PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 19085111-11 2008 Results showed that the maximum permissible cosolvent concentrations for hASBT uptake studies, without compromising assay results or causing cytotoxicity, are 1% DMAC, 1% DMF, 2.5% DMSO, 2.5% methanol, and 2.5% ethanol. dimethylacetamide 162-166 solute carrier family 10 member 2 Homo sapiens 73-78 17503240-8 2007 A 50% decline of serum alanine aminotransferase (ALT) levels after the cessation of DMAc exposure took less than 14 days and a 90% decline less than 31 days. dimethylacetamide 84-88 glutamic--pyruvic transaminase Homo sapiens 23-47 15680597-9 2005 As a trace of DMAc, the band at 1616cm(-1) is disappeared by washing for the cellulose treated with carbon dioxide (Cell 1-C and Cell 2/60-C). dimethylacetamide 14-18 carboxyl ester lipase pseudogene Homo sapiens 116-122 15680597-9 2005 As a trace of DMAc, the band at 1616cm(-1) is disappeared by washing for the cellulose treated with carbon dioxide (Cell 1-C and Cell 2/60-C). dimethylacetamide 14-18 carboxyl ester lipase pseudogene Homo sapiens 129-140 12794545-5 2003 Combinations of DRB1 alleles with or without specific DMA and DMB variants showed significant differences in distributions between the cases and controls, but both of the previously associated class II alleles (DRB1*1501 and DRB1*0701) showed stronger positive associations with DMAC in the absence than in the presence of DMA*0102. dimethylacetamide 279-283 major histocompatibility complex, class II, DR beta 1 Homo sapiens 211-215 12794545-5 2003 Combinations of DRB1 alleles with or without specific DMA and DMB variants showed significant differences in distributions between the cases and controls, but both of the previously associated class II alleles (DRB1*1501 and DRB1*0701) showed stronger positive associations with DMAC in the absence than in the presence of DMA*0102. dimethylacetamide 279-283 major histocompatibility complex, class II, DR beta 1 Homo sapiens 211-215 12794545-6 2003 Apparent joint effects of DRB1 and DM allelic combinations on occurrence and timing of DMAC suggest that class II disease relationships may be better predicted by biologically plausible interactive combinations than by polymorphisms in individual genes. dimethylacetamide 87-91 major histocompatibility complex, class II, DR beta 1 Homo sapiens 26-30 12425666-1 2002 Dynamics of cellulose diacetate (CDA, the total degree of substitution (TDS) = 2.44) in dimethylacetamide (DMAc) in dilute solution was investigated at 2, 10, 20, 30, 40, 49.7, and 61.5 degrees C through dynamic light scattering in the quiescent state. dimethylacetamide 88-105 cytidine deaminase Homo sapiens 33-36 12425666-3 2002 First, CDA existed in three types of structures in the polar solvent, DMAc; one is a single CDA chain, and the others are dynamic structures, or self-assemblies, which were formed temporarily and locally by the solvent-mediated hydrogen bonding between the intermolecular C-6 position hydroxyls of the anhydroglucose units in the CDA backbone. dimethylacetamide 70-74 cytidine deaminase Homo sapiens 7-10 12425666-4 2002 Second, CDA showed a nature of low-temperature solubility in DMAc, that is, CDA is expected to dissolve molecularly below -12 degrees C but to take a phase separation above 65 degrees C, where two structures such as collapses of a single CDA chain and an aggregate appear. dimethylacetamide 61-65 cytidine deaminase Homo sapiens 8-11 12425666-4 2002 Second, CDA showed a nature of low-temperature solubility in DMAc, that is, CDA is expected to dissolve molecularly below -12 degrees C but to take a phase separation above 65 degrees C, where two structures such as collapses of a single CDA chain and an aggregate