifentanil	19-31	caspase 3	Homo sapiens	166-175
23028840-14	2012	Our data suggest that remifentanil increases cellular respiration of human hepatocytes and prevents TNF-alpha-induced mitochondrial dysfunction.	Remifentanil	22-34	tumor necrosis factor	Homo sapiens	100-109
21935686-3	2011	In this study, to estimate the safe interval to avoid residual paralysis, we retrospectively selected patients in whom the TOF ratio was measured during remifentanil administration before extubation, and we studied the characteristics of recovery from the neuromuscular blockade produced by the empirical use of rocuronium.	Remifentanil	153-165	FEZ family zinc finger 2	Homo sapiens	123-126
21703258-8	2011	A 10-muM concentration of fentanyl and other opioids, including 1 muM morphine and 4 muM remifentanil, induced HIF-1alpha protein expression and HIF-1 target gene expression in an opioid receptor-dependent manner in SH-SY5Y cells with activity peaking at 24h.	Remifentanil	89-101	latexin	Homo sapiens	5-8
21703258-8	2011	A 10-muM concentration of fentanyl and other opioids, including 1 muM morphine and 4 muM remifentanil, induced HIF-1alpha protein expression and HIF-1 target gene expression in an opioid receptor-dependent manner in SH-SY5Y cells with activity peaking at 24h.	Remifentanil	89-101	hypoxia inducible factor 1 subunit alpha	Homo sapiens	111-121
21703258-8	2011	A 10-muM concentration of fentanyl and other opioids, including 1 muM morphine and 4 muM remifentanil, induced HIF-1alpha protein expression and HIF-1 target gene expression in an opioid receptor-dependent manner in SH-SY5Y cells with activity peaking at 24h.	Remifentanil	89-101	hypoxia inducible factor 1 subunit alpha	Homo sapiens	111-116
21399490-4	2011	Analgesia was provided by remifentanil (0.25 mug   kg-1   min-1).	Remifentanil	26-38	CD59 molecule (CD59 blood group)	Homo sapiens	58-63
21441549-2	2011	METHODS: This double-blind, randomized study tested the possibility to obtain a quicker onset of analgesia by using effect-compartment controlled remifentanil patient-controlled analgesia (remifentanil TCI-PCA) than by using i.v.	Remifentanil	146-158	latexin	Homo sapiens	202-205
21441549-11	2011	CONCLUSIONS: Remifentanil PCA-TCI with a slow and progressive adapted algorithm without any associated premedication or co-medication is feasible in young healthy women undergoing UAE.	Remifentanil	13-25	latexin	Homo sapiens	30-33
20501520-4	2011	In absence or presence of dithiothreitol (DTT), delta-ALA-D activity was reduced after hyperoxygenation in the group treated with remifentanil and was not modified in dexmedetomidine group.	Remifentanil	130-142	aminolevulinate dehydratase	Homo sapiens	48-59
20501520-7	2011	delta-ALA-D activity was only inhibited in remifentanil group, which indicates a possible interaction between oxygenation and the type of anesthetic.	Remifentanil	43-55	aminolevulinate dehydratase	Homo sapiens	0-11
21600128-0	2011	[Effect of pediatric TCI system for propofol plus remifentanil in pediatric short-duration surgery with laryngeal mask airway anesthesia].	Remifentanil	50-62	latexin	Homo sapiens	21-24
21600128-1	2011	OBJECTIVE: To study the effect of a pediatric TCI patent system for propofol plus remifentanil in pediatric short-duration surgery with laryngeal mask airway (LMA) anesthesia.	Remifentanil	82-94	latexin	Homo sapiens	46-49
21600128-11	2011	CONCLUSION: The patented system for propofol 3 microg/ml effect compartment concentration plus remifentanil 2.5 ng/ml plasma concentration TCI displays stable hemodynamics, less stress, fewer complications and better clinical outcomes in pediatric short-duration surgery with LMA anesthesia.	Remifentanil	95-107	latexin	Homo sapiens	139-142
21118844-9	2011	The decrease in MAP, HR, CI, and K-ICG was significantly lower in the remifentanil 0.5 and 1.0 microg kg-1 min-1 groups compared with the remifentanil 0 microg kg-1 min-1 group.	Remifentanil	70-82	CD59 molecule (CD59 blood group)	Homo sapiens	165-170
21267826-6	2011	Our protocol was proposed to associate an hypnotic agent (propofol) to an opioid one (remifentanil) using the technique of the TCI, with respectively Schnider and Minto models.	Remifentanil	86-98	transcobalamin 1	Homo sapiens	127-130
20960893-3	2010	The remifentanil infusion rate was set to maintain the systolic arterial pressure below 150 mmHg and heart rate below 100 beats x min(-1).	Remifentanil	4-16	CD59 molecule (CD59 blood group)	Homo sapiens	130-136
20848080-9	2010	The mean remifentanil dose administered was 0.07 +- 0.03 mug kg(-1) min(-1).	Remifentanil	9-21	CD59 molecule (CD59 blood group)	Homo sapiens	68-74
21117280-4	2010	EXPERIMENTAL APPROACH: Seven pregnant ewes received a continuous infusion of remifentanil (0.33 microg kg-1 min-1) for 1 h, and maternal and fetal arterial blood samples were drawn at regular intervals during and up to 1 h after the discontinuation of the infusion.	Remifentanil	77-89	CD59 molecule (CD59 blood group)	Homo sapiens	108-122
20056436-8	2010	MEASUREMENTS AND MAIN RESULTS: Patients in the remifentanil group had lower levels of CK-MB from T = 2 hours to 24 hours, cTnI from T = 10 minutes to T = 12 hours, IMA from T = 10 minutes to T = 2 hours and h-FABP from T = 10 minutes to T = 12 hours (p < 0.05).	Remifentanil	47-59	troponin I3, cardiac type	Homo sapiens	122-126
20056436-8	2010	MEASUREMENTS AND MAIN RESULTS: Patients in the remifentanil group had lower levels of CK-MB from T = 2 hours to 24 hours, cTnI from T = 10 minutes to T = 12 hours, IMA from T = 10 minutes to T = 2 hours and h-FABP from T = 10 minutes to T = 12 hours (p < 0.05).	Remifentanil	47-59	fatty acid binding protein 3	Homo sapiens	207-213
20960893-4	2010	In 2 of 3 cases, intraoperative hemodynamics were controlled by titrated remifentanil infusion with up to 2 and 3 microg x kg(-1) min(-1) in each case, without additional vasoactive agents.	Remifentanil	73-85	CD59 molecule (CD59 blood group)	Homo sapiens	130-136
20865877-2	2010	Seventy children were randomly allocated to two groups to receive remifentanil infusion at 0.2 microg x kg(-1) x min(-1) with either sevoflurane or propofol supplements for insertion of the rigid bronchoscope.	Remifentanil	66-78	CD59 molecule (CD59 blood group)	Homo sapiens	113-119
19757155-10	2010	Remifentanil could suppress inflammatory responses and inhibit iNOS expression in septic mice.	Remifentanil	0-12	nitric oxide synthase 2, inducible	Mus musculus	63-67
20715524-5	2010	RESULTS: Average infusion rate of remifentanil was 0.24 +/- 0.02 microg x kg(-1) x min(-1) and total infused dose of fentanyl was 0.27 +/- 0.05 mg. Average bispectral index values in both groups were comparable.	Remifentanil	34-46	CD59 molecule (CD59 blood group)	Homo sapiens	83-89
19647325-1	2010	BACKGROUND: Several treatment strategies for augmenting outcomes with ECT (concurrent antidepressant treatment, frequency of ECT treatments, hyperventilation and use of remifentanil) are discussed in the context of a difficult clinical case, accompanied by a review of the relevant existing literature.	Remifentanil	169-181	ECT	Homo sapiens	70-73
20486575-4	2010	Under continuous infusion of remifentanil at 0.1-0.2 microg x kg(-1) x min(-1), the patient became sedated while spontaneously breathing, and her pain and laryngeal reflexes were reduced.	Remifentanil	29-41	CD59 molecule (CD59 blood group)	Homo sapiens	71-77
20156668-4	2010	Remifentanil was administered at a dose of 0.5 microg x kg(-1) x min(-1) to obtain analgesia and a <2 surgical field level in Fromme"s modified scale.	Remifentanil	0-12	CD59 molecule (CD59 blood group)	Homo sapiens	65-71
19627530-6	2010	Remifentanil, a drug cleared by hydrolysis, can be modeled in all age groups by simple application of this model using a standardized clearance of 2790 ml x min(-1) for a 70-kg person.	Remifentanil	0-12	CD59 molecule (CD59 blood group)	Homo sapiens	157-163
19944681-8	2010	Remifentanil preconditioning increased expression of ERK1/2 and anti-apoptotic protein Bcl-2 and decreased expression of pro-apoptotic proteins, Bax and cytochrome c, compared to ischemia-reperfusion only in wild-type rats.	Remifentanil	0-12	mitogen activated protein kinase 3	Rattus norvegicus	53-59
19944681-8	2010	Remifentanil preconditioning increased expression of ERK1/2 and anti-apoptotic protein Bcl-2 and decreased expression of pro-apoptotic proteins, Bax and cytochrome c, compared to ischemia-reperfusion only in wild-type rats.	Remifentanil	0-12	BCL2 associated X, apoptosis regulator	Rattus norvegicus	145-148
19944681-8	2010	Remifentanil preconditioning increased expression of ERK1/2 and anti-apoptotic protein Bcl-2 and decreased expression of pro-apoptotic proteins, Bax and cytochrome c, compared to ischemia-reperfusion only in wild-type rats.	Remifentanil	0-12	BCL2, apoptosis regulator	Rattus norvegicus	87-92
19681651-7	2010	Remifentanil improved expression of ERK1/2 and anti-apoptotic protein Bcl2, and expression of sarcoplasmic reticulum genes which were significantly reduced in the I/R rats only.	Remifentanil	0-12	mitogen activated protein kinase 3	Rattus norvegicus	36-42
19825011-7	2010	Remifentanil pharmacokinetics was described with a two-compartment model, parameter estimates were 2.99 l x min(-1) x 70 kg(-1) for clearance and 16.23 l x 70 kg(-1) for steady state volume of distribution.	Remifentanil	0-12	CD59 molecule (CD59 blood group)	Homo sapiens	108-114
20077774-4	2010	RESULTS: The patients in PR group were infused remifentanil by 0.22 +/- 0.06 microg x kg(-1) x min(-1) and all needed controlled ventilation with laryngeal mask airway.	Remifentanil	47-59	CD59 molecule (CD59 blood group)	Homo sapiens	95-101
19681651-7	2010	Remifentanil improved expression of ERK1/2 and anti-apoptotic protein Bcl2, and expression of sarcoplasmic reticulum genes which were significantly reduced in the I/R rats only.	Remifentanil	0-12	BCL2, apoptosis regulator	Rattus norvegicus	70-74
19681651-8	2010	Remifentanil reduced expression of pro-apoptotic protein, Bax and cytochrome c. These suggested that remifentanil produced cardioprotective effect by preserving the expression of proteins involved in anti-apoptotic pathways, and the expression of sarcoplasmic reticulum genes in I/R rat heart, regardless of the timing of administration.	Remifentanil	0-12	BCL2 associated X, apoptosis regulator	Rattus norvegicus	58-61
19681651-8	2010	Remifentanil reduced expression of pro-apoptotic protein, Bax and cytochrome c. These suggested that remifentanil produced cardioprotective effect by preserving the expression of proteins involved in anti-apoptotic pathways, and the expression of sarcoplasmic reticulum genes in I/R rat heart, regardless of the timing of administration.	Remifentanil	101-113	BCL2 associated X, apoptosis regulator	Rattus norvegicus	58-61
19702213-3	2009	Anesthesia was induced with propofol, suxamethonium and remifentanil 0.26 microg x kg(-1) x min(-1).	Remifentanil	56-68	CD59 molecule (CD59 blood group)	Homo sapiens	92-98
20042082-3	2009	In the present study, we used a rat model of postoperative pain to investigate the role of tyrosine phosphorylation of NMDA receptor 2B (NR2B) subunit in spinal cord in the postoperative hyperalgesia induced by remifentanil and the intervention of pretreatment with ketamine.	Remifentanil	211-223	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	119-135
20042082-3	2009	In the present study, we used a rat model of postoperative pain to investigate the role of tyrosine phosphorylation of NMDA receptor 2B (NR2B) subunit in spinal cord in the postoperative hyperalgesia induced by remifentanil and the intervention of pretreatment with ketamine.	Remifentanil	211-223	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	137-141
20042082-5	2009	Correlated with the pain behavior changes, immunocytochemical and western blotting experiments in our study revealed that there was a marked increase in NR2B phosphorylation at Tyr1472 in the superficial dorsal horn after intraoperative infusion of remifentanil, which was attenuated by pretreatment with ketamine.	Remifentanil	249-261	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	153-157
20042082-6	2009	CONCLUSIONS: This study provides direct evidence that tyrosine phosphorylation of the NR2B at Tyr1472 in spinal dosal horn contributes to postoperative hyperalgesia induced by remifentanil and supports the potential therapeutic value of ketamine for improving postoperative hyperalgesia induced by remifentanil.	Remifentanil	176-188	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	86-90
20042082-6	2009	CONCLUSIONS: This study provides direct evidence that tyrosine phosphorylation of the NR2B at Tyr1472 in spinal dosal horn contributes to postoperative hyperalgesia induced by remifentanil and supports the potential therapeutic value of ketamine for improving postoperative hyperalgesia induced by remifentanil.	Remifentanil	298-310	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	86-90
19860224-4	2009	In R group, remifentanil was administered at 0.2 microg x kg(-1) x min(-1) from the induction of anesthesia.	Remifentanil	12-24	CD59 molecule (CD59 blood group)	Homo sapiens	67-73
19570226-0	2009	Genetic variation in the serotonin transporter gene (5-HTTLPR, rs25531) influences the analgesic response to the short acting opioid Remifentanil in humans.	Remifentanil	133-145	solute carrier family 6 member 4	Homo sapiens	25-46
19726290-0	2009	[Remifentanil preconditioning lowers cardiac troponin I levels in patients undergoing off-pump coronary artery bypass graft surgery].	Remifentanil	1-13	troponin I3, cardiac type	Homo sapiens	37-55
19726290-1	2009	OBJECTIVE: To investigate the value of cardiac troponin I (cTnI) levels in assessing myocardial protection by remifentanil precondition against myocardial injury induced by off-pump coronary artery bypass (OPCAB).	Remifentanil	110-122	troponin I3, cardiac type	Homo sapiens	39-57
19726290-1	2009	OBJECTIVE: To investigate the value of cardiac troponin I (cTnI) levels in assessing myocardial protection by remifentanil precondition against myocardial injury induced by off-pump coronary artery bypass (OPCAB).	Remifentanil	110-122	troponin I3, cardiac type	Homo sapiens	59-63
19726290-9	2009	The cTnI levels of remifentanil preconditioning group were markedly decreased after the operation in comparison with those of the control group (P<0.05).	Remifentanil	19-31	troponin I3, cardiac type	Homo sapiens	4-8
19726290-10	2009	CONCLUSION: Remifentanil preconditioning decreases the cTnI levels and reduces myocardial injury induced by OPCAB.	Remifentanil	12-24	troponin I3, cardiac type	Homo sapiens	55-59
30625832-7	2009	Following the tracheal intubation SBP and HR increased in both groups, the magnitude of which was lower in the remifentanil group.	Remifentanil	111-123	selenium binding protein 1	Homo sapiens	34-37
19570226-0	2009	Genetic variation in the serotonin transporter gene (5-HTTLPR, rs25531) influences the analgesic response to the short acting opioid Remifentanil in humans.	Remifentanil	133-145	solute carrier family 6 member 4	Homo sapiens	53-61
18575957-1	2009	Aim The present study sought insight into the effects of remifentanyl and fentanyl on LPS-induced release of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and IL-10 in human whole blood.	Remifentanil	57-69	interleukin 6	Homo sapiens	109-122
19522262-4	2009	Remifentanil at the rate of 0.5 microg x kg(-1) x min(-1) was administrated continuously, and tracheal intubation was performed by each anesthesiologist, at various times after administration of remifentanil.	Remifentanil	0-12	CD59 molecule (CD59 blood group)	Homo sapiens	50-56
19462805-3	2009	Anesthesia was induced with bolus infusion of propofol 1 mg x kg(-1) and continuous infusion of remifentanil at 0.15 microg x kg(-1) x min(-1) was started.	Remifentanil	96-108	CD59 molecule (CD59 blood group)	Homo sapiens	135-141
19462805-5	2009	Anesthesia was maintained with sevoflurane (0.4-1.0%), air and oxygen (33-50%) and with continuous infusion of 0.1-0.15 microg x kg(-1) x min(-1) of remifentanil without any muscle relaxant.	Remifentanil	149-161	CD59 molecule (CD59 blood group)	Homo sapiens	138-144
19522262-7	2009	We analyzed the P50, representing the duration of remifentanil infusion with 50% probability of blocking sympathetic response to tracheal intubation.	Remifentanil	50-62	nuclear factor kappa B subunit 1	Homo sapiens	16-19
19522262-10	2009	CONCLUSIONS: During sevoflurane anesthesia, remifentanil infusion at 0.5 microg x kg(-1) x min(-1) for more than 210 sec could provide the effective blocking of the sympathetic response to tracheal intubation with more than 50% probability.	Remifentanil	44-56	CD59 molecule (CD59 blood group)	Homo sapiens	91-97
19522267-5	2009	Infusion rate of remifentanil at the beginning of surgery was 0.24+/-0.02 microg x kg(-1) x min(-1), and minimal and maximal rate were 0.06+/-0.03 and 0.26+/-0.03 microg x kg(-1) min(-1).	Remifentanil	17-29	CD59 molecule (CD59 blood group)	Homo sapiens	92-98
19522267-5	2009	Infusion rate of remifentanil at the beginning of surgery was 0.24+/-0.02 microg x kg(-1) x min(-1), and minimal and maximal rate were 0.06+/-0.03 and 0.26+/-0.03 microg x kg(-1) min(-1).	Remifentanil	17-29	CD59 molecule (CD59 blood group)	Homo sapiens	179-185
18575957-4	2009	IL-6, TNF-alpha and IL-10 concentrations in activation groups treated with remifentanyl or fentanyl were significantly lower than those in LPS treated group (P < 0.05).	Remifentanil	75-87	interleukin 6	Homo sapiens	0-4
18575957-4	2009	IL-6, TNF-alpha and IL-10 concentrations in activation groups treated with remifentanyl or fentanyl were significantly lower than those in LPS treated group (P < 0.05).	Remifentanil	75-87	tumor necrosis factor	Homo sapiens	6-15
18575957-4	2009	IL-6, TNF-alpha and IL-10 concentrations in activation groups treated with remifentanyl or fentanyl were significantly lower than those in LPS treated group (P < 0.05).	Remifentanil	75-87	interleukin 10	Homo sapiens	20-25
18575957-6	2009	Conclusion Remifentanyl or fentanyl alone has no effects on IL-6, TNF-alpha and IL-10 production, but could attenuate LPS-induced IL-6,TNF-alpha and IL-10 production in human whole blood.	Remifentanil	11-23	interleukin 6	Homo sapiens	130-134
18575957-6	2009	Conclusion Remifentanyl or fentanyl alone has no effects on IL-6, TNF-alpha and IL-10 production, but could attenuate LPS-induced IL-6,TNF-alpha and IL-10 production in human whole blood.	Remifentanil	11-23	tumor necrosis factor	Homo sapiens	135-144
18575957-6	2009	Conclusion Remifentanyl or fentanyl alone has no effects on IL-6, TNF-alpha and IL-10 production, but could attenuate LPS-induced IL-6,TNF-alpha and IL-10 production in human whole blood.	Remifentanil	11-23	interleukin 10	Homo sapiens	149-154
18575957-7	2009	Remifentanyl and fentanyl could inhibit the expressions of IL-6, TNF-alpha and IL-10 induced by LPS.	Remifentanil	0-12	interleukin 6	Homo sapiens	59-63
18575957-7	2009	Remifentanyl and fentanyl could inhibit the expressions of IL-6, TNF-alpha and IL-10 induced by LPS.	Remifentanil	0-12	tumor necrosis factor	Homo sapiens	65-74
18575957-7	2009	Remifentanyl and fentanyl could inhibit the expressions of IL-6, TNF-alpha and IL-10 induced by LPS.	Remifentanil	0-12	interleukin 10	Homo sapiens	79-84
18626707-12	2008	CONCLUSIONS: We demonstrated the success of a multipharmacological treatment including opioid premedication with CR oxycodone used as transition opioid for TCI remifentanil infusion; the treatment group showed lower pain scores and rescue analgesic consumption, shorter time to discharge from recovery room and from surgical ward, and the same incidence of side effects, comparably to controls.	Remifentanil	160-172	latexin	Homo sapiens	156-159
19094432-1	2008	This prospective randomized pilot study compared the influence of fentanyl-based versus remifentanil-based anaesthesia on cytokine responses and expression of the suppressor of cytokine signalling (SOCS)-3 gene following coronary artery bypass graft surgery.	Remifentanil	88-100	suppressor of cytokine signaling 3	Homo sapiens	163-205
19094432-5	2008	The IFN-gamma/IL-10 ratio after concanavalin A stimulation in whole blood cells on post-operative day 1 and SOCS-3 gene expression on post-operative day 2 were significantly lower in the remifentanil group than in the fentanyl group.	Remifentanil	187-199	interferon gamma	Homo sapiens	4-13
19094432-5	2008	The IFN-gamma/IL-10 ratio after concanavalin A stimulation in whole blood cells on post-operative day 1 and SOCS-3 gene expression on post-operative day 2 were significantly lower in the remifentanil group than in the fentanyl group.	Remifentanil	187-199	interleukin 10	Homo sapiens	14-19
19094432-5	2008	The IFN-gamma/IL-10 ratio after concanavalin A stimulation in whole blood cells on post-operative day 1 and SOCS-3 gene expression on post-operative day 2 were significantly lower in the remifentanil group than in the fentanyl group.	Remifentanil	187-199	suppressor of cytokine signaling 3	Homo sapiens	108-114