appear. dimethylacetamide 61-65 cytidine deaminase Homo sapiens 76-79 12425666-4 2002 Second, CDA showed a nature of low-temperature solubility in DMAc, that is, CDA is expected to dissolve molecularly below -12 degrees C but to take a phase separation above 65 degrees C, where two structures such as collapses of a single CDA chain and an aggregate appear. dimethylacetamide 61-65 cytidine deaminase Homo sapiens 76-79 12425666-6 2002 In view of the low-temperature solubility of CDA in DMAc, this abnormal behavior around T was explained by dynamical critical-like fluctuations if T were treated as a kind of lower critical solution temperature (LCST) in the CDA/DMAc system. dimethylacetamide 52-56 cytidine deaminase Homo sapiens 45-48 12425666-6 2002 In view of the low-temperature solubility of CDA in DMAc, this abnormal behavior around T was explained by dynamical critical-like fluctuations if T were treated as a kind of lower critical solution temperature (LCST) in the CDA/DMAc system. dimethylacetamide 52-56 cytidine deaminase Homo sapiens 225-228 12425666-6 2002 In view of the low-temperature solubility of CDA in DMAc, this abnormal behavior around T was explained by dynamical critical-like fluctuations if T were treated as a kind of lower critical solution temperature (LCST) in the CDA/DMAc system. dimethylacetamide 229-233 cytidine deaminase Homo sapiens 45-48 11684362-0 2001 Inactivation of rat liver cytochrome P450 (P450) by N,N-dimethylformamide and N,N-dimethylacetamide. dimethylacetamide 78-99 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 26-41 11176565-12 2001 Analysis of CD4 counts at the time of DMAC, CMV and PCP provide validation for current prophylaxis guidelines in children > or =2 years old. dimethylacetamide 38-42 CD4 molecule Homo sapiens 12-15 9877361-4 1998 These guidelines incorporate age-specific CD4 counts at which DMAC prophylaxis should be used. dimethylacetamide 62-66 CD4 molecule Homo sapiens 42-45 9803090-12 1998 We concluded that the risk of DMAC infection in advanced AIDS patients in Thailand is high when low CD4 lymphocyte count is established. dimethylacetamide 30-34 CD4 molecule Homo sapiens 100-103 9696194-4 1998 We aim to determine if G-CSF administration is associated with improved survival in patients with DMAC in a retrospective, cohort study. dimethylacetamide 98-102 colony stimulating factor 3 Homo sapiens 23-28 9696194-13 1998 Addition of G-CSF to a regimen of clarithromycin and ethambutol may increase survival in DMAC and should be studied prospectively. dimethylacetamide 89-93 colony stimulating factor 3 Homo sapiens 12-17 8434128-2 1993 Dimethylsulfoxide (DMSO), dimethylformamide, dimethyl-acetamide, ethanol, and methanol all reduced NAT II activity in concentrations ranging from 1.25 to 10%. dimethylacetamide 45-63 N-acetyltransferase 1 Rattus norvegicus 99-102 1881866-4 1991 In contrast to a previous report, we find that incorporation of label into the B29 - B30 peptide bond occurs during the transformation with threonine methyl ester in aqueous N,N-dimethylacetamide. dimethylacetamide 174-195 CD79b molecule Homo sapiens 79-82 1820039-3 1991 Trypsin was used to convert the precursors, GRF(1-43)-OH and GRF(1-44)-OH, to GRF(1-44)-NH2 (60 and 15% conversion, respectively) in a 75% v:v N,N"-dimethylacetamide solution containing a large excess of leucine amide. dimethylacetamide 143-165 growth hormone releasing hormone Homo sapiens 44-47 34791877-3 2021 In the present study, a LiF-rich protection layer has been developed using self-driven chemical reactions between the Li3xLa2/3-xTiO3/polyvinylidene fluoride/dimethylacetamide (LLTO/PVDF/DMAc) solution and the Li metal. dimethylacetamide 158-175 LIF interleukin 6 family cytokine Homo sapiens 24-27 35429488-5 2022 Increasing both DMA and NMA concentration from 2 to 6% improved SMI, total motile sperm, progressive motile sperm (PMS), VCL, VSL and VAP values. dimethylacetamide 16-19 vinculin Gallus gallus 121-124 35349119-2 2022 Recently, we discovered that the common drug excipient, N,N-dimethylacetamide (DMA), delays inflammation-induced preterm birth in mice by inhibiting NF-kappaB. dimethylacetamide 56-77 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 149-158 35349119-2 2022 Recently, we discovered that the common drug excipient, N,N-dimethylacetamide (DMA), delays inflammation-induced preterm birth in mice by inhibiting NF-kappaB. dimethylacetamide 79-82 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 149-158 35349119-5 2022 Like DMA, DMF protects IkappaBalpha from degradation and prevents the p65 subunit of NF-kappaB from translocating to the nucleus. dimethylacetamide 5-8 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha Mus musculus 23-35 6271894-5 1981 Undifferentiated PCC4 cells could be differentiated when propagated in the presence of dimethylacetamide, as judged by changes in the expression of H-2 antigens on the cell surface. dimethylacetamide 87-104 histocompatibility-2, MHC Mus musculus 148-151 810367-1 1975 Penicillin V (S)-sulphoxide (I), treated with methanesulphonic acid in benzene and dimethylacetamide, gives the decarboxylated increment3-cephem compound (IV) and a new product of rearrangement to which the structure of the 4-[N-(1"-carboxy-2"-methylenepropyl)carbamoyl]-2-phenoxymethylthiazole (VIII) is ascribed. dimethylacetamide 83-100 cytochrome c oxidase subunit 8A Homo sapiens 296-300 33251424-5 2020 In contrast, the dielectric constants increased with the increase in temperature for the GBL/DMAC cosolvent system. dimethylacetamide 93-97 MTOR associated protein, LST8 homolog Homo sapiens 89-92 33156759-4 2020 Nevertheless, DMAC was characterised by a lower median CD4 count (5.0 cells/microL vs. 38.5 cells/microL, P < 0.001), lower median body mass index (BMI) (17.7 kg/m2 vs. 19.7 kg/m2, P = 0.002) and the absence of chest radiographic findings (P < 0.001). dimethylacetamide 14-18 CD4 molecule Homo sapiens 55-58 33156759-5 2020 Simultaneous presence of CD4 <20 cells/microl, BMI <18.5 kg/m2 and negative chest radiographic finding had a 98% specificity for diagnosing DMAC against TB or other types of mycobacterial infections.CONCLUSION: DMAC is an important differential diagnosis of TB in HIV patients. dimethylacetamide 140-144 CD4 molecule Homo sapiens 25-28 33156759-5 2020 Simultaneous presence of CD4 <20 cells/microl, BMI <18.5 kg/m2 and negative chest radiographic finding had a 98% specificity for diagnosing DMAC against TB or other types of mycobacterial infections.CONCLUSION: DMAC is an important differential diagnosis of TB in HIV patients. dimethylacetamide 211-215 CD4 molecule Homo sapiens 25-28 33156759-6 2020 A simple rule based on CD4, BMI and chest radiography may inform the decision to start anti-DMAC treatment in patients with mycobacterial infection. dimethylacetamide 92-96 CD4 molecule Homo sapiens 23-26 31693155-10 2020 CONCLUSIONS: The drugs above are sufficient to rescue functional loss in DMAc-induced toxic hepatitis, in part via the regulations of ALT, AST, LDH, bilirubin and ammonia. dimethylacetamide 73-77 solute carrier family 17 member 5 Homo sapiens 139-142 32212676-2 2020 Here, we report a highly concentrated 5.0 M lithium nitrate (LiNO3) in N,N-dimethylacetamide (DMA) with TEMPO as a redox mediator (RM) and with the LiF layer by adding DMTFA in the electrolyte, which reduces the charge voltage (3.6 V over 65 cycles), and allows stable cycling for 100 cycles without noticeably fading in