19299779-6	2009	During emergence, the remifentanil group (infusion rate 0.014 +/- 0.011 microg x kg(-1) x min(-1)) had a significantly lower incidence (40% vs 80%, P = 0.002) and less severe coughing compared with the control group, as well as a lower incidence of nonpurposeful movement (3.3% vs 30%, P = 0.006) and slower heart rates.	Remifentanil	22-34	CD59 molecule (CD59 blood group)	Homo sapiens	90-96
19058913-1	2009	The ultra-short-acting mu-opioid receptor (MOR) agonist remifentanil enhances postsurgical pain when used as main anesthetic in animal models and man.	Remifentanil	56-68	opioid receptor mu 1	Homo sapiens	23-41
19058913-1	2009	The ultra-short-acting mu-opioid receptor (MOR) agonist remifentanil enhances postsurgical pain when used as main anesthetic in animal models and man.	Remifentanil	56-68	opioid receptor mu 1	Homo sapiens	43-46
19058913-6	2009	Both remifentanil and surgery decreased DOR mRNA levels (up to days 2 and 4, respectively) in the dorsal root ganglia, but not in the spinal cord.	Remifentanil	5-17	opioid receptor, delta 1	Mus musculus	40-43
19058913-10	2009	The study suggests that down-regulation of DOR contributes to remifentanil and surgery-induced nociception, and that postoperative pain is completely reversed by increasing enkephalin levels in the spinal cord and the periphery.	Remifentanil	62-74	opioid receptor, delta 1	Mus musculus	43-46
18975538-5	2008	Remifentanil (0.1-0.25 microg x kg(-1) x min(-1)) maintained the patients" spontaneous ventilation and increased their tolerance to the pain and discomfort caused by insertion of the lightwand.	Remifentanil	0-12	CD59 molecule (CD59 blood group)	Homo sapiens	41-47
17666715-11	2007	This pilot study suggests that remifentanil intravenous PCA is efficacious for labour analgesia as a bolus of 0.25 microg x kg(-1), with a lockout interval of two minutes and continuous infusion of 0.025-0.1 microg x kg(-1) x min(-1).	Remifentanil	31-43	CD59 molecule (CD59 blood group)	Homo sapiens	226-232
18648240-8	2008	Selective delta-opioid agonists [D-Pen(2), D-Pen(5)]enkephalin and deltorphin II displayed a similar bell-shaped concentration-response relation for the enhancement of NMDA responses, and 10 nM deltorphin II occluded the effects of 4 nM remifentanil on NMDA responses.	Remifentanil	237-249	proenkephalin	Rattus norvegicus	52-62
18400142-0	2008	Remifentanil-TCI and propofol-TCI for conscious sedation during fibreoptic intubation in the acromegalic patient.	Remifentanil	0-12	transcobalamin 1	Homo sapiens	13-16
18400142-5	2008	During the fibreoptic procedure the target concentrations of remifentanil and propofol ranged between 1.0 and 5.0 ng mL(-1), and between 1.5 and 3.5 microg mL(-1), respectively.	Remifentanil	61-73	L1 cell adhesion molecule	Mus musculus	117-123
17996006-1	2008	BACKGROUND: Remifentanil"s short-acting analgesic effect and the potential of producing hyperalgesia is a challenge to post-operative pain control.	Remifentanil	12-24	solute carrier family 35 member G1	Homo sapiens	119-123
18165607-0	2008	Remifentanil-induced cerebral blood flow effects in normal humans: dose and ApoE genotype.	Remifentanil	0-12	apolipoprotein E	Homo sapiens	76-80
18027597-2	2007	Therefore, the time for remifentanil concentration to reach its steady state concentration (Css) is shorter than those of other anesthetic drugs such as propofol and fentanyl.	Remifentanil	24-36	cytidine monophosphate N-acetylneuraminic acid synthetase	Homo sapiens	92-95
18027597-3	2007	The Css and the time course of plasma concentration as well as effect-site concentration (Ce) during the continuous infusion of remifentanil could be helpful in our clinical practice.	Remifentanil	128-140	cytidine monophosphate N-acetylneuraminic acid synthetase	Homo sapiens	4-7
18027597-4	2007	Css is strongly affected by weight and age with Minto"s pharmacokinetic parameters of remifentanil.	Remifentanil	86-98	cytidine monophosphate N-acetylneuraminic acid synthetase	Homo sapiens	0-3
18027597-9	2007	For example, it will take about 5 min for remifentanil effect-site concentration to decrease from Css to a half of Css.	Remifentanil	42-54	cytidine monophosphate N-acetylneuraminic acid synthetase	Homo sapiens	98-101
18027597-9	2007	For example, it will take about 5 min for remifentanil effect-site concentration to decrease from Css to a half of Css.	Remifentanil	42-54	cytidine monophosphate N-acetylneuraminic acid synthetase	Homo sapiens	115-118
18027600-6	2007	In the near future, the introduction of reliable delivery systems for remifentanil combined with propofol would provide us with a new concept in intravenous anesthesia, the DOUBLE TCI Anesthesia.	Remifentanil	70-82	latexin	Homo sapiens	180-183
18234187-0	2008	Meperidine, remifentanil and tramadol but not sufentanil interact with alpha(2)-adrenoceptors in alpha(2A)-, alpha(2B)- and alpha(2C)-adrenoceptor knock out mice brain.	Remifentanil	12-24	adrenergic receptor, alpha 2b	Mus musculus	71-93
18234187-0	2008	Meperidine, remifentanil and tramadol but not sufentanil interact with alpha(2)-adrenoceptors in alpha(2A)-, alpha(2B)- and alpha(2C)-adrenoceptor knock out mice brain.	Remifentanil	12-24	adrenergic receptor, alpha 2b	Mus musculus	109-117
18234187-8	2008	Required concentrations of meperidine and remifentanil for [(125)I]-PIC displacement from alpha(2B)- and alpha(2C)-adrenoceptors were lower than from alpha(2A)-adrenoceptors, indicating higher binding affinity for alpha(2B)- and alpha(2C)-adrenoceptors.	Remifentanil	42-54	adrenergic receptor, alpha 2b	Mus musculus	90-98
18234187-8	2008	Required concentrations of meperidine and remifentanil for [(125)I]-PIC displacement from alpha(2B)- and alpha(2C)-adrenoceptors were lower than from alpha(2A)-adrenoceptors, indicating higher binding affinity for alpha(2B)- and alpha(2C)-adrenoceptors.	Remifentanil	42-54	adrenergic receptor, alpha 2b	Mus musculus	214-222
18234187-10	2008	Our results indicate that meperidine, remifentanil and tramadol interact with alpha(2)-adrenoceptors in mouse brain showing different affinity for alpha(2A)-, alpha(2B)- and alpha(2C)-adrenoceptors.	Remifentanil	38-50	adrenergic receptor, alpha 2b	Mus musculus	78-100
18234187-10	2008	Our results indicate that meperidine, remifentanil and tramadol interact with alpha(2)-adrenoceptors in mouse brain showing different affinity for alpha(2A)-, alpha(2B)- and alpha(2C)-adrenoceptors.	Remifentanil	38-50	adrenergic receptor, alpha 2b	Mus musculus	159-167
17065897-3	2006	The aim of the investigation was to determine analgesic and antihyperalgesic properties of the cyclooxygenase-2 inhibitor parecoxib on remifentanil-induced hypersensitivity in humans.	Remifentanil	135-147	prostaglandin-endoperoxide synthase 2	Homo sapiens	95-111
27771888-11	2007	This pilot study suggests that remifentanil intravenous PCA is efficacious for labour analgesia as a bolus of 0.25 mug kg-1, with a lockout interval of two minutes and continuous infusion of 0.025-0.1 mug kg-1 min-1.	Remifentanil	31-43	CD59 molecule (CD59 blood group)	Homo sapiens	210-215
17513631-9	2007	Coadministration of remifentanil led to synergistic analgesic effects (to 62% +/- 26% and 58% +/- 25% of control, for 0.025 or 0.05 microg x kg(-1) x min(-1), respectively), but upon withdrawal, pain and hyperalgesia increased above control level.	Remifentanil	20-32	CD59 molecule (CD59 blood group)	Homo sapiens	150-156
17426069-1	2007	BACKGROUND: High-dose remifentanil (1-5 microg kg-1 min-1), commonly used for cardiac surgery, has been associated with muscle rigidity, hypotension, bradycardia, and reduced cardiac output.	Remifentanil	22-34	CD59 molecule (CD59 blood group)	Homo sapiens	52-57
17426069-11	2007	CONCLUSIONS: Remifentanil at 0.3 and 0.4 microg kg-1 min-1 in combination with a target-controlled propofol infusion in the pre-bypass period is well tolerated.	Remifentanil	13-25	CD59 molecule (CD59 blood group)	Homo sapiens	53-58
17518172-0	2007	[Stress response under continuous infusion of remifentanil compared to bolus doses of fentanyl assessed by levels of cytokines, C-reactive protein, and cortisol during and after abdominal hysterectomy].	Remifentanil	46-58	C-reactive protein	Homo sapiens	128-146
17486919-1	2007	BACKGROUND: During total intravenous anaesthesia, the target controlled infusion concentration of remifentanil can be achieved either in limiting maximum plasma concentration (Cp) to the effect site target concentration which corresponds to a plasma TCI technique (pTCI) or as fast as possible to achieve the effect-site target without limiting Cp (eTCI).	Remifentanil	98-110	latexin	Homo sapiens	250-253
17578972-0	2007	Remifentanil-induced cerebral blood flow effects in normal humans: dose and ApoE genotype.	Remifentanil	0-12	apolipoprotein E	Homo sapiens	76-80
17578972-3	2007	We tested the hypothesis that, in the absence of surgery, small doses of remifentanil produce limbic system activation in humans which varies with dose and ApoE genotype.	Remifentanil	73-85	apolipoprotein E	Homo sapiens	156-160
16553341-3	2006	All received an infusion of remifentanil at a dose of 0.5 microg x Kg(-1) x min(-1) until tracheal intubation and then 0.25 microg x Kg(-1) x min(-1) during surgery.	Remifentanil	28-40	CD59 molecule (CD59 blood group)	Homo sapiens	76-82
16884977-2	2006	This study was designed to compare postoperative troponin I (cTnI) concentrations after sevoflurane-remifentanil versus propofol-remifentanil anesthesia.	Remifentanil	100-112	troponin I3, cardiac type	Homo sapiens	61-65
16052121-6	2005	RESULTS: The average (+/- sd) remifentanil dose was 0.035 +/- 0.012 microg x kg x min(-1).	Remifentanil	30-42	CD59 molecule (CD59 blood group)	Homo sapiens	82-88
16037145-11	2005	We studied remifentanil as a sole drug for ESWL and have shown that an infusion rate of 0.05 microg x kg-1 x min-1 plus patient-controlled analgesia demands of 10 microg provides adequate analgesia and has significantly less side effects than a dose of 0.1 microg x kg-1 x min-1 plus 10 microg demands.	Remifentanil	11-23	CD59 molecule (CD59 blood group)	Homo sapiens	109-114
16199414-8	2005	An infusion of remifentanil at the rate of 0.15 microg kg(-1) min(-1) was started, sevoflurane continued at 0.6 MAC and cisatracurium 0.2 mg kg(-1) was given.	Remifentanil	15-27	CD59 molecule (CD59 blood group)	Homo sapiens	62-68
16199414-10	2005	RESULTS: Baseline HR [mean (SD)] of 117 (20) beats min(-1) decreased significantly from 12.5 min onwards after starting the remifentanil infusion in the control group [106 (18) at 12.5 min and 99 (16) beats min(-1) at 45 min].	Remifentanil	124-136	CD59 molecule (CD59 blood group)	Homo sapiens	51-57
16211731-4	2005	Remifentanil was given to all patients at a constant infusion rate of 0.3 microg kg [-1] min[-1] throughout anaesthesia.	Remifentanil	0-12	CD59 molecule (CD59 blood group)	Homo sapiens	89-95
16037145-11	2005	We studied remifentanil as a sole drug for ESWL and have shown that an infusion rate of 0.05 microg x kg-1 x min-1 plus patient-controlled analgesia demands of 10 microg provides adequate analgesia and has significantly less side effects than a dose of 0.1 microg x kg-1 x min-1 plus 10 microg demands.	Remifentanil	11-23	CD59 molecule (CD59 blood group)	Homo sapiens	273-278
16052121-11	2005	CONCLUSIONS: The computer game was a more potent stimulus than pain in countering the depressant effect of remifentanil on AHR.	Remifentanil	107-119	aryl hydrocarbon receptor	Homo sapiens	123-126
24672137-13	2005	Changes in SAP and DAP followed a similar pattern in both groups, but SAP was significantly lower in the remifentanil group compared with that in the alfentanil group throughout the study period (all, P < 0.05).	Remifentanil	105-117	SH2 domain containing 1A	Homo sapiens	70-73
24672137-14	2005	After 1 minute of intubation, DAP was significantly lower in the remifentanil group compared with that in the alfentanil group (66 [9] mm Hg vs. 73 [20] mm Hg; P < 0.05).	Remifentanil	65-77	death associated protein	Homo sapiens	30-33
15675927-9	2005	RESULTS: The median tolerated dose of remifentanil was 0.127 microg.kg(-1).min(-1) (range: 0.053-0.3 microg.kg(-1).min(-1)).	Remifentanil	38-50	CD59 molecule (CD59 blood group)	Homo sapiens	75-81
15845659-26	2005	min(-1) was reached after 4 h. The combination of remifentanil with a nonsteroidal antiinflammatory drug provided adequate analgesia in 73% of patients 30 min after tracheal extubation.	Remifentanil	50-62	CD59 molecule (CD59 blood group)	Homo sapiens	0-6
15675927-9	2005	RESULTS: The median tolerated dose of remifentanil was 0.127 microg.kg(-1).min(-1) (range: 0.053-0.3 microg.kg(-1).min(-1)).	Remifentanil	38-50	CD59 molecule (CD59 blood group)	Homo sapiens	115-121
15986842-0	2005	Case report: Use of a remifentanil infusion with the tri-service anaesthetic apparatus.	Remifentanil	22-34	tRNA-Ile (anticodon AAT) 9-1	Homo sapiens	53-56
15986842-3	2005	We chose to adopt the technique of running a remifentanil infusion with the Tri-Service apparatus in an attempt to reduce the administered volatile and thus shorten recovery times.	Remifentanil	45-57	tRNA-Ile (anticodon AAT) 9-1	Homo sapiens	76-79
15385015-4	2004	METHODS: Twenty patients were randomized to receive a titrated infusion of remifentanil (0-1 microg x kg(-1) x min(-1)) or a standard dose of fentanyl (30 microg x kg(-1)) prebypass plus morphine (1 mg x kg(-1)) on rewarming.	Remifentanil	75-87	CD59 molecule (CD59 blood group)	Homo sapiens	111-118
15492595-9	2004	Preconditioning with remifentanil modestly reduced infarct size (49.6+/-20.1% CON versus 29.3+/-8.5% RP2; p<0.01).	Remifentanil	21-33	protein XRP2	Oryctolagus cuniculus	101-104
14749874-5	2004	Induction of anaesthesia was started with a remifentanil infusion at 0.4 micro g x kg(-1) x min(-1) and 5 min later 2 mg x kg(-1) propofol was given for hypnosis.	Remifentanil	44-56	CD59 molecule (CD59 blood group)	Homo sapiens	92-98
15025597-6	2004	was administrated followed by a continuous infusion of remifentanil (0.25 microg x kg(-1) x min(-1) i.v.)	Remifentanil	55-67	CD59 molecule (CD59 blood group)	Homo sapiens	92-98
14766716-7	2004	When pressure was applied to cause increasing pain in volunteers (n=11) 0.05 microg kg-1 min-1 remifentanil increased pain tolerance by 50%.	Remifentanil	95-107	CD59 molecule (CD59 blood group)	Homo sapiens	89-94
14997083-0	2004	Peri-intubation cardiovascular response during low dose remifentanil or sufentanil administration in association with propofol TCI.	Remifentanil	56-68	transcobalamin 1	Homo sapiens	127-130
15329588-9	2004	Remifentanil mean infusion rate was 0.13 +/- 0.03 microg x kg(-1) x min(-1), whereas morphine mean infusion rate was 0.68 +/- 0.28 microg x kg(-1) x min(-1).	Remifentanil	0-12	CD59 molecule (CD59 blood group)	Homo sapiens	68-74
15044556-5	2004	administration of mu opioid receptor (MOR) agonists (fentanyl, alfentanil, remifentanil, and morphine) evoked scratching in a dose- and time-dependent manner.	Remifentanil	75-87	opioid receptor mu 1	Homo sapiens	18-36
15044556-5	2004	administration of mu opioid receptor (MOR) agonists (fentanyl, alfentanil, remifentanil, and morphine) evoked scratching in a dose- and time-dependent manner.	Remifentanil	75-87	opioid receptor mu 1	Homo sapiens	38-41
19471732-9	2004	Anesthesia was maintained with 0.4 microg.kg-1.h-1 dexmedetomidine and 0.3 microg.kg-1.min-1 remifentanil in continuous infusion, and 3 microg.mL-1 propofol in target-controlled infusion.	Remifentanil	93-105	CD59 molecule (CD59 blood group)	Homo sapiens	87-92
15108975-4	2004	While maintenance of anesthesia was ensured by a continuous infusion of etomidate, increased concentrations of remifentanil (from 0.1 to 1 microg x kg(-1) x min(-1)) were infused in steps of 5 min under hemodynamic monitoring, including left and right atrial pressures, systemic and pulmonary arterial pressures, and left and right cardiac indices.	Remifentanil	111-123	CD59 molecule (CD59 blood group)	Homo sapiens	157-163
15108975-8	2004	RESULTS: Remifentanil produced a dose-dependent and significant decrease in systemic arterial pressure and vascular resistances (n = 9) from a concentration of 0.25 microg x kg(-1) x min(-1).	Remifentanil	9-21	CD59 molecule (CD59 blood group)	Homo sapiens	183-189
14674975-7	2004	RESULTS: Remifentanil decreases significantly the ventricular elastance (from 6.09 mmHg ml-1 m(-2) to 4.88) (P < 0.05), with a less, but however, significant decrease of arterial elastance (from 3.68 mmHg ml(-1) m(-2) to 3.13) (P < 0.05).	Remifentanil	9-21	interleukin 17F	Homo sapiens	88-92
12818956-0	2003	ARX-derived auditory evoked potential index and bispectral index during the induction of anesthesia with propofol and remifentanil.	Remifentanil	118-130	aristaless related homeobox	Homo sapiens	0-3
14508314-6	2003	Remifentanil infusion at 2 and 4 microg x kg-1 x min-1 significantly decreased rCBF and mean CBFv.	Remifentanil	0-12	CD59 molecule (CD59 blood group)	Homo sapiens	49-54
14508314-9	2003	100 g-1 x min-1 x mmHg-1 for 2 and 4 microg x kg-1 x min-1 remifentanil, respectively (relative change in percent/mmHg: 1.9 +/- 0.8 and 1.6 +/- 0.5, respectively).	Remifentanil	59-71	CD59 molecule (CD59 blood group)	Homo sapiens	10-58
14508314-10	2003	The average slopes for mean CBFv reactivity were 1.61 +/- 0.95 and 1.54 +/- 0.83 cm x s-1 x mmHg-1 for 2 and 4 microg x kg-1 x min-1 remifentanil, respectively (relative change in percent/mmHg: 1.86 +/- 0.59 and 1.79 +/- 0.59, respectively).	Remifentanil	133-145	CD59 molecule (CD59 blood group)	Homo sapiens	127-132
12950860-8	2003	Infusion of remifentanil started with a dose of 0.75-1 microg x kg-1x min-1, 1 h before surgery.	Remifentanil	12-24	CD59 molecule (CD59 blood group)	Homo sapiens	70-75
12477685-6	2002	CONCLUSIONS: Low doses of remifentanil (up to 0.05 microg x kg(-1) x min(-1)) can be useful in critically-ill patients in order to achieve calm and sedation.	Remifentanil	26-38	CD59 molecule (CD59 blood group)	Homo sapiens	69-75
12792580-8	2003	CONCLUSIONS: Remifentanil analgesia (mean dose of 0.37 microg.kg(-1).min-1) in patients undergoing endonasal endoscopic surgery of the sellar region provides a more efficacious cardiocirculatory control with reduced bleeding and faster psychosensorial recovery.	Remifentanil	13-25	CD59 molecule (CD59 blood group)	Homo sapiens	69-74
12756965-4	2003	For intubation the RF dosage was 0.26 +/- 0.06 microgram.kg-1.min-1 and the target concentration of P was 3.16 +/- 0.63 micrograms.ml-1.	Remifentanil	19-21	CD59 molecule (CD59 blood group)	Homo sapiens	62-67
12477685-2	2002	METHODS: Remifentanil infusion was started at 0.02 microg x kg(-1) x min(-1) in ten mechanically ventilated critically-ill patients, and the infusion rate was increased to 0.05, 0.10, 0.15, 0.20, and 0.25 microg x kg(-1) x min(-1) every 30 min.	Remifentanil	9-21	CD59 molecule (CD59 blood group)	Homo sapiens	69-75
15321493-7	2003	The median rate of infusion of remifentanil was 0.056 microg.kg(-1) min(-1) [10th-90th centiles: 0.037-0.15 ng.mL(-1)].	Remifentanil	31-43	CD59 molecule (CD59 blood group)	Homo sapiens	68-74
12625310-1	2003	In a randomised, double-blind study we compared the efficacy of continuous remifentanil infusion (0.25 microg x kg(-1) x min(-1) with 40 mg lidocaine and placebo in the prevention of injection pain due to intravenous propofol administration (1.5-2 mg x kg(-1)) in 155 patients scheduled for elective surgery.	Remifentanil	75-87	CD59 molecule (CD59 blood group)	Homo sapiens	121-127
12401616-0	2002	In vitro remifentanil metabolism: the effects of whole blood constituents and plasma butyrylcholinesterase.	Remifentanil	9-21	butyrylcholinesterase	Homo sapiens	85-106
12401616-1	2002	UNLABELLED: We designed this in vitro study to determine whether the half-life of remifentanil was altered in butyrylcholinesterase-deficient patients.	Remifentanil	82-94	butyrylcholinesterase	Homo sapiens	110-131
12401616-7	2002	IMPLICATIONS: This was a test-tube-designed study to determine whether an enzyme deficiency (butyrylcholinesterase deficiency) changes the way remifentanil is metabolized.	Remifentanil	143-155	butyrylcholinesterase	Homo sapiens	93-114
12413255-1	2002	After institutional approval and with written informed consent, eight surgical patients were infused intravenously with remifentanil at 250 ngkg lean body mass (LBM)(-1) x min(-1) for 30 min.	Remifentanil	120-132	CD59 molecule (CD59 blood group)	Homo sapiens	172-178
12455322-1	2002	We describe the cases of 3 patients who received anesthesia with remifentanil continuously infused at rates of 0.8 to 1.25 micrograms.kg-1.min-1 for at least 3 hours.	Remifentanil	65-77	CD59 molecule (CD59 blood group)	Homo sapiens	139-144