capacity. dimethylacetamide 94-97 LIF interleukin 6 family cytokine Homo sapiens 148-151 31659523-4 2019 RESULTS: Solid phase extraction with Cu (OTf)2 in dimethylacetamide is a suitable activation method for [18F]fluoride. dimethylacetamide 50-67 POU class 2 homeobox 2 Homo sapiens 41-46 31152802-5 2019 NMP and DMA pre-treatment recovered TNFalpha-inhibited expression of essential osteoblastic genes, Alp, Runx2, and Osterix as well as mineralization in multipotent stem cells, but not in pre-osteoblasts and calvarial osteoblasts. dimethylacetamide 8-11 tumor necrosis factor Homo sapiens 36-44 31152802-5 2019 NMP and DMA pre-treatment recovered TNFalpha-inhibited expression of essential osteoblastic genes, Alp, Runx2, and Osterix as well as mineralization in multipotent stem cells, but not in pre-osteoblasts and calvarial osteoblasts. dimethylacetamide 8-11 ATHS Homo sapiens 99-102 31152802-5 2019 NMP and DMA pre-treatment recovered TNFalpha-inhibited expression of essential osteoblastic genes, Alp, Runx2, and Osterix as well as mineralization in multipotent stem cells, but not in pre-osteoblasts and calvarial osteoblasts. dimethylacetamide 8-11 RUNX family transcription factor 2 Homo sapiens 104-109 31152802-5 2019 NMP and DMA pre-treatment recovered TNFalpha-inhibited expression of essential osteoblastic genes, Alp, Runx2, and Osterix as well as mineralization in multipotent stem cells, but not in pre-osteoblasts and calvarial osteoblasts. dimethylacetamide 8-11 Sp7 transcription factor Homo sapiens 115-122 31152802-9 2019 TNFalpha largely abrogated BMP-promoted growth of mineralized bone while pre-treatment of NMP and DMA prevented the deleterious effect of TNFalpha. dimethylacetamide 98-101 tumor necrosis factor Homo sapiens 138-146 31156337-0 2019 TNF-alpha and IL-6 as Biomarkers of Impaired Lung Functions in Dimethylacetamide Exposure. dimethylacetamide 63-80 tumor necrosis factor Homo sapiens 0-9 31156337-0 2019 TNF-alpha and IL-6 as Biomarkers of Impaired Lung Functions in Dimethylacetamide Exposure. dimethylacetamide 63-80 interleukin 6 Homo sapiens 14-18 29550560-4 2018 In this study, a composite safety electrolyte additive consisting of perfluoro-2-methyl-3-pentanone, N, N-Dimethylacetamide (and fluorocarbon surfactant is proved to be effective and simple in improving the thermal stability of NCM materials. dimethylacetamide 101-123 CWC22 spliceosome associated protein homolog Homo sapiens 228-231 29735925-8 2018 On the other hand, PSf/DMAc membrane pores were finger-like with lower water flux (63.1 &plusmn; 12.4 LMH) and slightly lower solute rejection (96 &plusmn; 2.00%) when compared to PSf/PolarClean membranes. dimethylacetamide 23-27 insulin like growth factor binding protein 7 Homo sapiens 19-22 29735925-8 2018 On the other hand, PSf/DMAc membrane pores were finger-like with lower water flux (63.1 &plusmn; 12.4 LMH) and slightly lower solute rejection (96 &plusmn; 2.00%) when compared to PSf/PolarClean membranes. dimethylacetamide 23-27 insulin like growth factor binding protein 7 Homo sapiens 188-191 28749186-0 2018 Correlation between CAT polymorphism and susceptibility to DMAc-induced abnormal liver function: a case-control study of Chinese population. dimethylacetamide 59-63 catalase Homo sapiens 20-23 28749186-6 2018 RESULTS: Subjects with the CAT rs769214 GA/GG genotypes had a reducing risk of abnormal liver function, which was more evident in the subgroups exposed to DMAc <10 years, exposed to DMAc <5 mg/m3, never smoked and never drank. dimethylacetamide 155-159 catalase Homo sapiens 27-30 28749186-6 2018 RESULTS: Subjects with the CAT rs769214 GA/GG genotypes had a reducing risk of abnormal liver function, which was more evident in the subgroups exposed to DMAc <10 years, exposed to DMAc <5 mg/m3, never smoked and never drank. dimethylacetamide 185-189 catalase Homo sapiens 27-30 28749186-7 2018 CONCLUSIONS: CAT rs769214 (-844 G > A) polymorphism may be associated with DMAc-induced abnormal liver function in Chinese population. dimethylacetamide 78-82 catalase Homo sapiens 13-16 29384052-6 2018 RESULTS: Interestingly, we found that DMA suppresses cytokine secretion by inhibiting nuclear factor-kappa B (NF-kappaB). dimethylacetamide 38-41 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 86-108 29384052-6 2018 RESULTS: Interestingly, we found that DMA suppresses cytokine secretion by inhibiting nuclear factor-kappa B (NF-kappaB). dimethylacetamide 38-41 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 110-119 31457282-7 2017 Solvates of L 1 with DMSO, dimethylformamide (DMF), and dimethylacetamide are quasi-isostructural. dimethylacetamide 56-73 L1 cell adhesion molecule Homo sapiens 12-15 28416085-4 2017 Further, NMR and Fourier transform infrared spectroscopy analysis of DMA sample after 1h, 2h, 3h, 4h and 8h of reaction with PCBs at 433K and PCB:DMA ratio (wt/vol) of 3:10 has been carried out to investigate the mechanism of dissolution of resin. dimethylacetamide 69-72 pyruvate carboxylase Homo sapiens 125-128 28663777-5 2017 GM-CSF should be considered as an adjunctive therapy in patients with refractory dMAC. dimethylacetamide 81-85 colony stimulating factor 2 Homo sapiens 0-6 31457224-5 2017 In addition, it was found that lithium-air batteries with an optimized electrolyte composition (DMA/TMS = 20:80, % v/v) showed a better cycle life and lower charge overpotential as compared to those with electrolytes with a single solvent, either DMA or TMS. dimethylacetamide 96-99 PYD and CARD domain containing Homo sapiens 254-257 27782292-0 2016 N,N-Dimethylacetamide Significantly Attenuates LPS- and TNFalpha-Induced Proinflammatory Responses Via Inhibition of the Nuclear Factor Kappa B Pathway. dimethylacetamide 0-21 tumor necrosis factor Homo sapiens 56-64 27782292-1 2016 Previously, we have shown that N,N-dimethylacetamide (DMA) prevents inflammation-induced preterm birth in a murine model, inhibits LPS-induced increases in placental pro-inflammatory cytokines and up-regulates the anti-inflammatory cytokine Interleukin-10 (IL-10). dimethylacetamide 31-52 interleukin 10 Mus musculus 241-255 27782292-1 2016 Previously, we have shown that N,N-dimethylacetamide (DMA) prevents inflammation-induced preterm birth in a murine model, inhibits LPS-induced increases in placental pro-inflammatory cytokines and up-regulates the anti-inflammatory cytokine Interleukin-10 (IL-10). dimethylacetamide 31-52 interleukin 10 Mus musculus 257-262 27782292-1 2016 Previously, we have shown that N,N-dimethylacetamide (DMA) prevents inflammation-induced preterm birth in a murine model, inhibits LPS-induced increases in placental pro-inflammatory cytokines and up-regulates the anti-inflammatory cytokine Interleukin-10 (IL-10). dimethylacetamide 54-57 interleukin 10 Mus musculus 241-255 27782292-1 2016 Previously, we have shown that N,N-dimethylacetamide (DMA) prevents inflammation-induced preterm birth in a murine model, inhibits LPS-induced increases in placental pro-inflammatory cytokines and up-regulates the anti-inflammatory cytokine Interleukin-10 (IL-10). dimethylacetamide 54-57 interleukin 10 Mus musculus 257-262 27782292-4 2016 Using in vitro and ex vivo models, we show that DMA suppresses secretion of pro-inflammatory cytokines in lipopolysaccharide (LPS)-induced RAW 264.7 cells, TNFalpha-challenged JEG-3 cells and LPS-stimulated human placental explants. dimethylacetamide 48-51 tumor necrosis factor Mus musculus 156-164 27782292-5 2016 DMA significantly attenuated the secretion of TNFalpha, IL-6, IL-10, and granulocyte macrophage colony stimulating factor (GM-CSF) from LPS-stimulated RAW 264.7 cells, IL-6 secretion from TNFalpha-stimulated JEG-3 cells and TNFalpha, IL-6, IL-10, GM-CSF and Interleukin-8 (IL-8) from LPS-stimulated human placental explants. dimethylacetamide 0-3 tumor necrosis factor Mus musculus 46-54 27782292-5 2016 DMA significantly attenuated the secretion of TNFalpha, IL-6, IL-10, and granulocyte macrophage colony stimulating factor (GM-CSF) from LPS-stimulated RAW 264.7 cells, IL-6 secretion from TNFalpha-stimulated JEG-3 cells and TNFalpha, IL-6, IL-10, GM-CSF and Interleukin-8 (IL-8) from LPS-stimulated human placental explants. dimethylacetamide 0-3 interleukin 6 Mus musculus 56-60 27782292-5 2016 DMA significantly attenuated the secretion of TNFalpha, IL-6, IL-10, and granulocyte macrophage colony stimulating factor (GM-CSF) from LPS-stimulated RAW 264.7 cells, IL-6 secretion from TNFalpha-stimulated JEG-3 cells and TNFalpha, IL-6, IL-10, GM-CSF and Interleukin-8 (IL-8) from LPS-stimulated human placental explants. dimethylacetamide 0-3 interleukin 10 Mus musculus 62-67 27782292-5 2016 DMA significantly attenuated the secretion of TNFalpha, IL-6, IL-10, and granulocyte macrophage colony stimulating factor (GM-CSF) from LPS-stimulated RAW 264.7 cells, IL-6 secretion from TNFalpha-stimulated JEG-3 cells and TNFalpha, IL-6, IL-10, GM-CSF and Interleukin-8 (IL-8) from LPS-stimulated human placental explants. dimethylacetamide 0-3 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 73-121 27782292-5 2016 DMA significantly attenuated the secretion of TNFalpha, IL-6, IL-10, and granulocyte macrophage colony stimulating factor (GM-CSF) from LPS-stimulated RAW 264.7 cells, IL-6 secretion from TNFalpha-stimulated JEG-3 cells and TNFalpha, IL-6, IL-10, GM-CSF and Interleukin-8 (IL-8) from LPS-stimulated human placental explants. dimethylacetamide 0-3 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 123-129 27782292-5 2016 DMA significantly attenuated the secretion of TNFalpha, IL-6, IL-10, and granulocyte macrophage colony stimulating factor (GM-CSF) from LPS-stimulated RAW 264.7 cells, IL-6 secretion from TNFalpha-stimulated JEG-3 cells and TNFalpha, IL-6, IL-10, GM-CSF and Interleukin-8 (IL-8) from LPS-stimulated human placental explants. dimethylacetamide 0-3 interleukin 6 Mus musculus 168-172 27782292-5 2016 DMA significantly attenuated the secretion of TNFalpha, IL-6, IL-10, and granulocyte macrophage colony stimulating factor (GM-CSF) from LPS-stimulated RAW 264.7 cells, IL-6 secretion from TNFalpha-stimulated JEG-3 cells and TNFalpha, IL-6, IL-10, GM-CSF and Interleukin-8 (IL-8) from LPS-stimulated human placental explants. dimethylacetamide 0-3 tumor necrosis factor Mus musculus 188-196 27782292-5 2016 DMA significantly attenuated the secretion of TNFalpha, IL-6, IL-10, and granulocyte macrophage colony stimulating factor (GM-CSF) from LPS-stimulated RAW 264.7 cells, IL-6 secretion from TNFalpha-stimulated JEG-3 cells and TNFalpha, IL-6, IL-10, GM-CSF and Interleukin-8 (IL-8) from LPS-stimulated human placental explants. dimethylacetamide 0-3 tumor necrosis factor Homo sapiens 188-196 27782292-5 2016 DMA significantly attenuated the secretion of TNFalpha, IL-6, IL-10, and granulocyte macrophage colony stimulating factor (GM-CSF) from LPS-stimulated RAW 264.7 cells, IL-6 secretion from TNFalpha-stimulated JEG-3 cells and TNFalpha, IL-6, IL-10, GM-CSF and Interleukin-8 (IL-8) from LPS-stimulated human placental explants. dimethylacetamide 0-3 interleukin 6 Homo sapiens 168-172 27782292-5 2016 DMA significantly attenuated the secretion of TNFalpha, IL-6, IL-10, and granulocyte macrophage colony