12377178-4	2002	Remifentanil increased rCBF above all in basal ganglia, whereas in supratentorial gray matter the increase in rCBF was equal or even more pronounced when using nitrous oxide.	Remifentanil	0-12	CCAAT/enhancer binding protein zeta	Rattus norvegicus	23-27
12455322-2	2002	Upon emergence from anesthesia, after withdrawal of the anesthetic gas, satisfactory levels of consciousness, spontaneous breathing and absence of pain were achieved under maintenance doses of remifentanil greater than 0.8 microgram.kg-1.min-1; such doses are related to the development of ventilatory depression, apnea and significant sedation.	Remifentanil	193-205	CD59 molecule (CD59 blood group)	Homo sapiens	238-243
12200947-11	2002	This was reduced to 1.55 micrograms mL-1 during co-induction with remifentanil and further reduced to 0.64 microgram mL-1 with midazolam premedication (P < 0.001; ANOVA).	Remifentanil	66-78	L1 cell adhesion molecule	Mus musculus	36-40
12370680-6	2002	The recovery profile was shorter in the remifentanil group the drug being rapidly metabolised by plasma cholinesterase.	Remifentanil	40-52	butyrylcholinesterase	Homo sapiens	104-118
11927475-2	2002	METHODS: Remifentanil was infused for 20 min at a rate of 0.1 microg x kg(-1) x min(-1).	Remifentanil	9-21	CD59 molecule (CD59 blood group)	Homo sapiens	80-86
11873028-8	2002	RESULTS: Determined from SEF, remifentanil had no effect on t(1/2)k(e0) (1.91 +/- 0.26 min [mean +/- standard error]) but caused an increase in C(50) (baseline = 1.48 +/- 0.12%; 80% increase at 8 ng/ml) and decrease in E(MIN) (baseline = 10.8 +/- 0.6 Hz; 80% reduction at 8 ng/ml).	Remifentanil	30-42	interleukin 17 receptor D	Homo sapiens	25-28
11553256-12	2001	Significantly fewer patients responded to tracheal intubation with remifentanil at 0.4 microg kg(-1) min(-1), supporting the use of a higher initial infusion rate before intubation.	Remifentanil	67-79	CD59 molecule (CD59 blood group)	Homo sapiens	101-107
11573525-7	2001	The median dose of remifentanil for maintenance of adequate anaesthesia (excluding the initial bolus dose) in the four groups was 0.21, 0.15, 0.11 and 0.13 microg kg(-1) min(-1) respectively (P=0.0026).	Remifentanil	19-31	CD59 molecule (CD59 blood group)	Homo sapiens	170-176
11388521-1	2001	BACKGROUND: The current study investigated dose-dependent effects of the mu-selective agonist remifentanil on regional cerebral blood flow (rCBF) in volunteers using positron emission tomography (PET).	Remifentanil	94-106	CCAAT/enhancer binding protein zeta	Rattus norvegicus	140-144
11388521-10	2001	At the low remifentanil dose, significant increases in relative rCBF were noted in the lateral prefrontal cortices, inferior parietal cortices, and supplementary motor area.	Remifentanil	11-23	CCAAT/enhancer binding protein zeta	Rattus norvegicus	64-68
11388521-14	2001	These dose-dependent effects of remifentanil on rCBF were confirmed by a correlation analysis.	Remifentanil	32-44	CCAAT/enhancer binding protein zeta	Rattus norvegicus	48-52
11388521-15	2001	CONCLUSION: Remifentanil induced dose-dependent changes in relative rCBF in areas involved in pain processing.	Remifentanil	12-24	CCAAT/enhancer binding protein zeta	Rattus norvegicus	68-72
11359587-6	2001	Adverse respiratory events (RR < 10.min-1 or SpO2 < 90%) occurred significantly more in the propofol/remifentanil group.	Remifentanil	107-119	CD59 molecule (CD59 blood group)	Homo sapiens	39-44
11065203-6	2000	RESULTS: Concentrations of remifentanil (50 ng/mL) similar to the relevant plasma concentration were able to inhibit PMNL migration through ECM significantly (migration compared to the control 82+/-7% SD; P<0.05), when both cell types were treated with the synthetic narcotic remifentanil.	Remifentanil	27-39	multimerin 1	Homo sapiens	140-143
11167470-4	2001	The median dosage of remifentanil required in the last three groups was 0.21, 0.25 and 0.34 microg x kg(-1) x min(-1), respectively (p < 0.05).	Remifentanil	21-33	CD59 molecule (CD59 blood group)	Homo sapiens	110-116
11135717-8	2001	Before and during the second rekindling, remifentanil 0.10 microg x kg(-1) x min(-1) or saline-placebo was infused for 35 min.	Remifentanil	41-53	CD59 molecule (CD59 blood group)	Homo sapiens	77-83
11575417-7	2001	Maximum increases in mean SAP after laryngoscopy and intubation were 35 and 41 mm Hg in the remifentanil and alfentanil groups, respectively.	Remifentanil	92-104	SH2 domain containing 1A	Homo sapiens	26-29
11065203-9	2000	CONCLUSION: The results of the present investigation indicate that remifentanil influences interaction of ECM against human neutrophils.	Remifentanil	67-79	multimerin 1	Homo sapiens	106-109
10926352-1	2000	Remifentanil (4-methoxycarbonyl-4-[(1-oxopropyl)phenylamino]-1-piperidinepropionic acid methyl ester) is a mu-opioid receptor agonist with considerable abuse potential in racing horses.	Remifentanil	0-12	mu-opioid receptor	Equus caballus	107-125
10992824-2	2000	Remifentanil increased rCBF and rCBV in white and grey matter (striatal, thalamic, occipital, parietal, frontal) regions, with a parallel decrease in rMTT in those regions with the exception of occipital grey matter.	Remifentanil	0-12	CCAAT/enhancer binding protein zeta	Rattus norvegicus	23-27
11213546-12	2000	RESULTS: Significant increases in PAS were recorded, at intubation and at 1 min after in patients treated with fentanyl; in the remifentanil group significant decreases in SAP at induction and at 4 min after intubation were recorded.	Remifentanil	128-140	SH2 domain containing 1A	Homo sapiens	172-175
10947750-2	2000	We compared the efficacy and safety of a remifentanil (0.25 microg x kg(-1) x min(-1)-based balanced anaesthetic technique with a bupivacaine-based regional anaesthetic technique in an open label, multicentre study in 271 ASA physical status 1 or 2 children aged 1-12 years.	Remifentanil	41-53	CD59 molecule (CD59 blood group)	Homo sapiens	78-84
10910490-11	2000	min-1 in the remifentanil group, which was significantly greater than in the desflurane group.	Remifentanil	13-25	CD59 molecule (CD59 blood group)	Homo sapiens	0-5
10740557-3	2000	followed by a bolus dose of remifentanil 1 microgram kg-1 over 30 s and an infusion of remifentanil at a rate of 0.5 microgram kg-1 min-1.	Remifentanil	87-99	CD59 molecule (CD59 blood group)	Homo sapiens	132-137
10831203-5	2000	Remifentanil was infused at 0.05 to 0.1 microg x kg(-1) x min(-1) with good sedation and analgesia for the placement of invasive monitors.	Remifentanil	0-12	CD59 molecule (CD59 blood group)	Homo sapiens	58-64
10965729-4	2000	"Slipping 8 channels patterns" were observed without spindless and K complexes; only in 2 patients N2O 50% can be used for increasing the depth of narcosys; ACTH levels increases only after remifentanil infusion stop.	Remifentanil	190-202	proopiomelanocortin	Homo sapiens	157-161
11194382-6	2000	The short-acting opioids alfentanil and remifentanil provide small volumes of distribution at steady state, a short blood-brain equilibration time and decreased t1/2 beta.	Remifentanil	40-52	interleukin 1 receptor like 1	Homo sapiens	161-170
10553851-14	1999	In conclusion, the recommended remifentanil infusion rate for controlling acute autonomic responses during neurosurgical anesthesia is 0.125 microg x kg(-1) x min(-1) when administered during a desflurane-based anesthetic.	Remifentanil	31-43	CD59 molecule (CD59 blood group)	Homo sapiens	159-165
10540089-6	1999	In these patients the median remifentanil target concentration was 1.6 ng x ml-1 and was achieved with a median infusion rate of 0.05 microg x kg-1 x min-1.	Remifentanil	29-41	CD59 molecule (CD59 blood group)	Homo sapiens	150-155
10549459-5	1999	During the maintenance fentanyl was delivered at 6.1 +/- 4.6 micrograms kg-1 h-1 and remifentanil at 0.15 +/- 0.07 microgram kg-1 min-1.	Remifentanil	85-97	CD59 molecule (CD59 blood group)	Homo sapiens	130-135
9286886-10	1997	The median remifentanil rate for successful analgesia was 0.125 microg x kg(-1) x min(-1) (range, 0.05-0.23 microg x kg(-1) x min(-1)), and the median number of 2-mg morphine boluses used was 2 (range, 0-5 boluses).	Remifentanil	11-23	CD59 molecule (CD59 blood group)	Homo sapiens	82-88
10389781-5	1999	The remifentanil group received remifentanil 0.2 microg x kg(-1) x min(-1) and enough desflurane to prevent movement, typically 3.2%-3.6%.	Remifentanil	4-16	CD59 molecule (CD59 blood group)	Homo sapiens	67-73
9637638-3	1998	METHODS: Nineteen parturients underwent nonemergent cesarean section with epidural anesthesia and received 0.1 microg kg(-1) x min(-1) remifentanil intravenously, which was continued until skin closure.	Remifentanil	135-147	CD59 molecule (CD59 blood group)	Homo sapiens	127-133
9640160-2	1998	Remifentanil was administered as a loading dose of 0.125, 0.25, 0.375 or 0.5 microgram kg-1 and at a maintenance infusion rate of 0.025, 0.05, 0.075 or 0.1 microgram kg-1 min-1, respectively, with an infusion of propofol 6 mg kg-1 h-1.	Remifentanil	0-12	CD59 molecule (CD59 blood group)	Homo sapiens	171-176
9640160-3	1998	Responses occurred in 88% of patients with remifentanil 0.025 microgram kg-1 min-1 compared with 30-40% in the other groups.	Remifentanil	43-55	CD59 molecule (CD59 blood group)	Homo sapiens	77-82
9640160-6	1998	Reductions in remifentanil doses to 0.025-0.05 microgram kg-1 min-1 resulted in adequate respiration at the end of surgery in 88% of patients.	Remifentanil	14-26	CD59 molecule (CD59 blood group)	Homo sapiens	62-67
10391607-4	1999	Remifentanil infusion, 0.2-1.0 microg x kg(-1) x min(-1), was used from induction to emergence of general anesthesia.	Remifentanil	0-12	CD59 molecule (CD59 blood group)	Homo sapiens	49-55
10201679-6	1999	ACh in the mPRF also was measured during either dialysis delivery or intravenous infusion of remifentanil and during dialysis delivery of fentanyl.	Remifentanil	93-105	Spi-C transcription factor (Spi-1/PU.1 related)	Mus musculus	11-15
9895070-12	1999	We conclude that TIVA/TCI anesthesia using propofol/remifentanil was associated with the highest intraoperative costs but the fewest postoperative side effects.	Remifentanil	52-64	transcobalamin 1	Homo sapiens	22-25
9895080-2	1999	They were randomized to receive one of the following initial dose regimens in double-blinded fashion: placebo or 0.04, 0.07, or 0.1 microg x kg(-1) x min(-1) remifentanil subsequently titrated to effect.	Remifentanil	158-170	CD59 molecule (CD59 blood group)	Homo sapiens	150-156
9895080-5	1999	The remifentanil 50% effective dose for a composite sedation level > or =2 within 15 min of the start of drug infusion was estimated as 0.043 microg x kg(-1) x min(-1) (95% confidence interval 0.01, 0.059).	Remifentanil	4-16	CD59 molecule (CD59 blood group)	Homo sapiens	163-169
10211013-2	1998	A single bolus infusion of remifentanil 10 micrograms kg-1 min-1 was given at the beginning of the dissection and anhepatic phases of OLT.	Remifentanil	27-39	CD59 molecule (CD59 blood group)	Homo sapiens	59-64
10211013-4	1998	Mean arterial clearance of remifentanil was significantly greater (P = 0.02) in the dissection phase (79.54 ml min-1 kg-1) than in the anhepatic phase (39.57 ml min-1 kg-1).	Remifentanil	27-39	CD59 molecule (CD59 blood group)	Homo sapiens	111-121
10211013-4	1998	Mean arterial clearance of remifentanil was significantly greater (P = 0.02) in the dissection phase (79.54 ml min-1 kg-1) than in the anhepatic phase (39.57 ml min-1 kg-1).	Remifentanil	27-39	CD59 molecule (CD59 blood group)	Homo sapiens	111-116
9778004-11	1998	Remifentanil pharmacokinetics were best described by a two-compartment model with lean body mass as a significant covariate, where V1 = 0.129(lean body mass-50) + 3.79 l, V2 = 6.87 l, CL1 = 0.0389(lean body mass-50) + 2.34 l/min and CL2 = 1.14 l/min.	Remifentanil	0-12	adhesion G protein-coupled receptor L1	Homo sapiens	184-187
9778004-11	1998	Remifentanil pharmacokinetics were best described by a two-compartment model with lean body mass as a significant covariate, where V1 = 0.129(lean body mass-50) + 3.79 l, V2 = 6.87 l, CL1 = 0.0389(lean body mass-50) + 2.34 l/min and CL2 = 1.14 l/min.	Remifentanil	0-12	endogenous retrovirus group W member 5	Homo sapiens	233-236
9847642-15	1998	The simulated constant infusion rate for remifentanil of 15 micrograms.min1 (8 micrograms.min-1 for fentanyl and 75 micrograms.min-1 for alfentanil) allowed the therapeutic threshold to be reached in 10 min with remifentanil, in 22 min with fentanyl and in 17 min with alfentanil.	Remifentanil	41-53	CD59 molecule (CD59 blood group)	Homo sapiens	90-95
9847642-15	1998	The simulated constant infusion rate for remifentanil of 15 micrograms.min1 (8 micrograms.min-1 for fentanyl and 75 micrograms.min-1 for alfentanil) allowed the therapeutic threshold to be reached in 10 min with remifentanil, in 22 min with fentanyl and in 17 min with alfentanil.	Remifentanil	41-53	CD59 molecule (CD59 blood group)	Homo sapiens	127-132
9847642-15	1998	The simulated constant infusion rate for remifentanil of 15 micrograms.min1 (8 micrograms.min-1 for fentanyl and 75 micrograms.min-1 for alfentanil) allowed the therapeutic threshold to be reached in 10 min with remifentanil, in 22 min with fentanyl and in 17 min with alfentanil.	Remifentanil	212-224	CD59 molecule (CD59 blood group)	Homo sapiens	90-95
9286886-14	1997	CONCLUSIONS: Remifentanil provided safe and effective postoperative analgesia when administered at a final rate of 0.05-0.23 microg x kg(-1) x min(-1) in the immediate postextubation period.	Remifentanil	13-25	CD59 molecule (CD59 blood group)	Homo sapiens	143-149
9060019-12	1997	In laminae I-II of the L4-L5 segment, the magnitude of the decrease in Fos expression was comparable for remifentanil (26.5%) and lidocaine (27.3%); the decrease was greater when both remifentanil and lidocaine were administered (50.5%), and even greater when bupivicaine and lidocaine were used (74.2%).	Remifentanil	105-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
9085949-3	1997	After surgery, remifentanil was infused at 1.0 microg x kg(-1) x min(-1) in all patients.	Remifentanil	15-27	CD59 molecule (CD59 blood group)	Homo sapiens	65-71
9253564-5	1997	A remifentanil post-operative infusion initiated during emergence was titrated in the recovery room for 30 min, at which time 14% of patients had a pain score of 2 and 86% had pain scores of 0 or 1 (0 = no pain; 1 = mild pain; 2 = moderate pain; 3 = severe pain), at a mean infusion rate of 0.086 microgram kg-1 min-1.	Remifentanil	2-14	CD59 molecule (CD59 blood group)	Homo sapiens	312-317
9135180-14	1997	An initial remifentanil infusion rate of 0.1 microgram.kg-1.min-1 titrated to individual need provided postoperative pain relief in the presence of adequate respiration in 71% of patients.	Remifentanil	11-23	CD59 molecule (CD59 blood group)	Homo sapiens	60-65
9135180-18	1997	Remifentanil can be administered as a postoperative analgesic agent at a starting dose of 0.1 microgram-.kg-1.min-1; however, it should only be used in the presence of adequate supervision and monitoring of the patient.	Remifentanil	0-12	CD59 molecule (CD59 blood group)	Homo sapiens	110-115
9060019-12	1997	In laminae I-II of the L4-L5 segment, the magnitude of the decrease in Fos expression was comparable for remifentanil (26.5%) and lidocaine (27.3%); the decrease was greater when both remifentanil and lidocaine were administered (50.5%), and even greater when bupivicaine and lidocaine were used (74.2%).	Remifentanil	184-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
9060019-13	1997	In laminae V-VI, remifentanil, by itself, decreased c-fos expression by 39.4%; for lidocaine alone, the decrease was 58.4%.	Remifentanil	17-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
33779892-4	2021	Remifentanil anesthesia reduced the paw withdrawal threshold from 2 h to 48 h postoperatively, with a decrease in the expression of TMEM16C and Slack in the dorsal root ganglia (DRG) and spinal cord.	Remifentanil	0-12	anoctamin 3	Rattus norvegicus	132-139
8105723-11	1993	The t1/2 ke0 (half-time for equilibration between plasma and the effect compartment) of remifentanil for analgesia was calculated as 1.3 min.	Remifentanil	88-100	interleukin 1 receptor like 1	Homo sapiens	4-12
33779892-0	2021	A Role for Transmembrane Protein 16C/Slack Impairment in Excitatory Nociceptive Synaptic Plasticity in the Pathogenesis of Remifentanil-induced Hyperalgesia in Rats.	Remifentanil	123-135	anoctamin 3	Rattus norvegicus	11-36
33779892-0	2021	A Role for Transmembrane Protein 16C/Slack Impairment in Excitatory Nociceptive Synaptic Plasticity in the Pathogenesis of Remifentanil-induced Hyperalgesia in Rats.	Remifentanil	123-135	potassium sodium-activated channel subfamily T member 1	Rattus norvegicus	37-42
33779892-3	2021	In this study, we investigated whether the impairment of transmembrane protein 16C (TMEM16C)/Slack is required for alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptor (AMPAR) activation in remifentanil-induced postoperative hyperalgesia.	Remifentanil	198-210	anoctamin 3	Rattus norvegicus	57-82
33779892-3	2021	In this study, we investigated whether the impairment of transmembrane protein 16C (TMEM16C)/Slack is required for alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptor (AMPAR) activation in remifentanil-induced postoperative hyperalgesia.	Remifentanil	198-210	anoctamin 3	Rattus norvegicus	84-91
8694306-14	1996	After tracheal intubation, remifentanil 0.25-4.0 micrograms.kg-1.min-1 effectively controlled intraoperative responses while allowing for rapid emergence from anesthesia.	Remifentanil	27-39	CD59 molecule (CD59 blood group)	Homo sapiens	65-70
8638836-9	1996	The NONMEM analysis population pharmacokinetic parameters for remifentanil include a CLc of 2.9 l x min(-1), a VDss of 21.81, and a terminal half-life of 35.1 min.	Remifentanil	62-74	CD59 molecule (CD59 blood group)	Homo sapiens	100-106
33779892-4	2021	Remifentanil anesthesia reduced the paw withdrawal threshold from 2 h to 48 h postoperatively, with a decrease in the expression of TMEM16C and Slack in the dorsal root ganglia (DRG) and spinal cord.	Remifentanil	0-12	potassium sodium-activated channel subfamily T member 1	Rattus norvegicus	144-149
33779892-6	2021	Overexpression of TMEM16C in the DRG impaired remifentanil-induced ERK1/2 phosphorylation and behavioral hyperalgesia.	Remifentanil	46-58	anoctamin 3	Rattus norvegicus	18-25
33779892-6	2021	Overexpression of TMEM16C in the DRG impaired remifentanil-induced ERK1/2 phosphorylation and behavioral hyperalgesia.	Remifentanil	46-58	mitogen activated protein kinase 3	Rattus norvegicus	67-73
33779892-8	2021	Taken together, these findings suggest that TMEM16C/Slack regulation of excitatory synaptic plasticity via GluA1-containing AMPARs is critical in the pathogenesis of remifentanil-induced postoperative hyperalgesia in rats.	Remifentanil	166-178	anoctamin 3	Rattus norvegicus	44-51
33779892-8	2021	Taken together, these findings suggest that TMEM16C/Slack regulation of excitatory synaptic plasticity via GluA1-containing AMPARs is critical in the pathogenesis of remifentanil-induced postoperative hyperalgesia in rats.	Remifentanil	166-178	potassium sodium-activated channel subfamily T member 1	Rattus norvegicus	52-57
33779892-8	2021	Taken together, these findings suggest that TMEM16C/Slack regulation of excitatory synaptic plasticity via GluA1-containing AMPARs is critical in the pathogenesis of remifentanil-induced postoperative hyperalgesia in rats.	Remifentanil	166-178	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	107-112
33779892-8	2021	Taken together, these findings suggest that TMEM16C/Slack regulation of excitatory synaptic plasticity via GluA1-containing AMPARs is critical in the pathogenesis of remifentanil-induced postoperative hyperalgesia in rats.	Remifentanil	166-178	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	124-130
34901039-9	2021	The receipt of remifentanil, propofol, Dex, and recovery time was significantly reduced in the RD2 group (P < 0.05).	Remifentanil	15-27	peripherin 2	Homo sapiens	95-98
34612779-0	2021	Remifentanil pretreatment ameliorates H/R-induced cardiac microvascular endothelial cell dysfunction by regulating the PI3K/Akt/HIF-1alpha signaling pathway.	Remifentanil	0-12	AKT serine/threonine kinase 1	Homo sapiens	124-127
34612779-0	2021	Remifentanil pretreatment ameliorates H/R-induced cardiac microvascular endothelial cell dysfunction by regulating the PI3K/Akt/HIF-1alpha signaling pathway.	Remifentanil	0-12	hypoxia inducible factor 1 subunit alpha	Homo sapiens	128-138
34166321-0	2021	P2Y1 Purinergic Receptor Contributes to Remifentanil-Induced Cold Hyperalgesia via Transient Receptor Potential Melastatin 8-Dependent Regulation of N-methyl-d-aspartate Receptor Phosphorylation in Dorsal Root Ganglion.	Remifentanil	40-52	transient receptor potential cation channel, subfamily M, member 8	Rattus norvegicus	83-124