stimulating factor (GM-CSF) from LPS-stimulated RAW 264.7 cells, IL-6 secretion from TNFalpha-stimulated JEG-3 cells and TNFalpha, IL-6, IL-10, GM-CSF and Interleukin-8 (IL-8) from LPS-stimulated human placental explants. dimethylacetamide 0-3 interleukin 10 Homo sapiens 240-245 27782292-5 2016 DMA significantly attenuated the secretion of TNFalpha, IL-6, IL-10, and granulocyte macrophage colony stimulating factor (GM-CSF) from LPS-stimulated RAW 264.7 cells, IL-6 secretion from TNFalpha-stimulated JEG-3 cells and TNFalpha, IL-6, IL-10, GM-CSF and Interleukin-8 (IL-8) from LPS-stimulated human placental explants. dimethylacetamide 0-3 colony stimulating factor 2 Homo sapiens 247-253 27782292-5 2016 DMA significantly attenuated the secretion of TNFalpha, IL-6, IL-10, and granulocyte macrophage colony stimulating factor (GM-CSF) from LPS-stimulated RAW 264.7 cells, IL-6 secretion from TNFalpha-stimulated JEG-3 cells and TNFalpha, IL-6, IL-10, GM-CSF and Interleukin-8 (IL-8) from LPS-stimulated human placental explants. dimethylacetamide 0-3 C-X-C motif chemokine ligand 8 Homo sapiens 258-271 27782292-5 2016 DMA significantly attenuated the secretion of TNFalpha, IL-6, IL-10, and granulocyte macrophage colony stimulating factor (GM-CSF) from LPS-stimulated RAW 264.7 cells, IL-6 secretion from TNFalpha-stimulated JEG-3 cells and TNFalpha, IL-6, IL-10, GM-CSF and Interleukin-8 (IL-8) from LPS-stimulated human placental explants. dimethylacetamide 0-3 C-X-C motif chemokine ligand 8 Homo sapiens 273-277 27782292-7 2016 DMA (10 mM) significantly inhibited nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkappaBalpha) degradation in LPS-stimulated RAW 264.7 cells, but there was no significant change in the expression of phosphorylated or native forms of downstream proteins in the MAPK pathway. dimethylacetamide 0-3 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha Mus musculus 36-119 27782292-7 2016 DMA (10 mM) significantly inhibited nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkappaBalpha) degradation in LPS-stimulated RAW 264.7 cells, but there was no significant change in the expression of phosphorylated or native forms of downstream proteins in the MAPK pathway. dimethylacetamide 0-3 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha Mus musculus 121-133 27782292-9 2016 Overall, our findings suggest that the anti-inflammatory activity of DMA is mediated by inhibition of the NF-kappaB pathway via decreased IkappaBalpha degradation. dimethylacetamide 69-72 NFKB inhibitor alpha Homo sapiens 138-150 27003174-4 2016 We found that DMAc triggered LO-2 apoptosis in a obviously dose-dependent manner, caused by increased ROS generation and activation of Bcl-2 pathway. dimethylacetamide 14-18 BCL2 apoptosis regulator Homo sapiens 135-140 25240216-3 2014 This dispersion process of the graphene flakes was achieved by the use of stable dimethylacetamide (DMAc), via solution intercalation with POSS-PCL nanocomposites. dimethylacetamide 100-104 PHD finger protein 1 Homo sapiens 144-147 24812029-0 2014 Induction of ROS-independent JNK-activation-mediated apoptosis by a novel coumarin-derivative, DMAC, in human colon cancer cells. dimethylacetamide 95-99 mitogen-activated protein kinase 8 Homo sapiens 29-32 24812029-3 2014 Induction of apoptotic characteristics, including cellular shrinkage, chromatin condensation, and Annexin V detection, was observed following DMAC treatment. dimethylacetamide 142-146 annexin A5 Homo sapiens 98-107 24812029-4 2014 Mechanistically, we observed that DMAC elicited induction of proteolytic cascade activation including cleavage of caspase-3 and poly ADP-ribose polymerase (PARP) expression and loss of the antiapoptotic proteins, Mcl-1 and Bcl-XL, accompanied