34101715-11	2021	The Apgar score at 1 min in the remifentanil group was lower than that in the dexmedetomidine group for both quantitative (weighted mean difference (WMD): 0.75; 95% CI, 0.44 to 1.07; tau2 = 0.00) and categorical outcomes (>=Apgar 7 vs. <Apgar 7) (risk ratio: 0.76; 95% CI, 0.59 to 0.99; tau2 = 0.01).	Remifentanil	32-44	microtubule associated protein tau	Homo sapiens	183-186
34101715-11	2021	The Apgar score at 1 min in the remifentanil group was lower than that in the dexmedetomidine group for both quantitative (weighted mean difference (WMD): 0.75; 95% CI, 0.44 to 1.07; tau2 = 0.00) and categorical outcomes (>=Apgar 7 vs. <Apgar 7) (risk ratio: 0.76; 95% CI, 0.59 to 0.99; tau2 = 0.01).	Remifentanil	32-44	microtubule associated protein tau	Homo sapiens	287-290
34732147-6	2021	Subsequently, the effects of fentanyl, sufentanil and remifentanil on Cx43 channel function and U937-HUVEC adhesion were explored.	Remifentanil	54-66	gap junction protein alpha 1	Homo sapiens	70-74
34166321-12	2021	NMDAR activation abolished inhibition of TRPM8 and P2Y1R antagonists on remifentanil-induced cold hyperalgesia.	Remifentanil	72-84	transient receptor potential cation channel, subfamily M, member 8	Rattus norvegicus	41-46
34166321-13	2021	P2Y1R antagonist inhibited remifentanil-evoked elevations in TRPM8 expression and membrane trafficking and P2Y1R-TRPM8 coexpression (remifentanil + 2"-deoxy-N6-methyl adenosine 3",5"-diphosphate (MRS2179) versus remifentanil + saline, coexpression, 8.33% +- 1.33% vs 22.19% +- 2.15%, P < .0001).	Remifentanil	27-39	transient receptor potential cation channel, subfamily M, member 8	Rattus norvegicus	61-66
34166321-13	2021	P2Y1R antagonist inhibited remifentanil-evoked elevations in TRPM8 expression and membrane trafficking and P2Y1R-TRPM8 coexpression (remifentanil + 2"-deoxy-N6-methyl adenosine 3",5"-diphosphate (MRS2179) versus remifentanil + saline, coexpression, 8.33% +- 1.33% vs 22.19% +- 2.15%, P < .0001).	Remifentanil	133-145	transient receptor potential cation channel, subfamily M, member 8	Rattus norvegicus	113-118
34166321-14	2021	CONCLUSIONS: Attenuation of remifentanil-induced cold hyperalgesia by P2Y1R inhibition is attributed to downregulations in NMDAR expression and phosphorylation via diminishing TRPM8 expression and membrane trafficking in DRG.	Remifentanil	28-40	transient receptor potential cation channel, subfamily M, member 8	Rattus norvegicus	176-181
35485905-0	2022	Remifentanil pretreatment attenuates brain nerve injury in response to cardiopulmonary bypass by blocking AKT/NRF2 signal pathway.	Remifentanil	0-12	AKT serine/threonine kinase 1	Rattus norvegicus	106-109
34486703-11	2021	CONCLUSIONS: Although RF does not exert direct pro-inflammatory actions on human adult microglia, its effects on BDNF, a crucial mediator of pain transmission, suggest a possible role on neuroinflammation and pain perception.	Remifentanil	22-24	brain derived neurotrophic factor	Homo sapiens	113-117
34567901-3	2021	Aims To investigate the association between intraoperative remifentanil dosage and postoperative opioid consumption in AIS in the setting of combined epidural analgesia for postoperative multimodal analgesia.	Remifentanil	59-71	IS1	Homo sapiens	119-122
34078833-0	2021	Remifentanil protects against myocardial ischemia/reperfusion injury via miR-205-mediated regulation of PINK1.	Remifentanil	0-12	microRNA 205	Rattus norvegicus	73-80
34078833-0	2021	Remifentanil protects against myocardial ischemia/reperfusion injury via miR-205-mediated regulation of PINK1.	Remifentanil	0-12	PTEN induced kinase 1	Rattus norvegicus	104-109
34078833-6	2021	The results demonstrated that cell viability of hypoxia/reoxygenation-induced cardiomyocytes was increased post remifentanil, while the apoptosis was decreased accompanied with reduced cleaved caspase-3 expression.	Remifentanil	112-124	caspase 3	Rattus norvegicus	193-202
34078833-8	2021	However, preconditioning with remifentanil reduced miR-205 and enhanced PINK1.	Remifentanil	30-42	microRNA 205	Rattus norvegicus	51-58
34078833-8	2021	However, preconditioning with remifentanil reduced miR-205 and enhanced PINK1.	Remifentanil	30-42	PTEN induced kinase 1	Rattus norvegicus	72-77
34078833-9	2021	Moreover, over-expression of miR-205 decreased PINK1 expression and counteracted the effects of remifentanil-induced increase of cell viability and decrease of cell apoptosis in hypoxia/reoxygenation-induced cardiomyocytes.	Remifentanil	96-108	microRNA 205	Rattus norvegicus	29-36
34078833-9	2021	Moreover, over-expression of miR-205 decreased PINK1 expression and counteracted the effects of remifentanil-induced increase of cell viability and decrease of cell apoptosis in hypoxia/reoxygenation-induced cardiomyocytes.	Remifentanil	96-108	PTEN induced kinase 1	Rattus norvegicus	47-52
34078833-10	2021	Injection with miR-205 antagomir improved remifentanil-induced decrease of infarct size and LDH (lactic acid dehydrogenase) activity in rat model with I/R injury.	Remifentanil	42-54	microRNA 205	Rattus norvegicus	15-22
34078833-11	2021	In conclusion, miR-205 might participate in the protective effect of remifentanil in rat myocardial I/R injury via regulation of PINK1, providing a potential target for amelioration of cardiovascular ischemic disease.	Remifentanil	69-81	microRNA 205	Rattus norvegicus	15-22
34078833-11	2021	In conclusion, miR-205 might participate in the protective effect of remifentanil in rat myocardial I/R injury via regulation of PINK1, providing a potential target for amelioration of cardiovascular ischemic disease.	Remifentanil	69-81	PTEN induced kinase 1	Rattus norvegicus	129-134
35349908-2	2022	The objective of this work is to design a PID-based control system for the regulation of the depth of hypnosis by propofol and remifentanil coadministration that takes into account the clinical practice.	Remifentanil	127-139	metastasis associated 1 family member 2	Homo sapiens	42-45
35485905-0	2022	Remifentanil pretreatment attenuates brain nerve injury in response to cardiopulmonary bypass by blocking AKT/NRF2 signal pathway.	Remifentanil	0-12	NFE2 like bZIP transcription factor 2	Rattus norvegicus	110-114
35485905-8	2022	The preconditioning of remifentanil or DEX partially attenuated CPB-induced injury and -decreased expressions on p-AKT and HO-1, while further promoting CPB-induced expression of nuclear Nrf2 expression and inhibiting that of cytoplasm Nrf2.	Remifentanil	23-35	AKT serine/threonine kinase 1	Rattus norvegicus	115-118
35485905-8	2022	The preconditioning of remifentanil or DEX partially attenuated CPB-induced injury and -decreased expressions on p-AKT and HO-1, while further promoting CPB-induced expression of nuclear Nrf2 expression and inhibiting that of cytoplasm Nrf2.	Remifentanil	23-35	heme oxygenase 1	Rattus norvegicus	123-127
35485905-8	2022	The preconditioning of remifentanil or DEX partially attenuated CPB-induced injury and -decreased expressions on p-AKT and HO-1, while further promoting CPB-induced expression of nuclear Nrf2 expression and inhibiting that of cytoplasm Nrf2.	Remifentanil	23-35	NFE2 like bZIP transcription factor 2	Rattus norvegicus	187-191
35485905-8	2022	The preconditioning of remifentanil or DEX partially attenuated CPB-induced injury and -decreased expressions on p-AKT and HO-1, while further promoting CPB-induced expression of nuclear Nrf2 expression and inhibiting that of cytoplasm Nrf2.	Remifentanil	23-35	NFE2 like bZIP transcription factor 2	Rattus norvegicus	236-240
35244055-0	2022	Desflurane and remifentanil anesthesia in a child with citrin deficiency: A case report.	Remifentanil	15-27	solute carrier family 25 member 13	Homo sapiens	55-61
35156240-0	2022	Remifentanil reduces the proliferation, migration and invasion of HCC cells via lncRNA NBR2/miR-650/TIMP3 axis.	Remifentanil	0-12	neighbor of BRCA1 lncRNA 2	Homo sapiens	87-91
35156240-0	2022	Remifentanil reduces the proliferation, migration and invasion of HCC cells via lncRNA NBR2/miR-650/TIMP3 axis.	Remifentanil	0-12	microRNA 650	Homo sapiens	92-99
35156240-0	2022	Remifentanil reduces the proliferation, migration and invasion of HCC cells via lncRNA NBR2/miR-650/TIMP3 axis.	Remifentanil	0-12	TIMP metallopeptidase inhibitor 3	Homo sapiens	100-105
35156240-9	2022	Remifentanil treatment significantly increased the expression of lncRNA NBR2 and TIMP3, and repressed miR-650 expression in HCC cells.	Remifentanil	0-12	neighbor of BRCA1 lncRNA 2	Homo sapiens	72-76
35156240-9	2022	Remifentanil treatment significantly increased the expression of lncRNA NBR2 and TIMP3, and repressed miR-650 expression in HCC cells.	Remifentanil	0-12	TIMP metallopeptidase inhibitor 3	Homo sapiens	81-86
35156240-9	2022	Remifentanil treatment significantly increased the expression of lncRNA NBR2 and TIMP3, and repressed miR-650 expression in HCC cells.	Remifentanil	0-12	microRNA 650	Homo sapiens	102-109
35156240-10	2022	Decreased lncRNA NBR2 or increased miR-650 promoted the proliferation, migration and invasion of remifentanil-treated HCC cells.	Remifentanil	97-109	neighbor of BRCA1 lncRNA 2	Homo sapiens	17-21
35156240-10	2022	Decreased lncRNA NBR2 or increased miR-650 promoted the proliferation, migration and invasion of remifentanil-treated HCC cells.	Remifentanil	97-109	microRNA 650	Homo sapiens	35-42
35156240-12	2022	Moreover, miR-650 down-regulation or TIMP3 up-regulation reversed the effects of lncRNA NBR2 knockdown that caused an enhancement of cell viability, migration and invasiveness in remifentanil-treated HCC cells.	Remifentanil	179-191	microRNA 650	Homo sapiens	10-17
35156240-12	2022	Moreover, miR-650 down-regulation or TIMP3 up-regulation reversed the effects of lncRNA NBR2 knockdown that caused an enhancement of cell viability, migration and invasiveness in remifentanil-treated HCC cells.	Remifentanil	179-191	TIMP metallopeptidase inhibitor 3	Homo sapiens	37-42
35156240-12	2022	Moreover, miR-650 down-regulation or TIMP3 up-regulation reversed the effects of lncRNA NBR2 knockdown that caused an enhancement of cell viability, migration and invasiveness in remifentanil-treated HCC cells.	Remifentanil	179-191	neighbor of BRCA1 lncRNA 2	Homo sapiens	88-92
35156240-13	2022	Thus remifentanil reduces the proliferation, migration and invasion of HCC cells via the lncRNA NBR2/miR-650/TIMP3 axis in vitro.	Remifentanil	5-17	neighbor of BRCA1 lncRNA 2	Homo sapiens	96-100
35156240-13	2022	Thus remifentanil reduces the proliferation, migration and invasion of HCC cells via the lncRNA NBR2/miR-650/TIMP3 axis in vitro.	Remifentanil	5-17	microRNA 650	Homo sapiens	101-108
35156240-13	2022	Thus remifentanil reduces the proliferation, migration and invasion of HCC cells via the lncRNA NBR2/miR-650/TIMP3 axis in vitro.	Remifentanil	5-17	TIMP metallopeptidase inhibitor 3	Homo sapiens	109-114
35345251-3	2022	Both remifentanil and dexmedetomidine are used as sedatives in cardiac surgery (CS) patients with NIV intolerance.	Remifentanil	5-17	citrate synthase	Homo sapiens	80-82
35244055-10	2022	LESSIONS: General anesthesia of the shortest duration with the least metabolized drugs using desflurane and remifentanil, would be beneficial for rapid emergence in surgical patients with citrin deficiency.	Remifentanil	108-120	solute carrier family 25 member 13	Homo sapiens	188-194
35198576-11	2022	The prevalence of moderate-to-severe pain, number of patients using vasoactive agents, duration of PACU stay, as well as consumption of propofol, remifentanil, and DEX were significantly lower in the RD2 group (P < 0.05).	Remifentanil	146-158	peripherin 2	Homo sapiens	200-203
34850055-0	2022	Remifentanil protects heart from myocardial ischaemia/reperfusion (I/R) injury via miR-206-3p/TLR4/NF-kappaB signalling axis.	Remifentanil	0-12	toll-like receptor 4	Rattus norvegicus	94-98
34850055-12	2022	TLR4 overexpression destroyed cardiac function, exacerbated oxidative stress, increased levels of p-IkappaBalpha and p-p65 and aggravated pathology manifestation affected by remifentanil.	Remifentanil	174-186	toll-like receptor 4	Rattus norvegicus	0-4
34850055-13	2022	CONCLUSIONS: Our results elucidated that remifentanil alleviated myocardial I/R injury by miR-206-3p/TLR4/NF-kappaB signalling axis.	Remifentanil	41-53	toll-like receptor 4	Rattus norvegicus	101-105
34985213-13	2022	Similarly, compounds such as remifentanil bearing a methyl formate substituent at the piperidine para-position also produced numerous fragment ions, which were more prone to the rH pathway to lose methyl formate or methanol neutral molecules and furnish fragment ions with m/z 317 or 345.	Remifentanil	29-41	Rh blood group, D antigen	Rattus norvegicus	178-180
35155431-0	2022	Remifentanil Promotes PDIA3 Expression by Activating p38MAPK to Inhibit Intestinal Ischemia/Reperfusion-Induced Oxidative and Endoplasmic Reticulum Stress.	Remifentanil	0-12	protein disulfide isomerase associated 3	Mus musculus	22-27
35155431-0	2022	Remifentanil Promotes PDIA3 Expression by Activating p38MAPK to Inhibit Intestinal Ischemia/Reperfusion-Induced Oxidative and Endoplasmic Reticulum Stress.	Remifentanil	0-12	mitogen-activated protein kinase 14	Mus musculus	53-60
35352582-0	2022	KCC2 receptor upregulation potentiates antinociceptive effect of GABAAR agonist on remifentanil-induced hyperalgesia.	Remifentanil	83-95	solute carrier family 12 member 5	Homo sapiens	0-4
35352582-11	2022	Both muscimol and CLP257 could dose-dependently inhibit mechanical hypersensitivity caused by remifentanil-induced downregulation of GABAAalpha2R and KCC2, respectively.	Remifentanil	94-106	solute carrier family 12 member 5	Homo sapiens	150-154
35155431-7	2022	Moreover, the deletion of intestinal epithelium PDIA3 blocked the protective effects of remifentanil.	Remifentanil	88-100	protein disulfide isomerase associated 3	Mus musculus	48-53
35155431-9	2022	Conclusion: Remifentanil appears to act via p38MAPK to protect the small intestine from intestinal I/R injury by its PDIA3-mediated antioxidant and anti-ER stress properties.	Remifentanil	12-24	mitogen-activated protein kinase 14	Mus musculus	44-51
35155431-9	2022	Conclusion: Remifentanil appears to act via p38MAPK to protect the small intestine from intestinal I/R injury by its PDIA3-mediated antioxidant and anti-ER stress properties.	Remifentanil	12-24	protein disulfide isomerase associated 3	Mus musculus	117-122
33895216-6	2021	Remifentanil was added at three different doses for 24 hours, after which evaluation was performed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Total Antioxidant Capacity (TAC), Total Oxidant Status (TOS), and Annexin V.	Remifentanil	0-12	annexin A5	Rattus norvegicus	239-248
33862462-0	2021	Remifentanil preconditioning promotes liver regeneration via upregulation of beta-arrestin 2/ERK/cyclin D1 pathway.	Remifentanil	0-12	arrestin, beta 2	Mus musculus	77-92
33862462-0	2021	Remifentanil preconditioning promotes liver regeneration via upregulation of beta-arrestin 2/ERK/cyclin D1 pathway.	Remifentanil	0-12	mitogen-activated protein kinase 1	Mus musculus	93-96
33862462-0	2021	Remifentanil preconditioning promotes liver regeneration via upregulation of beta-arrestin 2/ERK/cyclin D1 pathway.	Remifentanil	0-12	cyclin D1	Mus musculus	97-106
33862462-5	2021	We further identified that remifentanil treatment increased the expression of beta-arrestin 2 in vivo and in vitro.	Remifentanil	27-39	arrestin, beta 2	Mus musculus	78-93
33862462-7	2021	While remifentanil increased the expression of activated (phosphorylated)-ERK and cyclin D1 in PHx livers, their levels were not significantly changed in remifentanil-treated CKO mice nor in WT mice pretreated with the ERK inhibitor U0126.	Remifentanil	6-18	mitogen-activated protein kinase 1	Mus musculus	74-77
33862462-7	2021	While remifentanil increased the expression of activated (phosphorylated)-ERK and cyclin D1 in PHx livers, their levels were not significantly changed in remifentanil-treated CKO mice nor in WT mice pretreated with the ERK inhibitor U0126.	Remifentanil	6-18	cyclin D1	Mus musculus	82-91
33862462-8	2021	Our findings suggest that remifentanil promotes liver regeneration via upregulation of a beta-arrestin 2/ERK/cyclin D1 axis, with implications for improving regeneration process after hepatectomy.	Remifentanil	26-38	arrestin, beta 2	Mus musculus	89-104
33862462-8	2021	Our findings suggest that remifentanil promotes liver regeneration via upregulation of a beta-arrestin 2/ERK/cyclin D1 axis, with implications for improving regeneration process after hepatectomy.	Remifentanil	26-38	mitogen-activated protein kinase 1	Mus musculus	105-108
33862462-8	2021	Our findings suggest that remifentanil promotes liver regeneration via upregulation of a beta-arrestin 2/ERK/cyclin D1 axis, with implications for improving regeneration process after hepatectomy.	Remifentanil	26-38	cyclin D1	Mus musculus	109-118
33969379-0	2021	Remifentanil preconditioning alleviates myocardial ischemia/reperfusion injury in rats via activating Jagged-1/Notch signaling pathway.	Remifentanil	0-12	jagged canonical Notch ligand 1	Rattus norvegicus	102-110
33969379-11	2021	In addition, mechanistic studies revealed that remifentanil preconditioning could up-regulate Jagged-1 expression and that Jagged-1 mediated the cardioprotective effects of remifentanil preconditioning through activating Notch signaling pathway.	Remifentanil	47-59	jagged canonical Notch ligand 1	Rattus norvegicus	94-102
33969379-11	2021	In addition, mechanistic studies revealed that remifentanil preconditioning could up-regulate Jagged-1 expression and that Jagged-1 mediated the cardioprotective effects of remifentanil preconditioning through activating Notch signaling pathway.	Remifentanil	173-185	jagged canonical Notch ligand 1	Rattus norvegicus	123-131
33969379-12	2021	Taken together, our data indicate that remifentanil preconditioning ameliorates myocardial damage in rat MI/RI models via Jagged-1-mediated Notch signaling pathway activation.	Remifentanil	39-51	jagged canonical Notch ligand 1	Rattus norvegicus	122-130
33310997-9	2021	Remifentanil may interfere with dexmedetomidine-induced diuresis and inhibition of AVP secretion.	Remifentanil	0-12	arginine vasopressin	Canis lupus familiaris	83-86
33639220-0	2021	P2X4 receptor in the dorsal horn contributes to BDNF/TrkB and AMPA receptor activation in the pathogenesis of remifentanil-induced postoperative hyperalgesia in rats.	Remifentanil	110-122	brain-derived neurotrophic factor	Rattus norvegicus	48-52
33228979-5	2021	Intraoperative cessation of remifentanil administration occurred in different numbers (%) of patients: control 0 (0%), SPI 1 (4.3%), PPI 18 (75.0%), and NOL 11 (47.8%); P=0.002.	Remifentanil	28-40	nucleolar protein 11	Homo sapiens	153-159
32996684-0	2020	Remifentanil up-regulates HIF1alpha expression to ameliorate hepatic ischaemia/reperfusion injury via the ZEB1/LIF axis.	Remifentanil	0-12	hypoxia inducible factor 1, alpha subunit	Mus musculus	26-35
33273982-4	2021	The results of the present study indicated that the addition of desflurane significantly reduced the amount of propofol and remifentanil that was administered in the PRD group, compared with that in the PR group.	Remifentanil	124-136	transmembrane protein 37	Homo sapiens	166-168
32574785-0	2021	NMDA receptor modulates spinal iron accumulation via activating DMT1(-)IRE in remifentanil-induced hyperalgesia.	Remifentanil	78-90	RoBo-1	Rattus norvegicus	64-68
32574785-10	2021	Our data revealed that spinal DMT1(-)IRE and iron content significantly increased in remifentanil-treated rats, and MK-801 inhibited the enhancements.	Remifentanil	85-97	RoBo-1	Rattus norvegicus	30-34
32574785-11	2021	DMT1(-)IRE knockdown and DFO prevented against remifentanil-induced hyperalgesia.	Remifentanil	47-59	RoBo-1	Rattus norvegicus	0-4
32574785-14	2021	This study suggests that DMT1(-)IRE-mediated iron accumulation is likely to be the downstream event following NMDA receptor activation and Ca2+ influx, contributing to remifentanil-induced hyperalgesia.	Remifentanil	168-180	RoBo-1	Rattus norvegicus	25-29
33300097-3	2020	CASE PRESENTATION: In case 1, MEP monitoring was successfully performed with the use of a fixed dose of remimazolam at 0.5 mg/kg/h and remifentanil at 0.2 mug/kg/min.	Remifentanil	135-147	neurolysin	Homo sapiens	30-33
33449539-3	2021	We present a case report of peripartum anesthetic management of a pregnant patient with congenital methemoglobinemia type 1 who received remifentanil labor analgesia and continuous methemoglobin monitoring.	Remifentanil	137-149	hemoglobin subunit gamma 2	Homo sapiens	99-112
33313232-0	2020	Remifentanil repairs cartilage damage and reduces the degradation of cartilage matrix in post-traumatic osteoarthritis, and inhibits IL-1beta-induced apoptosis of articular chondrocytes via inhibition of PI3K/AKT/NF-kappaB phosphorylation.	Remifentanil	0-12	interleukin 1 alpha	Rattus norvegicus	133-141
33313232-0	2020	Remifentanil repairs cartilage damage and reduces the degradation of cartilage matrix in post-traumatic osteoarthritis, and inhibits IL-1beta-induced apoptosis of articular chondrocytes via inhibition of PI3K/AKT/NF-kappaB phosphorylation.	Remifentanil	0-12	AKT serine/threonine kinase 1	Rattus norvegicus	209-212
33194033-0	2020	Remifentanil ameliorates lung injury in neonate rats with acute respiratory distress by down-regulating TIMP1 expression.	Remifentanil	0-12	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	104-109
33194033-9	2020	Remifentanil inhibited the expression of TIMP-1 in rats with acute respiratory distress, and TIMP-1 overexpression inhibited the protective effect of Remifentanil on rats with acute respiratory distress.	Remifentanil	0-12	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	41-47
33194033-9	2020	Remifentanil inhibited the expression of TIMP-1 in rats with acute respiratory distress, and TIMP-1 overexpression inhibited the protective effect of Remifentanil on rats with acute respiratory distress.	Remifentanil	150-162	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	93-99
33194033-10	2020	Remifentanil can reduce lung injury and inflammatory response in young mice with acute respiratory distress and play a protective role by down-regulating the expression of TIMP-1.	Remifentanil	0-12	tissue inhibitor of metalloproteinase 1	Mus musculus	172-178
32818602-3	2020	Phosphorylation of p38 mitogen-activated protein kinase (p38MAPK) in the dorsal root ganglion (DRG) neurons after remifentanil infusion, and the effect of a p38MAPK inhibitor on remifentanil-induced hyperalgesia were analyzed to investigate involvement of p38MAPK in the peripheral mechanisms of remifentanil-induced hyperalgesia.	Remifentanil	114-126	mitogen-activated protein kinase 14	Homo sapiens	19-55
32818602-3	2020	Phosphorylation of p38 mitogen-activated protein kinase (p38MAPK) in the dorsal root ganglion (DRG) neurons after remifentanil infusion, and the effect of a p38MAPK inhibitor on remifentanil-induced hyperalgesia were analyzed to investigate involvement of p38MAPK in the peripheral mechanisms of remifentanil-induced hyperalgesia.	Remifentanil	114-126	mitogen-activated protein kinase 14	Homo sapiens	57-64
32818602-10	2020	Remifentanil-induced exacerbation of incisional hyperalgesia was inhibited by methylnaltrexone and the BK2 antagonist.	Remifentanil	0-12	bradykinin receptor B2	Homo sapiens	103-106
32247539-1	2020	BACKGROUND: This study investigated whether remifentanil infusion decreased intraoperative hyperglycaemia and insulin resistance compared with intermittent fentanyl administration in patients undergoing elective cardiac surgery.	Remifentanil	44-56	insulin	Homo sapiens	110-117
32996684-0	2020	Remifentanil up-regulates HIF1alpha expression to ameliorate hepatic ischaemia/reperfusion injury via the ZEB1/LIF axis.	Remifentanil	0-12	zinc finger E-box binding homeobox 1	Mus musculus	106-110
32996684-0	2020	Remifentanil up-regulates HIF1alpha expression to ameliorate hepatic ischaemia/reperfusion injury via the ZEB1/LIF axis.	Remifentanil	0-12	leukemia inhibitory factor	Mus musculus	111-114
32996684-7	2020	Furthermore, hypoxia-induced NCTC-1469 cells exhibited decreased HIF1alpha and ZEB1 expression, reduced cell viability, as well as increased LIF expression and cell apoptosis (P < .05), which were reversed by remifentanil treatment (P < .05).	Remifentanil	209-221	hypoxia inducible factor 1, alpha subunit	Mus musculus	65-74
32996684-7	2020	Furthermore, hypoxia-induced NCTC-1469 cells exhibited decreased HIF1alpha and ZEB1 expression, reduced cell viability, as well as increased LIF expression and cell apoptosis (P < .05), which were reversed by remifentanil treatment (P < .05).	Remifentanil	209-221	zinc finger E-box binding homeobox 1	Mus musculus	79-83
32996684-7	2020	Furthermore, hypoxia-induced NCTC-1469 cells exhibited decreased HIF1alpha and ZEB1 expression, reduced cell viability, as well as increased LIF expression and cell apoptosis (P < .05), which were reversed by remifentanil treatment (P < .05).	Remifentanil	209-221	leukemia inhibitory factor	Mus musculus	141-144
32996684-10	2020	In summary, remifentanil protects against hepatic I/R injury through HIF1alpha and downstream effectors.	Remifentanil	12-24	hypoxia inducible factor 1, alpha subunit	Mus musculus	69-78
32925338-19	2020	CONCLUSIONS: Moderate-to-deep sedation by propofol and remifentanil TCI has a low incidence of catastrophic and severe events.	Remifentanil	55-67	transcobalamin 1	Homo sapiens	68-71
32654750-7	2020	RESULTS: For the Minto, Eleveld, and Kim remifentanil models, a plasma target concentration of ~ 4 ng ml-1 achieves drug administration consistent with product label recommended initial doses for all groups with minor exceptions.	Remifentanil	41-53	interleukin 17F	Homo sapiens	102-106
33103411-0	2020	Remifentanil protects neurological function of rats with cerebral ischemia-reperfusion injury via NR2B/CaMKIIalpha signaling pathway.	Remifentanil	0-12	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	98-102
33103411-9	2020	Remifentanil can repress the NR2B/ CaMKIIalpha signaling pathway in the neurons of rats with cerebral IRI to decrease the p-CREB expression, ROS level and MDA content in neurons, neuronal apoptosis level and cerebral infarct size, and increase the mitochondrial membrane potential, thereby protecting the neurological function.	Remifentanil	0-12	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	29-33
33103411-9	2020	Remifentanil can repress the NR2B/ CaMKIIalpha signaling pathway in the neurons of rats with cerebral IRI to decrease the p-CREB expression, ROS level and MDA content in neurons, neuronal apoptosis level and cerebral infarct size, and increase the mitochondrial membrane potential, thereby protecting the neurological function.	Remifentanil	0-12	cAMP responsive element binding protein 1	Rattus norvegicus	124-128
32636353-5	2020	The prediction probability model was: P=ex/1+ex, where e is the natural logarithm, X=-4.337+0.020x(CRP)+1.014 (whether the examination time was greater than 30 minutes)+1.912x(whether remifentanil was used during anesthesia)+1.514x(whether nausea or vomiting occurred during surgery or during recovery).	Remifentanil	184-196	peroxisomal biogenesis factor 1	Homo sapiens	38-44
32584786-4	2020	Remifentanil preconditioning was able to lower hypoxia-mediated protein carbonylation and limit MLKL-based signaling and pro-inflammatory response to almost normoxic control levels, and decrease hypoxia-induced pro-senescent activity of about 21% compared to control hypoxic conditions.	Remifentanil	0-12	mixed lineage kinase domain like pseudokinase	Homo sapiens	96-100
32247539-12	2020	CONCLUSIONS: Compared with patients treated with intermittent fentanyl, patients receiving continuous remifentanil infusion had fewer episodes of hyperglycaemia and less need for insulin administration during the intraoperative period of cardiac surgery.	Remifentanil	102-114	insulin	Homo sapiens	179-186
32466796-10	2020	One study reported lower cortisol levels with midazolam vs. placebo, while another study found significant variation in perioperative renin levels with remifentanil vs. placebo.	Remifentanil	152-164	renin	Homo sapiens	134-139
32547170-10	2020	Results: Remifentanil infusion could induce overexpression of beta-catenin and wnt3a in rats.	Remifentanil	9-21	Wnt family member 3A	Rattus norvegicus	79-84
32547170-14	2020	Conclusion: Remifentanil exposure could induce overexpression of wnt3a and enhance the production of beta-catenin in the spinal dorsal horn.	Remifentanil	12-24	Wnt family member 3A	Rattus norvegicus	65-70
32547170-14	2020	Conclusion: Remifentanil exposure could induce overexpression of wnt3a and enhance the production of beta-catenin in the spinal dorsal horn.	Remifentanil	12-24	catenin beta 1	Rattus norvegicus	101-113
32329867-7	2020	Besides, remifentanil reduced the mRNA expressions of IL-18, INF-gamma, TNF-beta, and IL-1beta (p<0.01), significantly decreased the protein expression of IL-18, and raised the protein expression of IL-18BP, thereby improving myocardial pathological damage.	Remifentanil	9-21	interleukin 1 alpha	Rattus norvegicus	86-94
32547170-0	2020	Wnt3a Inhibitor Attenuates Remifentanil-Induced Hyperalgesia via Downregulating Spinal NMDA Receptor in Rats.	Remifentanil	27-39	Wnt family member 3A	Rattus norvegicus	0-5
32547170-10	2020	Results: Remifentanil infusion could induce overexpression of beta-catenin and wnt3a in rats.	Remifentanil	9-21	catenin beta 1	Rattus norvegicus	62-74
30741729-4	2020	The TLR4 antagonist (+)-naltrexone decreased responding in rats trained to self-administer the micro-opioid receptor agonist remifentanil, but with a potency that was not significantly different from that observed in another group of subjects in which responding was maintained by food reinforcement.	Remifentanil	125-137	toll-like receptor 4	Rattus norvegicus	4-8
32329867-0	2020	Remifentanil improves myocardial ischemia-reperfusion injury in rats through inhibiting IL-18 signaling pathway.	Remifentanil	0-12	interleukin 18	Rattus norvegicus	88-93
32329867-7	2020	Besides, remifentanil reduced the mRNA expressions of IL-18, INF-gamma, TNF-beta, and IL-1beta (p<0.01), significantly decreased the protein expression of IL-18, and raised the protein expression of IL-18BP, thereby improving myocardial pathological damage.	Remifentanil	9-21	interleukin 18	Rattus norvegicus	54-59
32329867-7	2020	Besides, remifentanil reduced the mRNA expressions of IL-18, INF-gamma, TNF-beta, and IL-1beta (p<0.01), significantly decreased the protein expression of IL-18, and raised the protein expression of IL-18BP, thereby improving myocardial pathological damage.	Remifentanil	9-21	tumor necrosis factor	Rattus norvegicus	72-80
32088196-0	2020	Spinal Hevin Mediates Membrane Trafficking of GluA1-containing AMPA Receptors in Remifentanil-induced Postoperative Hyperalgesia in Mice.	Remifentanil	81-93	SPARC-like 1	Mus musculus	7-12
32088196-0	2020	Spinal Hevin Mediates Membrane Trafficking of GluA1-containing AMPA Receptors in Remifentanil-induced Postoperative Hyperalgesia in Mice.	Remifentanil	81-93	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	46-51
32088196-3	2020	This study aimed to investigate the correlation between spinal Hevin and AMPA receptors in remifentanil-induced postoperative hyperalgesia in mice.	Remifentanil	91-103	SPARC-like 1	Mus musculus	63-68
32088196-9	2020	Treatment with remifentanil increased the expression of spinal Hevin and the membrane trafficking of AMPA receptors.	Remifentanil	15-27	SPARC-like 1	Mus musculus	63-68
32088196-10	2020	Additionally, knockdown of spinal Hevin attenuated pain hypersensitivity and downregulated membrane trafficking of AMPA receptors after treatment with remifentanil.	Remifentanil	151-163	SPARC-like 1	Mus musculus	34-39
32088196-12	2020	CONCLUSIONS: Spinal Hevin was involved in the maintenance of remifentanil-induced postoperative hyperalgesia via modulating membrane trafficking of AMPA receptors.	Remifentanil	61-73	SPARC-like 1	Mus musculus	20-25
32329867-7	2020	Besides, remifentanil reduced the mRNA expressions of IL-18, INF-gamma, TNF-beta, and IL-1beta (p<0.01), significantly decreased the protein expression of IL-18, and raised the protein expression of IL-18BP, thereby improving myocardial pathological damage.	Remifentanil	9-21	interleukin 18	Rattus norvegicus	155-160
32329867-7	2020	Besides, remifentanil reduced the mRNA expressions of IL-18, INF-gamma, TNF-beta, and IL-1beta (p<0.01), significantly decreased the protein expression of IL-18, and raised the protein expression of IL-18BP, thereby improving myocardial pathological damage.	Remifentanil	9-21	interleukin 18 binding protein	Rattus norvegicus	199-206
32329867-8	2020	CONCLUSIONS: The protective mechanism of remifentanil on the myocardium of MIRI rats may be related to the inhibition on the IL-18 signaling pathway.	Remifentanil	41-53	interleukin 18	Rattus norvegicus	125-130
32082073-0	2019	Remifentanil Protects against Lipopolysaccharide-Induced Inflammation through PARP-1/NF-kappaB Signaling Pathway.	Remifentanil	0-12	poly(ADP-ribose) polymerase 1	Homo sapiens	78-84
32082073-8	2019	Compared with the control group, pretreatment with remifentanil significantly reduced superoxide anion production and DNA damage, with downregulation of iNOS, ICAM-1, and PARP-1 expressions as well as PAR expression.	Remifentanil	51-63	nitric oxide synthase 2	Homo sapiens	153-157
32082073-8	2019	Compared with the control group, pretreatment with remifentanil significantly reduced superoxide anion production and DNA damage, with downregulation of iNOS, ICAM-1, and PARP-1 expressions as well as PAR expression.	Remifentanil	51-63	intercellular adhesion molecule 1	Homo sapiens	159-165
32082073-8	2019	Compared with the control group, pretreatment with remifentanil significantly reduced superoxide anion production and DNA damage, with downregulation of iNOS, ICAM-1, and PARP-1 expressions as well as PAR expression.	Remifentanil	51-63	poly(ADP-ribose) polymerase 1	Homo sapiens	171-177
32082073-9	2019	Moreover, pretreatment with PARP-1 siRNA or remifentanil inhibited LPS-induced NF-kappaB p65 expression and nuclear translocation.	Remifentanil	44-56	RELA proto-oncogene, NF-kB subunit	Homo sapiens	89-92
32082073-10	2019	Remifentanil reduced LPS-induced inflammatory response through PARP-1/NF-kappaB signaling pathway.	Remifentanil	0-12	poly(ADP-ribose) polymerase 1	Homo sapiens	63-69
31583053-0	2019	Hyperglycemia-Induced Oxidative Stress Abrogates Remifentanil Preconditioning-Mediated Cardioprotection in Diabetic Rats by Impairing Caveolin-3-Modulated PI3K/Akt and JAK2/STAT3 Signaling.	Remifentanil	49-61	caveolin 3	Rattus norvegicus	134-144
31430547-0	2019	Chemokine CCL7 regulates spinal phosphorylation of GluA1-containing AMPA receptor via interleukin-18 in remifentanil-induced hyperalgesia in rats.	Remifentanil	104-116	C-C motif chemokine ligand 7	Rattus norvegicus	10-14
31430547-0	2019	Chemokine CCL7 regulates spinal phosphorylation of GluA1-containing AMPA receptor via interleukin-18 in remifentanil-induced hyperalgesia in rats.	Remifentanil	104-116	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	51-56
31430547-0	2019	Chemokine CCL7 regulates spinal phosphorylation of GluA1-containing AMPA receptor via interleukin-18 in remifentanil-induced hyperalgesia in rats.	Remifentanil	104-116	interleukin 18	Rattus norvegicus	86-100
31430547-8	2019	RESULTS: We reported that acute exposure to remifentanil caused and maintained behavioral RIH with up-regulation of expression in CCL7/CCR2 and IL-18/IL-18R and the phosphorylation of GluA1 in the dorsal horn.	Remifentanil	44-56	C-C motif chemokine ligand 7	Rattus norvegicus	130-134
31430547-8	2019	RESULTS: We reported that acute exposure to remifentanil caused and maintained behavioral RIH with up-regulation of expression in CCL7/CCR2 and IL-18/IL-18R and the phosphorylation of GluA1 in the dorsal horn.	Remifentanil	44-56	C-C motif chemokine receptor 2	Rattus norvegicus	135-139
31430547-8	2019	RESULTS: We reported that acute exposure to remifentanil caused and maintained behavioral RIH with up-regulation of expression in CCL7/CCR2 and IL-18/IL-18R and the phosphorylation of GluA1 in the dorsal horn.	Remifentanil	44-56	interleukin 18	Rattus norvegicus	144-149
31430547-8	2019	RESULTS: We reported that acute exposure to remifentanil caused and maintained behavioral RIH with up-regulation of expression in CCL7/CCR2 and IL-18/IL-18R and the phosphorylation of GluA1 in the dorsal horn.	Remifentanil	44-56	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	184-189
31430547-12	2019	CONCLUSION: Our current findings demonstrate that spinal CCL7/CCR2 modulation of GluA1-containing AMPA receptor activation via IL-18 and IL-18R over-expression is an important pathogenesis of remifentanil-induced hyperalgesia in rats.	Remifentanil	192-204	C-C motif chemokine ligand 7	Rattus norvegicus	57-61
31430547-12	2019	CONCLUSION: Our current findings demonstrate that spinal CCL7/CCR2 modulation of GluA1-containing AMPA receptor activation via IL-18 and IL-18R over-expression is an important pathogenesis of remifentanil-induced hyperalgesia in rats.	Remifentanil	192-204	C-C motif chemokine receptor 2	Rattus norvegicus	62-66
31430547-12	2019	CONCLUSION: Our current findings demonstrate that spinal CCL7/CCR2 modulation of GluA1-containing AMPA receptor activation via IL-18 and IL-18R over-expression is an important pathogenesis of remifentanil-induced hyperalgesia in rats.	Remifentanil	192-204	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	81-86
31430547-12	2019	CONCLUSION: Our current findings demonstrate that spinal CCL7/CCR2 modulation of GluA1-containing AMPA receptor activation via IL-18 and IL-18R over-expression is an important pathogenesis of remifentanil-induced hyperalgesia in rats.	Remifentanil	192-204	interleukin 18	Rattus norvegicus	127-132
31583053-0	2019	Hyperglycemia-Induced Oxidative Stress Abrogates Remifentanil Preconditioning-Mediated Cardioprotection in Diabetic Rats by Impairing Caveolin-3-Modulated PI3K/Akt and JAK2/STAT3 Signaling.	Remifentanil	49-61	AKT serine/threonine kinase 1	Rattus norvegicus	160-163
31583053-0	2019	Hyperglycemia-Induced Oxidative Stress Abrogates Remifentanil Preconditioning-Mediated Cardioprotection in Diabetic Rats by Impairing Caveolin-3-Modulated PI3K/Akt and JAK2/STAT3 Signaling.	Remifentanil	49-61	Janus kinase 2	Rattus norvegicus	168-172
31583053-0	2019	Hyperglycemia-Induced Oxidative Stress Abrogates Remifentanil Preconditioning-Mediated Cardioprotection in Diabetic Rats by Impairing Caveolin-3-Modulated PI3K/Akt and JAK2/STAT3 Signaling.	Remifentanil	49-61	signal transducer and activator of transcription 3	Rattus norvegicus	173-178
31112988-2	2019	Orexin-1 receptor (OxR1) antagonism reduces demand for cocaine and remifentanil, indicating that orexin-based therapies may reduce demand for many classes of abused drugs.	Remifentanil	67-79	hypocretin neuropeptide precursor	Rattus norvegicus	0-6
31112988-2	2019	Orexin-1 receptor (OxR1) antagonism reduces demand for cocaine and remifentanil, indicating that orexin-based therapies may reduce demand for many classes of abused drugs.	Remifentanil	67-79	oxidation resistance 1	Rattus norvegicus	19-23
31112988-2	2019	Orexin-1 receptor (OxR1) antagonism reduces demand for cocaine and remifentanil, indicating that orexin-based therapies may reduce demand for many classes of abused drugs.	Remifentanil	67-79	hypocretin neuropeptide precursor	Rattus norvegicus	97-103
31346154-0	2019	Influence of (ATP)-Binding Cassette Transporter Subfamily B Member 1 (ABCB1) Gene Polymorphism on the Efficacy of Remifentanil.	Remifentanil	114-126	ATP binding cassette subfamily B member 1	Homo sapiens	70-75
31346154-1	2019	<strong>BACKGROUND</strong> The aim of this study was to investigate the influence of adenosine triphosphate (ATP)-binding cassette transporter subfamily B member 1 (ABCB1) gene polymorphism on the efficacy of Remifentanil.	Remifentanil	210-222	ATP binding cassette subfamily B member 1	Homo sapiens	166-171
31346154-8	2019	<strong>CONCLUSIONS</strong> ABCB1 gene polymorphism can affect the clinical efficacy of Remifentanil.	Remifentanil	89-101	ATP binding cassette subfamily B member 1	Homo sapiens	29-34
30923248-3	2019	This study aims to determine if patients undergoing operative management of AIS have decreased opioid consumption and pain scores when an intraoperative fentanyl infusion is used as compared with a remifentanil infusion.	Remifentanil	198-210	IS1	Homo sapiens	76-79
30120960-0	2019	Annexin 1 inhibits remifentanil-induced hyperalgesia and NMDA receptor phosphorylation via regulating spinal CXCL12/CXCR4 in rats.	Remifentanil	19-31	annexin A1	Rattus norvegicus	0-9
30120960-0	2019	Annexin 1 inhibits remifentanil-induced hyperalgesia and NMDA receptor phosphorylation via regulating spinal CXCL12/CXCR4 in rats.	Remifentanil	19-31	C-X-C motif chemokine ligand 12	Rattus norvegicus	109-115
30120960-0	2019	Annexin 1 inhibits remifentanil-induced hyperalgesia and NMDA receptor phosphorylation via regulating spinal CXCL12/CXCR4 in rats.	Remifentanil	19-31	C-X-C motif chemokine receptor 4	Rattus norvegicus	116-121
30120960-4	2019	This study examined whether ANXA1 prevented remifentanil-caused OIH through modulating CXCL12 and NMDAR pathway in rats.	Remifentanil	44-56	annexin A1	Rattus norvegicus	28-33
30120960-5	2019	Acute exposure to remifentanil induced mechanical allodynia and thermal hyperalgesia, which was accompanied by the increase of spinal ANXA1 and CXCL12/CXCR4 expression.	Remifentanil	18-30	annexin A1	Rattus norvegicus	134-139
30120960-5	2019	Acute exposure to remifentanil induced mechanical allodynia and thermal hyperalgesia, which was accompanied by the increase of spinal ANXA1 and CXCL12/CXCR4 expression.	Remifentanil	18-30	C-X-C motif chemokine ligand 12	Rattus norvegicus	144-150
30120960-5	2019	Acute exposure to remifentanil induced mechanical allodynia and thermal hyperalgesia, which was accompanied by the increase of spinal ANXA1 and CXCL12/CXCR4 expression.	Remifentanil	18-30	C-X-C motif chemokine receptor 4	Rattus norvegicus	151-156
30759061-0	2019	COX-2 contributed to the remifentanil-induced hyperalgesia related to ephrinB/EphB signaling.	Remifentanil	25-37	cytochrome c oxidase II, mitochondrial	Mus musculus	0-5
30759061-4	2019	The objective of this research was to investigate the role of COX-2 in remifentanil-induced hyperalgesia and its relationship with ephrinB/EphB signaling.	Remifentanil	71-83	cytochrome c oxidase II, mitochondrial	Mus musculus	62-67
30759061-7	2019	Results: Continuing infusion of remifentanil produced thermal hyperalgesia and mechanical allodynia, which was accompanied by increased expression of spinal COX-2 protein and mRNA.	Remifentanil	32-44	cytochrome c oxidase II, mitochondrial	Mus musculus	157-162
30759061-9	2019	SC58125 and NS398, inhibitors of COX-2, suppressed pain behaviours induced by remifentanil infusion and reversed the increased pain behaviours induced by intrathecal injection of ephrinB2-Fc, an agonist of ephrinB/EphB.	Remifentanil	78-90	cytochrome c oxidase II, mitochondrial	Mus musculus	33-38
30759061-10	2019	Conclusions: Our findings confirmed that COX-2 is involved in remifentanil-induced hyperalgesia related to ephrinB/EphB signaling.	Remifentanil	62-74	cytochrome c oxidase II, mitochondrial	Mus musculus	41-46
30923248-12	2019	DISCUSSION: Despite concerns for hyperalgesia and acute tolerance, remifentanil is widely used for intraoperative opioid infusions for surgical correction of AIS.	Remifentanil	67-79	IS1	Homo sapiens	158-161
30988754-7	2019	The anesthesia of propofol combined with remifentanil could contribute to the balance of NO/ET-1 and the inhibition of inflammatory factors during the hepatectomy operation in patients with liver cirrhosis, and help to protect the liver function of patients, reducing the incidence of liver ischemia-reperfusion injury in patients.	Remifentanil	41-53	endothelin 1	Homo sapiens	92-96
30808671-4	2019	The present study examined whether clinically employed synthetic (fentanyl, remifentanil) and the semisynthetic opioid (oxycodone) would also potentiate sustained ASIC currents, which arise from ASIC3 channel isoforms.	Remifentanil	76-88	acid sensing ion channel subunit 3	Rattus norvegicus	195-200
30863139-0	2019	TRPV1 channel contributes to remifentanil-induced postoperative hyperalgesia via regulation of NMDA receptor trafficking in dorsal root ganglion.	Remifentanil	29-41	transient receptor potential cation channel subfamily V member 1	Homo sapiens	0-5
31068895-6	2019	Results: In the injured neonatal brain, remifentanil significantly decreased ROS production, cortical caspase activity, DNA fragmentation, interleukin-1beta levels, and reactive astrogliosis.	Remifentanil	40-52	interleukin 1 beta	Mus musculus	139-156
31068895-8	2019	Performance on negative geotaxis (P6-8) and grasping reflex (P10-12) tests was improved in the remifentanil group.	Remifentanil	95-107	annexin A6	Mus musculus	34-38
31068895-8	2019	Performance on negative geotaxis (P6-8) and grasping reflex (P10-12) tests was improved in the remifentanil group.	Remifentanil	95-107	S100 calcium binding protein A10 (calpactin)	Mus musculus	61-64
31068895-9	2019	At P18, a sex specificity was noticed; remifentanil-treated females spent more time in the open field center than did the controls, suggesting less anxiety in young female mice.	Remifentanil	39-51	stathmin 1	Mus musculus	3-6
31065591-0	2019	Remifentanil promotes osteoblastogenesis by upregulating Runx2/osterix expression in preosteoblastic C2C12 cells.	Remifentanil	0-12	runt related transcription factor 2	Mus musculus	57-62
31065591-0	2019	Remifentanil promotes osteoblastogenesis by upregulating Runx2/osterix expression in preosteoblastic C2C12 cells.	Remifentanil	0-12	Sp7 transcription factor 7	Mus musculus	63-70
31065591-8	2019	The expression of Runx2 and osterix was evaluated by RT-PCT and western blot analysis to investigate the mechanism involved in remifentanil-mediated osteoblast differentiation.	Remifentanil	127-139	runt related transcription factor 2	Mus musculus	18-23
31065591-8	2019	The expression of Runx2 and osterix was evaluated by RT-PCT and western blot analysis to investigate the mechanism involved in remifentanil-mediated osteoblast differentiation.	Remifentanil	127-139	Sp7 transcription factor 7	Mus musculus	28-35
31065591-11	2019	RT-PCR and western blot analysis showed that the expression of Runx2 and osterix was upregulated by remifentanil.	Remifentanil	100-112	runt related transcription factor 2	Mus musculus	63-68
31065591-11	2019	RT-PCR and western blot analysis showed that the expression of Runx2 and osterix was upregulated by remifentanil.	Remifentanil	100-112	Sp7 transcription factor 7	Mus musculus	73-80
31065591-12	2019	Conclusions: We demonstrated that remifentanil increased osteoblast differentiation in vitro by upregulation of Runx2 and osterix expression.	Remifentanil	34-46	runt related transcription factor 2	Mus musculus	112-117
31065591-12	2019	Conclusions: We demonstrated that remifentanil increased osteoblast differentiation in vitro by upregulation of Runx2 and osterix expression.	Remifentanil	34-46	Sp7 transcription factor 7	Mus musculus	122-129
30863139-4	2019	However, the contribution of TRPV1 in modulating remifentanil-induced postoperative hyperalgesia is still unknown.	Remifentanil	49-61	transient receptor potential cation channel subfamily V member 1	Homo sapiens	29-34
30863139-5	2019	The aim of this study is the contribution of TRPV1 to the surface expression of N-methyl-d-aspartate (NMDA) receptors in remifentanil-induced postoperative hyperalgesia.	Remifentanil	121-133	transient receptor potential cation channel subfamily V member 1	Homo sapiens	45-50
30863139-11	2019	Here, we found the membrane trafficking of NR1, possibly due to the activation of TRPV1 in DRG neurons after remifentanil infusion.	Remifentanil	109-121	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	43-46
30863139-11	2019	Here, we found the membrane trafficking of NR1, possibly due to the activation of TRPV1 in DRG neurons after remifentanil infusion.	Remifentanil	109-121	transient receptor potential cation channel subfamily V member 1	Homo sapiens	82-87
30863139-12	2019	Furthermore, intrathecal injection of CPZ was able to relieve remifentanil-induced postoperative hyperalgesia according to a behavioral test and CPZ confirmed that TRPV1 is involved in NR1 trafficking.	Remifentanil	62-74	transient receptor potential cation channel subfamily V member 1	Homo sapiens	164-169
30863139-12	2019	Furthermore, intrathecal injection of CPZ was able to relieve remifentanil-induced postoperative hyperalgesia according to a behavioral test and CPZ confirmed that TRPV1 is involved in NR1 trafficking.	Remifentanil	62-74	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	185-188
30863139-14	2019	Conclusion: Our study demonstrates that TRPV1 receptors are involved in remifentanil-induced postoperative hyperalgesia.	Remifentanil	72-84	transient receptor potential cation channel subfamily V member 1	Homo sapiens	40-45
30863139-15	2019	TRPV1 contributes to the persistence of remifentanil-induced postoperative hyperalgesia through the trafficking of NMDA receptors via the activation of CaMKII-PKC signaling pathways in DRG neurons.	Remifentanil	40-52	transient receptor potential cation channel subfamily V member 1	Homo sapiens	0-5
30765766-0	2019	Indispensable role of beta-arrestin2 in the protection of remifentanil preconditioning against hepatic ischemic reperfusion injury.	Remifentanil	58-70	arrestin, beta 2	Mus musculus	22-36
30765766-3	2019	Using the rodent models of hepatic ischemia reperfusion injury both in wild type and TLR4 knockout (TLR4 KO) mice, we found that remifentanil preconditioning could inhibit the expression of TLR4 and reduce the inflammatory response induced by HIRI in wild type but not in TLR4 KO mice.	Remifentanil	129-141	toll-like receptor 4	Mus musculus	85-89
30765766-3	2019	Using the rodent models of hepatic ischemia reperfusion injury both in wild type and TLR4 knockout (TLR4 KO) mice, we found that remifentanil preconditioning could inhibit the expression of TLR4 and reduce the inflammatory response induced by HIRI in wild type but not in TLR4 KO mice.	Remifentanil	129-141	toll-like receptor 4	Mus musculus	100-104
30765766-3	2019	Using the rodent models of hepatic ischemia reperfusion injury both in wild type and TLR4 knockout (TLR4 KO) mice, we found that remifentanil preconditioning could inhibit the expression of TLR4 and reduce the inflammatory response induced by HIRI in wild type but not in TLR4 KO mice.	Remifentanil	129-141	toll-like receptor 4	Mus musculus	100-104
30765766-3	2019	Using the rodent models of hepatic ischemia reperfusion injury both in wild type and TLR4 knockout (TLR4 KO) mice, we found that remifentanil preconditioning could inhibit the expression of TLR4 and reduce the inflammatory response induced by HIRI in wild type but not in TLR4 KO mice.	Remifentanil	129-141	toll-like receptor 4	Mus musculus	100-104
30765766-5	2019	Remifentanil increased beta-arrestin2 expression both in vivo and in vitro, while after silencing beta-arrestin2 RNA, the effect of remifentanil in reducing cell death and apoptosis, as well as decreasing phosphorylation of ERK and JNK were abolished in RAW264.7 cells.	Remifentanil	0-12	arrestin, beta 2	Mus musculus	23-37
30765766-5	2019	Remifentanil increased beta-arrestin2 expression both in vivo and in vitro, while after silencing beta-arrestin2 RNA, the effect of remifentanil in reducing cell death and apoptosis, as well as decreasing phosphorylation of ERK and JNK were abolished in RAW264.7 cells.	Remifentanil	132-144	arrestin, beta 2	Mus musculus	98-112
30765766-5	2019	Remifentanil increased beta-arrestin2 expression both in vivo and in vitro, while after silencing beta-arrestin2 RNA, the effect of remifentanil in reducing cell death and apoptosis, as well as decreasing phosphorylation of ERK and JNK were abolished in RAW264.7 cells.	Remifentanil	132-144	mitogen-activated protein kinase 8	Mus musculus	232-235
30765766-6	2019	These data suggested that remifentanil could ameliorate mice HIRI through upregulating beta-arrestin2 expression, which may function as a key molecule in bridging opioid receptor and TLR4 pathway.	Remifentanil	26-38	arrestin, beta 2	Mus musculus	87-101
30765766-6	2019	These data suggested that remifentanil could ameliorate mice HIRI through upregulating beta-arrestin2 expression, which may function as a key molecule in bridging opioid receptor and TLR4 pathway.	Remifentanil	26-38	toll-like receptor 4	Mus musculus	183-187
30575939-16	2018	CONCLUSIONS: Remifentanil can effectively reduce myocardial cell injury caused by myocardial ischemia-reperfusion in rats, improve cardiac function, reduce the myocardial infarction area, decrease cleaved caspase-3 in myocardial cells, and increase Bcl-2/Bax.	Remifentanil	13-25	BCL2, apoptosis regulator	Rattus norvegicus	249-254
30864483-0	2019	IgE-mediated allergy to remifentanil?	Remifentanil	24-36	immunoglobulin heavy constant epsilon	Homo sapiens	0-3
30630559-18	2019	CONCLUSION: Compared with midazolam-remifentanil intravenous anaesthesia, the dezocine-remifentanil method has a better analgesic effect, shorter wake-up time, and can effectively regulate the expression of inflammatory cytokines TNF-&amp;alpha; and IL-6.	Remifentanil	87-99	tumor necrosis factor	Homo sapiens	230-233
30630559-18	2019	CONCLUSION: Compared with midazolam-remifentanil intravenous anaesthesia, the dezocine-remifentanil method has a better analgesic effect, shorter wake-up time, and can effectively regulate the expression of inflammatory cytokines TNF-&amp;alpha; and IL-6.	Remifentanil	87-99	interleukin 6	Homo sapiens	250-254
30630560-10	2019	CONCLUSION: Compared with fentanyl combined anesthesia, the remifentanil combined anesthesia can significantly reduce serum levels of cytokines IL-8, IL-6, CRP, TNF- &amp;alpha; and oxidative stress level, and is, therefore, more secure for patients undergoing laparoscopic surgery for colon cancer.	Remifentanil	60-72	C-X-C motif chemokine ligand 8	Homo sapiens	144-148
30630560-10	2019	CONCLUSION: Compared with fentanyl combined anesthesia, the remifentanil combined anesthesia can significantly reduce serum levels of cytokines IL-8, IL-6, CRP, TNF- &amp;alpha; and oxidative stress level, and is, therefore, more secure for patients undergoing laparoscopic surgery for colon cancer.	Remifentanil	60-72	interleukin 6	Homo sapiens	150-154
30575939-16	2018	CONCLUSIONS: Remifentanil can effectively reduce myocardial cell injury caused by myocardial ischemia-reperfusion in rats, improve cardiac function, reduce the myocardial infarction area, decrease cleaved caspase-3 in myocardial cells, and increase Bcl-2/Bax.	Remifentanil	13-25	BCL2 associated X, apoptosis regulator	Rattus norvegicus	255-258
30089853-0	2018	Remifentanil upregulates hepatic IL-18 binding protein (IL-18BP) expression through transcriptional control.	Remifentanil	0-12	interleukin 18	Homo sapiens	33-38
30089853-0	2018	Remifentanil upregulates hepatic IL-18 binding protein (IL-18BP) expression through transcriptional control.	Remifentanil	0-12	interleukin 18 binding protein	Homo sapiens	56-63
30089853-2	2018	We have previously demonstrated that remifentanil protects against liver I/R injury by upregulating the hepatic expression of IL-18-binding protein (IL-18BP), a natural IL-18 inhibitor.	Remifentanil	37-49	interleukin 18 binding protein	Homo sapiens	126-147
30089853-2	2018	We have previously demonstrated that remifentanil protects against liver I/R injury by upregulating the hepatic expression of IL-18-binding protein (IL-18BP), a natural IL-18 inhibitor.	Remifentanil	37-49	interleukin 18 binding protein	Homo sapiens	149-156
30089853-2	2018	We have previously demonstrated that remifentanil protects against liver I/R injury by upregulating the hepatic expression of IL-18-binding protein (IL-18BP), a natural IL-18 inhibitor.	Remifentanil	37-49	interleukin 18	Homo sapiens	126-131
30089853-3	2018	The current study was performed to further clarify the effects of remifentanil on IL-18BP expression in the liver as well as investigate the underlying mechanisms.	Remifentanil	66-78	interleukin 18 binding protein	Homo sapiens	82-89
30089853-4	2018	In Sprague-Dawley (SD) rats, we demonstrated that remifentanil significantly increased the expression of IL-18BP in normal rat liver tissue over a 24-h time period with maximal expression at 24 h after treatment.	Remifentanil	50-62	interleukin 18 binding protein	Rattus norvegicus	105-112
30089853-5	2018	The upregulation of remifentanil on IL-18BP expression displayed similar trends in in vitro cellular studies, including mouse primary hepatocytes, normal human hepatocyte LO2, and mouse hepatoma cells Hep1-6.	Remifentanil	20-32	interleukin 18 binding protein	Mus musculus	36-43
30089853-5	2018	The upregulation of remifentanil on IL-18BP expression displayed similar trends in in vitro cellular studies, including mouse primary hepatocytes, normal human hepatocyte LO2, and mouse hepatoma cells Hep1-6.	Remifentanil	20-32	DNL-type zinc finger	Mus musculus	201-207
30089853-6	2018	In LO2 cells, preexposure of the cells to remifentanil significantly inhibited IL-18-activated p65 NF-kappaB phosphorylation, and the inhibition was absent when the cells were transfected with IL-18BP siRNA, indicating the functional effects of IL-18BP induced by remifentanil.	Remifentanil	42-54	interleukin 18	Homo sapiens	79-84
30089853-6	2018	In LO2 cells, preexposure of the cells to remifentanil significantly inhibited IL-18-activated p65 NF-kappaB phosphorylation, and the inhibition was absent when the cells were transfected with IL-18BP siRNA, indicating the functional effects of IL-18BP induced by remifentanil.	Remifentanil	42-54	RELA proto-oncogene, NF-kB subunit	Homo sapiens	95-98
30089853-6	2018	In LO2 cells, preexposure of the cells to remifentanil significantly inhibited IL-18-activated p65 NF-kappaB phosphorylation, and the inhibition was absent when the cells were transfected with IL-18BP siRNA, indicating the functional effects of IL-18BP induced by remifentanil.	Remifentanil	42-54	interleukin 18 binding protein	Homo sapiens	193-200
30089853-6	2018	In LO2 cells, preexposure of the cells to remifentanil significantly inhibited IL-18-activated p65 NF-kappaB phosphorylation, and the inhibition was absent when the cells were transfected with IL-18BP siRNA, indicating the functional effects of IL-18BP induced by remifentanil.	Remifentanil	42-54	interleukin 18 binding protein	Homo sapiens	245-252
30089853-6	2018	In LO2 cells, preexposure of the cells to remifentanil significantly inhibited IL-18-activated p65 NF-kappaB phosphorylation, and the inhibition was absent when the cells were transfected with IL-18BP siRNA, indicating the functional effects of IL-18BP induced by remifentanil.	Remifentanil	264-276	interleukin 18	Homo sapiens	79-84
30089853-6	2018	In LO2 cells, preexposure of the cells to remifentanil significantly inhibited IL-18-activated p65 NF-kappaB phosphorylation, and the inhibition was absent when the cells were transfected with IL-18BP siRNA, indicating the functional effects of IL-18BP induced by remifentanil.	Remifentanil	264-276	RELA proto-oncogene, NF-kB subunit	Homo sapiens	95-98
30089853-6	2018	In LO2 cells, preexposure of the cells to remifentanil significantly inhibited IL-18-activated p65 NF-kappaB phosphorylation, and the inhibition was absent when the cells were transfected with IL-18BP siRNA, indicating the functional effects of IL-18BP induced by remifentanil.	Remifentanil	264-276	interleukin 18 binding protein	Homo sapiens	193-200
30089853-7	2018	Pretreatment with actinomycin D abolished remifentanil-induced upregulation of IL-18BP mRNA, suggesting that the induction occurred at the transcriptional level.	Remifentanil	42-54	interleukin 18 binding protein	Homo sapiens	79-86
30089853-8	2018	This was further supported by the luciferase reporter assay, which demonstrated that remifentanil treatment significantly increased transcription of the IL-18BP promoter.	Remifentanil	85-97	interleukin 18 binding protein	Homo sapiens	153-160
30089853-9	2018	Both western blot analysis and ChIP assays showed that STAT1 and C/EBP beta were activated by remifentanil.	Remifentanil	94-106	signal transducer and activator of transcription 1	Homo sapiens	55-60
30089853-9	2018	Both western blot analysis and ChIP assays showed that STAT1 and C/EBP beta were activated by remifentanil.	Remifentanil	94-106	CCAAT enhancer binding protein beta	Homo sapiens	65-75
30089853-11	2018	These findings demonstrate that remifentanil could upregulate hepatic IL-18BP expression through transcriptional activation of the IL-18BP promoter, and STAT1 and C/EBP beta are two key transcriptional factors involved in this process.	Remifentanil	32-44	interleukin 18 binding protein	Homo sapiens	70-77
30089853-11	2018	These findings demonstrate that remifentanil could upregulate hepatic IL-18BP expression through transcriptional activation of the IL-18BP promoter, and STAT1 and C/EBP beta are two key transcriptional factors involved in this process.	Remifentanil	32-44	interleukin 18 binding protein	Homo sapiens	131-138
30167784-0	2018	Remifentanil suppresses increase in interleukin-6 mRNA in the brain by inhibiting cyclic AMP synthesis.	Remifentanil	0-12	interleukin 6	Mus musculus	36-49
30336856-9	2018	RESULTS: Mean remifentanil infusion rate [mean (standard deviation)] was significantly higher in the sevoflurane group than in the desflurane group [0.192 (0.064) vs. 0.099 (0.033) mug kg-1 min-1; difference, 0.093 (95% confidence interval, 0.071-0.115); P&lt;0.001].	Remifentanil	14-26	CD59 molecule (CD59 blood group)	Homo sapiens	190-195
30167784-9	2018	RESULTS: Remifentanil suppressed increase in IL-6 mRNA levels in the mouse brain, and also inhibited the responses of plasma IL-6, corticosterone, and noradrenaline in an inflammatory state.	Remifentanil	9-21	interleukin 6	Mus musculus	45-49
30167784-9	2018	RESULTS: Remifentanil suppressed increase in IL-6 mRNA levels in the mouse brain, and also inhibited the responses of plasma IL-6, corticosterone, and noradrenaline in an inflammatory state.	Remifentanil	9-21	interleukin 6	Mus musculus	125-129
30167784-11	2018	In cultured cells, remifentanil suppressed increase in IL-6 mRNA levels and intracellular cAMP levels after the administration of LPS, and this enhanced IL-6 mRNA expression in response to LPS.	Remifentanil	19-31	interleukin 6	Mus musculus	55-59
30167784-11	2018	In cultured cells, remifentanil suppressed increase in IL-6 mRNA levels and intracellular cAMP levels after the administration of LPS, and this enhanced IL-6 mRNA expression in response to LPS.	Remifentanil	19-31	interleukin 6	Mus musculus	153-157
30167784-12	2018	CONCLUSION: Remifentanil suppressed increase in IL-6 mRNA levels in the brain in an inflammatory state, and this effect may be attributed to its direct action on neuronal cells through the inhibition of intracellular cAMP rather than corticosterone.	Remifentanil	12-24	interleukin 6	Mus musculus	48-52
30243294-12	2018	CONCLUSION: In comparison with sevoflurane-based inhalational anesthesia, propofol/remifentanil -based total intravenous anesthesia can effectively inhibit the release of VEGF-C induced by breast surgery, but didn"t seem to be beneficial in the short-term recurrence rate of breast cancer.	Remifentanil	83-95	vascular endothelial growth factor C	Homo sapiens	171-177
29959648-4	2018	Remifentanil withdrawal could activate Src family kinases (SFKs) in microglia, and upregulate the expression of tumor necrosis factor alpha (TNFalpha) in spinal dorsal horn.	Remifentanil	0-12	tumor necrosis factor	Rattus norvegicus	141-149
30243294-0	2018	Effects of propofol/remifentanil-based total intravenous anesthesia versus sevoflurane-based inhalational anesthesia on the release of VEGF-C and TGF-beta and prognosis after breast cancer surgery: a prospective, randomized and controlled study.	Remifentanil	20-32	vascular endothelial growth factor C	Homo sapiens	135-141
30243294-3	2018	In this study, we compared the effects of propofol/remifentanil-based total intravenous anesthesia (TIVA) and sevoflurane-based inhalational anesthesia on the release of VEGF-C and TGF-beta, as well as recurrence- free survival (RFS) rates in the patients undergoing breast cancer surgery.	Remifentanil	51-63	vascular endothelial growth factor C	Homo sapiens	170-176
29959648-5	2018	Furthermore, pretreatment with either microglia inhibitor Minocycline, SFKs inhibitor PP2 or TNF alphaneutralization antibody could block remifentanil withdrawal induced spinal LTP, whereas supplement of recombinant rat TNFalpha to the spinal cord could reverse the inhibitory effect of Minocycline or PP2 on remifentanil withdrawal induced LTP.	Remifentanil	138-150	tumor necrosis factor	Rattus norvegicus	93-96
29538008-12	2018	CONCLUSION: Tlr4 receptor involvement is suggested in the development of remifentanil-induced hyperalgesia in mice.	Remifentanil	73-85	toll-like receptor 4	Mus musculus	12-16
28957873-0	2018	HDAC3 Mediates Cardioprotection of Remifentanil Postconditioning by Targeting GSK-3beta in H9c2 Cardiomyocytes in Hypoxia/Reoxygenation Injury.	Remifentanil	35-47	histone deacetylase 3	Rattus norvegicus	0-5
28957873-0	2018	HDAC3 Mediates Cardioprotection of Remifentanil Postconditioning by Targeting GSK-3beta in H9c2 Cardiomyocytes in Hypoxia/Reoxygenation Injury.	Remifentanil	35-47	glycogen synthase kinase 3 beta	Rattus norvegicus	78-87
29578864-4	2018	This study examines whether protein kinase Mzeta and Kalirin-7 contribute to remifentanil-induced postincisional hyperalgesia via AMPA receptor.	Remifentanil	77-89	kalirin, RhoGEF kinase	Rattus norvegicus	53-60
29578864-10	2018	Protein kinase Mzeta inhibitor reduced remifentanil-induced hyperalgesia, Kalirin-7 expression, and GluA1 trafficking.	Remifentanil	39-51	kalirin, RhoGEF kinase	Rattus norvegicus	74-81
29578864-10	2018	Protein kinase Mzeta inhibitor reduced remifentanil-induced hyperalgesia, Kalirin-7 expression, and GluA1 trafficking.	Remifentanil	39-51	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	100-105
29578864-14	2018	CONCLUSIONS: Spinal protein kinase Mzeta regulation of GluA1-containing AMPA receptor trafficking and spine morphology via Kalirin-7 overexpression is a fundamental pathogenesis of remifentanil-induced hyperalgesia in rats.	Remifentanil	181-193	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	55-60
29578864-14	2018	CONCLUSIONS: Spinal protein kinase Mzeta regulation of GluA1-containing AMPA receptor trafficking and spine morphology via Kalirin-7 overexpression is a fundamental pathogenesis of remifentanil-induced hyperalgesia in rats.	Remifentanil	181-193	kalirin, RhoGEF kinase	Rattus norvegicus	123-130
29896261-8	2018	CD11b, TNF-alpha, IL-1beta and IL-6 levels were increased following remifentanil administration and these effects were counteracted by EA (all P&lt;0.05).	Remifentanil	68-80	integrin subunit alpha M	Rattus norvegicus	0-5
29896261-8	2018	CD11b, TNF-alpha, IL-1beta and IL-6 levels were increased following remifentanil administration and these effects were counteracted by EA (all P&lt;0.05).	Remifentanil	68-80	tumor necrosis factor	Rattus norvegicus	7-16
29896261-8	2018	CD11b, TNF-alpha, IL-1beta and IL-6 levels were increased following remifentanil administration and these effects were counteracted by EA (all P&lt;0.05).	Remifentanil	68-80	interleukin 1 beta	Rattus norvegicus	18-26
29896261-8	2018	CD11b, TNF-alpha, IL-1beta and IL-6 levels were increased following remifentanil administration and these effects were counteracted by EA (all P&lt;0.05).	Remifentanil	68-80	interleukin 6	Rattus norvegicus	31-35
29896261-10	2018	The results of the present study demonstrated that EA at the Huantiao and Yanglingquan acupoints may reduce remifentanil-induced postoperative hyperalgesia, likely by inhibiting spinal microglia via reduction of CD11b and pro-inflammatory cytokine expression.	Remifentanil	108-120	integrin subunit alpha M	Rattus norvegicus	212-217
29861656-5	2018	c-Fos immunofluorescence of the brain stem showed that dorsal motor nucleus of the vagus was activated after remifentanil preconditioning.	Remifentanil	109-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
29867405-10	2018	We found that the addition of remifentanil to N2O anesthesia improves the ability of traditional frequency-derived measures, including the Bispectral Index (BIS), to discriminate between loss and ROR.	Remifentanil	30-42	long intergenic non-protein coding RNA, regulator of reprogramming	Homo sapiens	196-199
29728964-0	2018	The Mechanism of Hyperalgesia and Anxiety Induced by Remifentanil: Phosphorylation of GluR1 Receptors in the Anterior Cingulate Cortex.	Remifentanil	53-65	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	86-91
29661389-5	2018	RESULTS: Remifentanil reduced isohypercapnic ventilation (end-tidal PCO2 6.5 kPa) by approximately 40% (from 20 to 12 litre min-1) in esketamine and placebo arms of the study, through an effect on baseline ventilation and ventilatory CO2 sensitivity.	Remifentanil	9-21	CD59 molecule (CD59 blood group)	Homo sapiens	124-129
29363836-7	2018	Together, our data demonstrate that MCU plays a critical role in remifentanil-induced postoperative mechanical allodynia, with NMDA receptor and ERK as possible downstream effectors.	Remifentanil	65-77	mitochondrial calcium uniporter	Homo sapiens	36-39
30603558-0	2018	Remifentanil Negatively Regulates RANKL-Induced Osteoclast Differentiation and Bone Resorption by Inhibiting c-Fos/NFATc1 Expression.	Remifentanil	0-12	TNF superfamily member 11	Homo sapiens	34-39
30603558-0	2018	Remifentanil Negatively Regulates RANKL-Induced Osteoclast Differentiation and Bone Resorption by Inhibiting c-Fos/NFATc1 Expression.	Remifentanil	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	109-114
30603558-0	2018	Remifentanil Negatively Regulates RANKL-Induced Osteoclast Differentiation and Bone Resorption by Inhibiting c-Fos/NFATc1 Expression.	Remifentanil	0-12	nuclear factor of activated T cells 1	Homo sapiens	115-121
30603558-9	2018	Expression of c-Fos and NFATC1 was most strongly decreased in the presence of RANKL and remifentanil, and the activity of ERK was also inhibited by remifentanil.	Remifentanil	88-100	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	14-19
30603558-9	2018	Expression of c-Fos and NFATC1 was most strongly decreased in the presence of RANKL and remifentanil, and the activity of ERK was also inhibited by remifentanil.	Remifentanil	88-100	nuclear factor of activated T cells 1	Homo sapiens	24-30
30603558-9	2018	Expression of c-Fos and NFATC1 was most strongly decreased in the presence of RANKL and remifentanil, and the activity of ERK was also inhibited by remifentanil.	Remifentanil	148-160	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	14-19
30603558-9	2018	Expression of c-Fos and NFATC1 was most strongly decreased in the presence of RANKL and remifentanil, and the activity of ERK was also inhibited by remifentanil.	Remifentanil	148-160	mitogen-activated protein kinase 1	Homo sapiens	122-125
29363836-7	2018	Together, our data demonstrate that MCU plays a critical role in remifentanil-induced postoperative mechanical allodynia, with NMDA receptor and ERK as possible downstream effectors.	Remifentanil	65-77	mitogen-activated protein kinase 1	Homo sapiens	145-148
29363836-8	2018	Our findings provide novel mechanisms for remifentanil-induced mechanical allodynia and encourage future studies to examine the mitochondrial Ca2+ uniporter as a potential therapeutic target for prevention of OIH.	Remifentanil	42-54	mitochondrial calcium uniporter	Homo sapiens	128-156
29434817-9	2018	Remifentanil infusion led to upregulation of membrane expression of the AMPAR subunit GluR1 and DOR (P=0.003 and 0.001, respectively) no change in total GluR1 and DOR expression levels (P=0.244 and 0.531, respectively).	Remifentanil	0-12	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	86-91
29363836-0	2018	Role of mitochondrial Ca2+ uniporter in remifentanil-induced postoperative allodynia.	Remifentanil	40-52	mitochondrial calcium uniporter	Homo sapiens	8-36
29363836-3	2018	This study investigated the role of mitochondrial Ca2+ uniporter (MCU) in remifentanil (a commonly used opioid analgesic)-induced allodynia.	Remifentanil	74-86	mitochondrial calcium uniporter	Homo sapiens	36-64
29363836-3	2018	This study investigated the role of mitochondrial Ca2+ uniporter (MCU) in remifentanil (a commonly used opioid analgesic)-induced allodynia.	Remifentanil	74-86	mitochondrial calcium uniporter	Homo sapiens	66-69
29434817-13	2018	Combined behavioral, western blot and electrophysiological evidence indicated that remifentanil-induced hyperalgesia was mediated by DOR activation, followed by phosphorylation-dependent GluR1 trafficking and AMPAR function enhancement in the spinal cord.	Remifentanil	83-95	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	187-192
29372092-0	2017	Intravenous Remifentanil Analgaesia for an Obstetric Patient with Type I Neurofibromatosis and a Factor V Leiden Mutation.	Remifentanil	12-24	coagulation factor V	Homo sapiens	97-112
29363836-4	2018	Using a rat model of OIH, we found that incision- and remifentanil-induced mechanical allodynia were remarkably attenuated by pretreatment with Ru360, a specific MCU antagonist, suggesting a critical role of MCU in both incision- and opioid-induced allodynia.	Remifentanil	54-66	mitochondrial calcium uniporter	Rattus norvegicus	162-165
29363836-4	2018	Using a rat model of OIH, we found that incision- and remifentanil-induced mechanical allodynia were remarkably attenuated by pretreatment with Ru360, a specific MCU antagonist, suggesting a critical role of MCU in both incision- and opioid-induced allodynia.	Remifentanil	54-66	mitochondrial calcium uniporter	Rattus norvegicus	208-211
29363836-6	2018	Western blot and immunohistochemistry showed that pNR [phosphorylated N-methyl-D-aspartate (NMDA) receptor] and pERK (phosphorylated extracellular signal-regulated kinase) are increased during both incision-induced hyperalgesia and remifentanil-induced hyperalgesia, and again the increases in pNR and pERK were remarkably attenuated by Ru360.	Remifentanil	232-244	trace amine associated receptor 5	Homo sapiens	50-53
29363836-6	2018	Western blot and immunohistochemistry showed that pNR [phosphorylated N-methyl-D-aspartate (NMDA) receptor] and pERK (phosphorylated extracellular signal-regulated kinase) are increased during both incision-induced hyperalgesia and remifentanil-induced hyperalgesia, and again the increases in pNR and pERK were remarkably attenuated by Ru360.	Remifentanil	232-244	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	112-116
29643876-6	2018	FLA and FGA groups used less propofol, remifentanil and fentanyl than GA group (P&lt;0.01), with shorter recovery time and extubation time (P&lt;0.05).	Remifentanil	39-51	fibrinogen alpha chain	Homo sapiens	8-11
29755652-0	2018	Correlation of MDR1 gene polymorphism with propofol combined with remifentanil anesthesia in pediatric tonsillectomy.	Remifentanil	66-78	ATP binding cassette subfamily B member 1	Homo sapiens	15-19
29434817-0	2018	Delta-opioid receptor inhibition prevents remifentanil-induced post-operative hyperalgesia via regulating GluR1 trafficking and AMPA receptor function.	Remifentanil	42-54	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	106-111
29434817-2	2018	A previous study by our group suggested that the trafficking and function of glutamate receptor 1 (GluR1) subunits contributes to remifentanil-induced hyperalgesia by regulating the phosphorylation of GluR1 in dorsal horn neurons.	Remifentanil	130-142	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	77-97
29434817-2	2018	A previous study by our group suggested that the trafficking and function of glutamate receptor 1 (GluR1) subunits contributes to remifentanil-induced hyperalgesia by regulating the phosphorylation of GluR1 in dorsal horn neurons.	Remifentanil	130-142	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	99-104
29434817-2	2018	A previous study by our group suggested that the trafficking and function of glutamate receptor 1 (GluR1) subunits contributes to remifentanil-induced hyperalgesia by regulating the phosphorylation of GluR1 in dorsal horn neurons.	Remifentanil	130-142	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	201-206
28763358-4	2017	Like remifentanil, the beta-1-adrenoreceptor antagonist may be used to attenuate the stress reaction to tracheal intubation and to modify perioperative anesthetic requirements.	Remifentanil	5-17	adrenoceptor beta 1	Homo sapiens	23-44
29118914-6	2017	In addition, in response to a nociceptive stimulus, the infusion of 10 microg kg-1 h-1 remifentanil reduced isoflurane-induced apoptosis in the hippocampus (P = 0.003 in CA1, P = 0.002 in CA3) but not in the cortex or thalamus.	Remifentanil	87-99	carbonic anhydrase 1	Rattus norvegicus	170-173
29118914-6	2017	In addition, in response to a nociceptive stimulus, the infusion of 10 microg kg-1 h-1 remifentanil reduced isoflurane-induced apoptosis in the hippocampus (P = 0.003 in CA1, P = 0.002 in CA3) but not in the cortex or thalamus.	Remifentanil	87-99	carbonic anhydrase 3	Rattus norvegicus	188-191
29077151-3	2017	Therefore, the aim of the present study was to assess the association between blood remifentanil concentrations measured after pneumoperitoneum and cortisol (CORT) or prolactin (PRL) ratio (intraoperative/preoperative value), in patients undergoing laparoscopic cholecystectomy.	Remifentanil	84-96	cortistatin	Homo sapiens	158-162
29077151-9	2017	RESULTS: A significant inverse correlation was found between CORT ratio and measured blood remifentanil concentration (p=0.03) or planned remifentanil dose (p=0.04).	Remifentanil	91-103	cortistatin	Homo sapiens	61-65
29077151-9	2017	RESULTS: A significant inverse correlation was found between CORT ratio and measured blood remifentanil concentration (p=0.03) or planned remifentanil dose (p=0.04).	Remifentanil	138-150	cortistatin	Homo sapiens	61-65
29077151-11	2017	CONCLUSIONS: Our data suggest that the CORT response to surgical stress is more efficiently counteracted by increased blood remifentanil concentration.	Remifentanil	124-136	cortistatin	Homo sapiens	39-43
28436446-8	2017	We discovered that pDNA-IL-10 treatment reduces remifentanil self-administration in a drug-concentration-dependent manner, similar to the effect of handling.	Remifentanil	48-60	interleukin 10	Rattus norvegicus	19-29
29114415-9	2017	Results: The mean dosage of remifentanil administered as a continuous infusion was 0.029+-0.0042 mug kg-1 min-1.	Remifentanil	28-40	CD59 molecule (CD59 blood group)	Homo sapiens	106-111
28673877-5	2017	In comparison to baseline, remifentanil infusion &gt;0.05mug/Kg-1/min-1 produced a significant reduction of Ti/Ttotneu and Ti/Ttotmec, by prolonging the expiratory time.	Remifentanil	27-39	CD59 molecule (CD59 blood group)	Homo sapiens	66-71
28853509-4	2017	In group PR, a remifentanil infusion with a target plasma concentration of 1 ng mL-1 was started until the operation was finished.	Remifentanil	15-27	L1 cell adhesion molecule	Mus musculus	80-84
28199982-0	2017	N-acetyl-cysteine attenuates remifentanil-induced postoperative hyperalgesia via inhibiting matrix metalloproteinase-9 in dorsal root ganglia.	Remifentanil	29-41	matrix metallopeptidase 9	Rattus norvegicus	92-118
28743151-0	2017	[Remifentanil Up2date - Part 1].	Remifentanil	1-13	uroplakin 2	Homo sapiens	14-17
28693245-12	2017	In conclusion, anesthesia with remifentanil better maintained the stability of hemodynamics, played a protective role against hepatic ischemia-reperfusion injury, and reduced ICAM-1 expression.	Remifentanil	31-43	intercellular adhesion molecule 1	Homo sapiens	175-181
28558702-1	2017	BACKGROUND: Administration of arginine vasopressin (AVP) is associated with reducing jugular venous (SjvO2) and regional cerebral (rScO2) oxygen saturation under propofol-remifentanil (P/R) anaesthesia.	Remifentanil	171-183	arginine vasopressin	Homo sapiens	39-50
27380044-1	2017	Up-regulation of GluN2B-containing N-methyl-D-aspartate receptors (NMDARs) expression and trafficking is the key mechanism for remifentanil-induced hyperalgesia (RIH), nevertheless, the signaling pathway and pivotal proteins involved in RIH remain equivocal.	Remifentanil	127-139	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	17-23
27380044-7	2017	ZIP (10 ng) could block behavioral sensitization induced by remifentanil.	Remifentanil	60-72	sequestosome 1	Rattus norvegicus	0-3
28359934-0	2017	CXCL13 regulates the trafficking of GluN2B-containing NMDA receptor via IL-17 in the development of remifentanil-induced hyperalgesia in rats.	Remifentanil	100-112	C-X-C motif chemokine ligand 13	Rattus norvegicus	0-6
28359934-0	2017	CXCL13 regulates the trafficking of GluN2B-containing NMDA receptor via IL-17 in the development of remifentanil-induced hyperalgesia in rats.	Remifentanil	100-112	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	36-42
28359934-0	2017	CXCL13 regulates the trafficking of GluN2B-containing NMDA receptor via IL-17 in the development of remifentanil-induced hyperalgesia in rats.	Remifentanil	100-112	interleukin 17A	Rattus norvegicus	72-77
28359934-1	2017	BACKGROUND: This study aimed to investigate whether CXCL13 modulated the trafficking of NMDA receptor via interleukin (IL)-17 in a rat model of remifentanil-induced hyperalgesia (RIH).Although chemokines are crucial regulators of neuroinflammation, spinal N-methyl-d-aspartate (NMDA) receptor activation, and development of hypernociceptive process, little is known about specific pathogenesis and effective treatment.	Remifentanil	144-156	C-X-C motif chemokine ligand 13	Rattus norvegicus	52-58
28359934-7	2017	RESULTS: This study found mechanical allodynia and thermal hyperalgesia with a remarkable increase in the expression of spinal CXCL13/CXCR5 and IL-17/IL-17RA and trafficking of GluN2B-containing NMDA receptor after remifentanil exposure.	Remifentanil	215-227	C-X-C motif chemokine ligand 13	Rattus norvegicus	127-133
28359934-7	2017	RESULTS: This study found mechanical allodynia and thermal hyperalgesia with a remarkable increase in the expression of spinal CXCL13/CXCR5 and IL-17/IL-17RA and trafficking of GluN2B-containing NMDA receptor after remifentanil exposure.	Remifentanil	215-227	C-X-C motif chemokine receptor 5	Rattus norvegicus	134-139
28359934-7	2017	RESULTS: This study found mechanical allodynia and thermal hyperalgesia with a remarkable increase in the expression of spinal CXCL13/CXCR5 and IL-17/IL-17RA and trafficking of GluN2B-containing NMDA receptor after remifentanil exposure.	Remifentanil	215-227	interleukin 17A	Rattus norvegicus	144-149
28359934-7	2017	RESULTS: This study found mechanical allodynia and thermal hyperalgesia with a remarkable increase in the expression of spinal CXCL13/CXCR5 and IL-17/IL-17RA and trafficking of GluN2B-containing NMDA receptor after remifentanil exposure.	Remifentanil	215-227	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	177-183
28199982-6	2017	The results indicated that intraoperative remifentanil induced an up-regulation and activation of MMP-9 in DRGs but not spinal cords.	Remifentanil	42-54	matrix metallopeptidase 9	Rattus norvegicus	98-103
26598295-7	2017	Similarly, the Ox1R antagonist attenuated cue-induced, but not drug-induced, reinstatement of remifentanil seeking in low takers but had no significant effect on reinstatement of drug seeking in high takers.	Remifentanil	94-106	hypocretin receptor 1	Rattus norvegicus	15-19
28039043-0	2017	Cathepsin S in the spinal microglia contributes to remifentanil-induced hyperalgesia in rats.	Remifentanil	51-63	cathepsin S	Rattus norvegicus	0-11
28039043-3	2017	In the present study, intravenous remifentanil infusion induced a significant increase in the expression of premature and mature form of CatS in the activated microglia in the spinal cord.	Remifentanil	34-46	cathepsin S	Felis catus	137-141
28039043-4	2017	Spinal delivery of irreversible CatS inhibitor LHVS reduced hyperalgesia, attenuated activation of spinal microglia and blocked phosphorylation of NMDA receptor NR1 subunit induced by remifentanil.	Remifentanil	184-196	cathepsin S	Felis catus	32-36
28133690-2	2017	OBJECTIVES: To evaluate the influence of the ORM1 variants in codon 118 on the intra-operative remifentanil consumption under general anesthesia.	Remifentanil	95-107	orosomucoid 1	Homo sapiens	45-49
28145661-0	2017	The Effects of Remifentanil on Expression of High Mobility Group Box 1 in Septic Rats.	Remifentanil	15-27	high mobility group box 1	Rattus norvegicus	45-70
28145661-3	2017	However, it is not yet known whether remifentanil affects the expression of HMGB1.	Remifentanil	37-49	high mobility group box 1	Rattus norvegicus	76-81
28145661-4	2017	We investigated the effects of remifentanil on HMGB1 expression and the underlying mechanism in septic rats.	Remifentanil	31-43	high mobility group box 1	Rattus norvegicus	47-52
28145661-8	2017	We found that remifentanil treatment suppressed the level of serum interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha 6 hours after CLP, and serum HMGB1 24 hours after CLP.	Remifentanil	14-26	interleukin 6	Rattus norvegicus	67-85
28145661-8	2017	We found that remifentanil treatment suppressed the level of serum interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha 6 hours after CLP, and serum HMGB1 24 hours after CLP.	Remifentanil	14-26	tumor necrosis factor	Rattus norvegicus	90-123
28145661-8	2017	We found that remifentanil treatment suppressed the level of serum interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha 6 hours after CLP, and serum HMGB1 24 hours after CLP.	Remifentanil	14-26	high mobility group box 1	Rattus norvegicus	153-158
28145661-9	2017	HMGB1 mRNA levels and the activity of NF-kappaB in multiple organs decreased by remifentanil treatment 24 hours after CLP.	Remifentanil	80-92	high mobility group box 1	Rattus norvegicus	0-5
28145661-11	2017	Altogether, these results suggested that remifentanil inhibited expression of HMGB1 in vital organs and release of HMGB1 into plasma.	Remifentanil	41-53	high mobility group box 1	Rattus norvegicus	78-83
28145661-11	2017	Altogether, these results suggested that remifentanil inhibited expression of HMGB1 in vital organs and release of HMGB1 into plasma.	Remifentanil	41-53	high mobility group box 1	Rattus norvegicus	115-120
28296782-11	2017	Total cumulative dose of dexmedetomidine was more in DR2 and DR3 groups (P = 0.000), while the amount of remifentanil was more in DR1 and DR2 groups (P = 0.000).	Remifentanil	105-117	down-regulator of transcription 1	Homo sapiens	130-133
28222697-0	2017	Magnesium sulphate attenuate remifentanil-induced postoperative hyperalgesia via regulating tyrosine phosphorylation of the NR2B subunit of the NMDA receptor in the spinal cord.	Remifentanil	29-41	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	124-128
28222697-3	2017	We hypothesized that intrathecal MgSO4 could relieve hyperalgesia after remifentanil infusion via regulating phosphorylation of NMDA receptor NR2B subunit activity in this study.	Remifentanil	72-84	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	142-146
28222697-10	2017	CONCLUSIONS: Remifentanil induced hyperalgesia/allodynia could be ameliorated by Mg-mediated blockade targeting the NR2B subunit in NMDA receptors.	Remifentanil	13-25	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	116-120
28182698-0	2017	Prevention of Remifentanil Induced Postoperative Hyperalgesia by Dexmedetomidine via Regulating the Trafficking and Function of Spinal NMDA Receptors as well as PKC and CaMKII Level In Vivo and In Vitro.	Remifentanil	14-26	protein kinase C, gamma	Rattus norvegicus	161-164
28182698-3	2017	In the current study, it was demonstrated that dexmedetomidine could prevent remifentanil-induced hyperalgesia (RIH) via regulating spinal NMDAR-PKC-Ca2+/ CaMKII pathway in vivo and in vitro.	Remifentanil	77-89	protein kinase C, gamma	Rattus norvegicus	145-148
28182698-9	2017	Subcutaneously injection of dexmedetomidine at the dose of 50 mug/kg at 30 min before plantar incision significantly attenuated remifentanil-induced mechanical and thermal hyperalgesia from 2 h to 48 h after infusion, and this was associated with reversal of up-regulated NR1 and NR2B subunits in both membrane fraction and total lysate as well as increased PKC and CaMKII expression in spinal cord dorsal horn.	Remifentanil	128-140	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	272-275
28182698-9	2017	Subcutaneously injection of dexmedetomidine at the dose of 50 mug/kg at 30 min before plantar incision significantly attenuated remifentanil-induced mechanical and thermal hyperalgesia from 2 h to 48 h after infusion, and this was associated with reversal of up-regulated NR1 and NR2B subunits in both membrane fraction and total lysate as well as increased PKC and CaMKII expression in spinal cord dorsal horn.	Remifentanil	128-140	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	280-284
28182698-9	2017	Subcutaneously injection of dexmedetomidine at the dose of 50 mug/kg at 30 min before plantar incision significantly attenuated remifentanil-induced mechanical and thermal hyperalgesia from 2 h to 48 h after infusion, and this was associated with reversal of up-regulated NR1 and NR2B subunits in both membrane fraction and total lysate as well as increased PKC and CaMKII expression in spinal cord dorsal horn.	Remifentanil	128-140	protein kinase C, gamma	Rattus norvegicus	358-361
28184263-2	2017	We reported previously that supplemental DHB decreased the BIS after the administration of sevoflurane and remifentanil.	Remifentanil	107-119	DNA helicase B	Homo sapiens	41-44
28133690-7	2017	The Remifentanil dose was calculated and correlated with ORM1 genotype variance.	Remifentanil	4-16	orosomucoid 1	Homo sapiens	57-61
28133690-11	2017	There was a significant effect of ORM1 genotype variant and the amount of remifentanil consumed.	Remifentanil	74-86	orosomucoid 1	Homo sapiens	34-38
28133690-13	2017	Conclusion: The ORM1 gene has a role in intra-operative remifentanil consumption in patients who underwent septoplasty surgery under general anesthesia.	Remifentanil	56-68	orosomucoid 1	Homo sapiens	16-20
27492364-0	2016	Remifentanil preconditioning protects rat cardiomyocytes against hypoxia-reoxygenation injury via delta-opioid receptor mediated activation of PI3K/Akt and ERK pathways.	Remifentanil	0-12	AKT serine/threonine kinase 1	Rattus norvegicus	148-151
27752976-7	2017	Changes in cholinesterase enzyme function may affect the disposition of succinylcholine, benzylisoquinoline muscle relaxants, remifentanil, and hydralazine.	Remifentanil	126-138	butyrylcholinesterase	Homo sapiens	11-25
28425312-0	2017	Activation of spinal alpha-7 nicotinic acetylcholine receptor shortens the duration of remifentanil-induced postoperative hyperalgesia by upregulating KCC2 in the spinal dorsal horn in rats.	Remifentanil	87-99	solute carrier family 12 member 5	Rattus norvegicus	151-155
28425312-4	2017	Results We demonstrated that the brain-derived neurotrophic factor/tyrosine receptor kinase B-K+-Cl- cotransporter-2 signal played a critical role in the development of remifentanil-induced postoperative hyperalgesia.	Remifentanil	169-181	solute carrier family 12 member 5	Rattus norvegicus	94-116
28425312-6	2017	Simultaneously, remifentanil-induced postoperative hyperalgesia-induced K+-Cl- cotransporter-2 downregulation was partly reversed and coincided with a decreased expression of brain-derived neurotrophic factor/tyrosine receptor kinase B in the spinal dorsal horn, approximately correlating with the time course of the nociceptive behavior.	Remifentanil	16-28	solute carrier family 12 member 5	Rattus norvegicus	72-94
28425312-7	2017	Moreover, intrathecal administration of the K+-Cl- cotransporter-2 inhibitor VU0240551 significantly reduced the analgesic effect of PNU-120596 on remifentanil-induced postoperative hyperalgesia.	Remifentanil	147-159	solute carrier family 12 member 5	Rattus norvegicus	44-66
28425312-8	2017	Conclusions The activation of alpha-7 nicotinic acetylcholine receptors induced a shorter duration of remifentanil-induced postoperative hyperalgesia by restoring the brain-derived neurotrophic factor/tyrosine receptor kinase B-K+-Cl- cotransporter-2 signal in the spinal dorsal horn of rats, which provides new insight into treatment in clinical postoperative pain management.	Remifentanil	102-114	solute carrier family 12 member 5	Rattus norvegicus	228-250
27871564-7	2016	The groups were comparable regarding to POCD incidence; however, IL-6 levels were lower the seventh day after surgery for remifentanil group (P= .04).	Remifentanil	122-134	interleukin 6	Homo sapiens	65-69
27637388-8	2016	ROS production, phosphorylated NR1 and NR2B subunits of NMDA receptor were found to be significantly increased in the spinal dorsal horn after intraoperative remifentanil infusion.	Remifentanil	158-170	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	31-34
27637388-8	2016	ROS production, phosphorylated NR1 and NR2B subunits of NMDA receptor were found to be significantly increased in the spinal dorsal horn after intraoperative remifentanil infusion.	Remifentanil	158-170	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	39-43
27734470-4	2016	However, it appears that intra-operative remifentanil infusion rates of above 0.25 mug.kg-1 .min-1 are associated with higher postoperative opioid consumption, suggesting tolerance.	Remifentanil	41-53	CD59 molecule (CD59 blood group)	Homo sapiens	93-98
27616703-0	2016	Spinal WNT pathway contributes to remifentanil induced hyperalgesia through regulating fractalkine and CX3CR1 in rats.	Remifentanil	34-46	Wnt family member 2	Rattus norvegicus	7-10
27616703-0	2016	Spinal WNT pathway contributes to remifentanil induced hyperalgesia through regulating fractalkine and CX3CR1 in rats.	Remifentanil	34-46	C-X3-C motif chemokine ligand 1	Rattus norvegicus	87-98
27616703-0	2016	Spinal WNT pathway contributes to remifentanil induced hyperalgesia through regulating fractalkine and CX3CR1 in rats.	Remifentanil	34-46	C-X3-C motif chemokine receptor 1	Rattus norvegicus	103-109
27616703-8	2016	RESULTS: We found that postsurgical mechanical and thermal hyperalgesia could be engendered after remifentanil exposure, which was accompanied by a dramatical rise of spinal WNT3a, FZ8, beta-catenin, fractalkine and CX3CR1 levels.	Remifentanil	98-110	Wnt family member 3A	Rattus norvegicus	174-179
27616703-8	2016	RESULTS: We found that postsurgical mechanical and thermal hyperalgesia could be engendered after remifentanil exposure, which was accompanied by a dramatical rise of spinal WNT3a, FZ8, beta-catenin, fractalkine and CX3CR1 levels.	Remifentanil	98-110	frizzled class receptor 8	Rattus norvegicus	181-184
27616703-8	2016	RESULTS: We found that postsurgical mechanical and thermal hyperalgesia could be engendered after remifentanil exposure, which was accompanied by a dramatical rise of spinal WNT3a, FZ8, beta-catenin, fractalkine and CX3CR1 levels.	Remifentanil	98-110	catenin beta 1	Rattus norvegicus	186-198
27616703-8	2016	RESULTS: We found that postsurgical mechanical and thermal hyperalgesia could be engendered after remifentanil exposure, which was accompanied by a dramatical rise of spinal WNT3a, FZ8, beta-catenin, fractalkine and CX3CR1 levels.	Remifentanil	98-110	C-X3-C motif chemokine ligand 1	Rattus norvegicus	200-211
27616703-8	2016	RESULTS: We found that postsurgical mechanical and thermal hyperalgesia could be engendered after remifentanil exposure, which was accompanied by a dramatical rise of spinal WNT3a, FZ8, beta-catenin, fractalkine and CX3CR1 levels.	Remifentanil	98-110	C-X3-C motif chemokine receptor 1	Rattus norvegicus	216-222
27616703-10	2016	Up-regulation of spinal fractalkine and CX3CR1 expression after remifentanil anesthesia was reversed by Fz-8/Fc.	Remifentanil	64-76	C-X3-C motif chemokine ligand 1	Rattus norvegicus	24-35
27616703-10	2016	Up-regulation of spinal fractalkine and CX3CR1 expression after remifentanil anesthesia was reversed by Fz-8/Fc.	Remifentanil	64-76	C-X3-C motif chemokine receptor 1	Rattus norvegicus	40-46
27616703-10	2016	Up-regulation of spinal fractalkine and CX3CR1 expression after remifentanil anesthesia was reversed by Fz-8/Fc.	Remifentanil	64-76	frizzled class receptor 8	Rattus norvegicus	104-108
28714352-2	2017	However, the mechanism of opioid-induced hyperalgesia development and in particular the potential interplay between N-methyl-D-aspartate receptors and protein kinase C or calcium/calmodulin-dependent protein kinase II or extracellular signal-regulated kinase 1/2 in the development of remifentanil-induced hyperalgesia is unclear.	Remifentanil	285-297	mitogen activated protein kinase 3	Rattus norvegicus	221-262
28714352-8	2017	The expressions of NR1, NR2B, p-NR1, and p-NR2B were increased significantly and progressively over time after remifentanil administration, and these increases were all significantly attenuated by either chelerythrine or KN93 but not PD98059.	Remifentanil	111-123	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	19-22
28714352-8	2017	The expressions of NR1, NR2B, p-NR1, and p-NR2B were increased significantly and progressively over time after remifentanil administration, and these increases were all significantly attenuated by either chelerythrine or KN93 but not PD98059.	Remifentanil	111-123	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	24-28
28714352-8	2017	The expressions of NR1, NR2B, p-NR1, and p-NR2B were increased significantly and progressively over time after remifentanil administration, and these increases were all significantly attenuated by either chelerythrine or KN93 but not PD98059.	Remifentanil	111-123	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	32-35
28714352-8	2017	The expressions of NR1, NR2B, p-NR1, and p-NR2B were increased significantly and progressively over time after remifentanil administration, and these increases were all significantly attenuated by either chelerythrine or KN93 but not PD98059.	Remifentanil	111-123	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	43-47
26462495-4	2016	At the beginning of anaesthesia induction, continuous infusion of remifentanil (1 mug min-1 kg-1) preceded hypnosis with propofol in 13 patients [non-hypnosis group; mean age, 67.8 (17.5) years], while propofol bolus (30-50 mg) was injected together with continuous remifentanil medication in 18 patients [hypnosis group; mean age, 62.9 (16.5) years].	Remifentanil	66-78	CD59 molecule (CD59 blood group)	Homo sapiens	86-96
28879314-11	2016	As determined via western blot analysis, remifentanil pretreatment increased the expression of bone-related genes (Col I, BMP-2, osterix, and TGF-beta).	Remifentanil	41-53	bone morphogenetic protein 2	Homo sapiens	122-127
28879314-11	2016	As determined via western blot analysis, remifentanil pretreatment increased the expression of bone-related genes (Col I, BMP-2, osterix, and TGF-beta).	Remifentanil	41-53	Sp7 transcription factor	Homo sapiens	129-136
30379462-3	2016	The patient received inhalation induction with 5% sevoflurane and an infusion of remifentanil (0.2mug   kg-1   min-1).	Remifentanil	81-93	CD59 molecule (CD59 blood group)	Homo sapiens	111-116
27492364-0	2016	Remifentanil preconditioning protects rat cardiomyocytes against hypoxia-reoxygenation injury via delta-opioid receptor mediated activation of PI3K/Akt and ERK pathways.	Remifentanil	0-12	Eph receptor B1	Rattus norvegicus	156-159
27492364-8	2016	Following remifentanil preconditioning, the phosphorylation level of Akt reached peak at 10min of reoxygenation.	Remifentanil	10-22	AKT serine/threonine kinase 1	Rattus norvegicus	69-72
27492364-12	2016	In conclusion, our results suggested that remifentanil protected adult rat cardiomyocytes from hypoxia-reoxygenation injury and its effects appears to be dependent on the delta-opioid receptor mediated activation of PI3K/Akt and subsequent ERK signaling pathways.	Remifentanil	42-54	AKT serine/threonine kinase 1	Rattus norvegicus	221-224
27492364-12	2016	In conclusion, our results suggested that remifentanil protected adult rat cardiomyocytes from hypoxia-reoxygenation injury and its effects appears to be dependent on the delta-opioid receptor mediated activation of PI3K/Akt and subsequent ERK signaling pathways.	Remifentanil	42-54	Eph receptor B1	Rattus norvegicus	240-243
27537764-0	2016	PICK1 Regulates the Expression and Trafficking of AMPA Receptors in Remifentanil-Induced Hyperalgesia.	Remifentanil	68-80	protein interacting with PRKCA 1	Rattus norvegicus	0-5
27537764-5	2016	This study aimed to test the hypothesis that PICK1 contributes to remifentanil-induced hyperalgesia by regulating AMPAR expression and trafficking in the spinal cord.	Remifentanil	66-78	protein interacting with PRKCA 1	Rattus norvegicus	45-50
27537764-10	2016	Remifentanil infusion induced distinct hyperalgesia at different time points (P &lt; .0001), which was partly reversed by PICK1 knockdown (P &lt; .007).	Remifentanil	0-12	protein interacting with PRKCA 1	Rattus norvegicus	122-127
27537764-11	2016	Besides, remifentanil infusion increased the expression of PICK1 mRNA and protein (P &lt; .0001) and the membrane GluR1 and GluR2 internalization in spinal dorsal horn neurons (P &lt; .0011).	Remifentanil	9-21	protein interacting with PRKCA 1	Rattus norvegicus	59-64
27537764-11	2016	Besides, remifentanil infusion increased the expression of PICK1 mRNA and protein (P &lt; .0001) and the membrane GluR1 and GluR2 internalization in spinal dorsal horn neurons (P &lt; .0011).	Remifentanil	9-21	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	114-119
27537764-11	2016	Besides, remifentanil infusion increased the expression of PICK1 mRNA and protein (P &lt; .0001) and the membrane GluR1 and GluR2 internalization in spinal dorsal horn neurons (P &lt; .0011).	Remifentanil	9-21	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	124-129
27537764-12	2016	More importantly, PICK1 deficiency could attenuate remifentanil-induced GluR2 internalization in the spinal cord dorsal horn (P &lt; .01) but had no effect on remifentanil-induced membrane GluR1 expression (P &gt;= .985).	Remifentanil	51-63	protein interacting with PRKCA 1	Rattus norvegicus	18-23
27537764-12	2016	More importantly, PICK1 deficiency could attenuate remifentanil-induced GluR2 internalization in the spinal cord dorsal horn (P &lt; .01) but had no effect on remifentanil-induced membrane GluR1 expression (P &gt;= .985).	Remifentanil	51-63	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	72-77
27537764-13	2016	CONCLUSIONS: These results indicate that PICK1 deficiency might reverse remifentanil-induced hyperalgesia through regulating GluR2-containing AMPAR expression and trafficking in the spinal cord dorsal horn.	Remifentanil	72-84	protein interacting with PRKCA 1	Rattus norvegicus	41-46
27537764-13	2016	CONCLUSIONS: These results indicate that PICK1 deficiency might reverse remifentanil-induced hyperalgesia through regulating GluR2-containing AMPAR expression and trafficking in the spinal cord dorsal horn.	Remifentanil	72-84	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	125-130
27687719-0	2016	The role of p38MAPK activation in spinal dorsal horn in remifentanil-induced postoperative hyperalgesia in rats.	Remifentanil	56-68	mitogen activated protein kinase 14	Rattus norvegicus	12-19
27687719-3	2016	This study aimed to investigate whether the combination of post-surgical and remifentanil-induced hyperalgesia worsens post-operative pain and whether phosphorylated p38MAPK (phospho-p38MAPK) in the spinal dorsal horn in rats is involved in remifentanil-induced postoperative hyperalgesia.	Remifentanil	241-253	mitogen activated protein kinase 14	Rattus norvegicus	183-190
27687719-9	2016	There was a significant increase in the number of dorsal horn phospho-p38MAPK-positive cells in the remifentanil + incision group compared to the incision group, but no increase in the number of these cells when remifentanil was given alone.	Remifentanil	100-112	mitogen activated protein kinase 14	Rattus norvegicus	70-77