by an increase in expression of the proapoptotic protein, Bak. dimethylacetamide 34-38 caspase 3 Homo sapiens 114-123 24812029-4 2014 Mechanistically, we observed that DMAC elicited induction of proteolytic cascade activation including cleavage of caspase-3 and poly ADP-ribose polymerase (PARP) expression and loss of the antiapoptotic proteins, Mcl-1 and Bcl-XL, accompanied by an increase in expression of the proapoptotic protein, Bak. dimethylacetamide 34-38 poly(ADP-ribose) polymerase 1 Homo sapiens 128-154 24812029-4 2014 Mechanistically, we observed that DMAC elicited induction of proteolytic cascade activation including cleavage of caspase-3 and poly ADP-ribose polymerase (PARP) expression and loss of the antiapoptotic proteins, Mcl-1 and Bcl-XL, accompanied by an increase in expression of the proapoptotic protein, Bak. dimethylacetamide 34-38 poly(ADP-ribose) polymerase 1 Homo sapiens 156-160 24812029-4 2014 Mechanistically, we observed that DMAC elicited induction of proteolytic cascade activation including cleavage of caspase-3 and poly ADP-ribose polymerase (PARP) expression and loss of the antiapoptotic proteins, Mcl-1 and Bcl-XL, accompanied by an increase in expression of the proapoptotic protein, Bak. dimethylacetamide 34-38 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 213-218 24812029-4 2014 Mechanistically, we observed that DMAC elicited induction of proteolytic cascade activation including cleavage of caspase-3 and poly ADP-ribose polymerase (PARP) expression and loss of the antiapoptotic proteins, Mcl-1 and Bcl-XL, accompanied by an increase in expression of the proapoptotic protein, Bak. dimethylacetamide 34-38 BCL2 like 1 Homo sapiens 223-229 24812029-4 2014 Mechanistically, we observed that DMAC elicited induction of proteolytic cascade activation including cleavage of caspase-3 and poly ADP-ribose polymerase (PARP) expression and loss of the antiapoptotic proteins, Mcl-1 and Bcl-XL, accompanied by an increase in expression of the proapoptotic protein, Bak. dimethylacetamide 34-38 BCL2 antagonist/killer 1 Homo sapiens 301-304 24812029-5 2014 In addition, suppressing c-Jun N-terminal protein kinase (JNK), but not extracellular-regulated protein kinase (ERK) or p38, substantially diminished DMAC-induced cell death and caspase-3 and PARP cleavage. dimethylacetamide 150-154 mitogen-activated protein kinase 8 Homo sapiens 25-56 24812029-5 2014 In addition, suppressing c-Jun N-terminal protein kinase (JNK), but not extracellular-regulated protein kinase (ERK) or p38, substantially diminished DMAC-induced cell death and caspase-3 and PARP cleavage. dimethylacetamide 150-154 mitogen-activated protein kinase 8 Homo sapiens 58-61 24812029-5 2014 In addition, suppressing c-Jun N-terminal protein kinase (JNK), but not extracellular-regulated protein kinase (ERK) or p38, substantially diminished DMAC-induced cell death and caspase-3 and PARP cleavage. dimethylacetamide 150-154 caspase 3 Homo sapiens 178-187 24812029-5 2014 In addition, suppressing c-Jun N-terminal protein kinase (JNK), but not extracellular-regulated protein kinase (ERK) or p38, substantially diminished DMAC-induced cell death and caspase-3 and PARP cleavage. dimethylacetamide 150-154 poly(ADP-ribose) polymerase 1 Homo sapiens 192-196 24812029-7 2014 Pretreatment with the JNK inhibitor, SP600125, suppressed DMAC-induced JNK phosphorylation, which was accompanied by a reversal of Bcl-XL expression. dimethylacetamide 58-62 mitogen-activated protein kinase 8 Homo sapiens 22-25 24812029-7 2014 Pretreatment with the JNK inhibitor, SP600125, suppressed DMAC-induced JNK phosphorylation, which was accompanied by a reversal of Bcl-XL expression. dimethylacetamide 58-62 mitogen-activated protein kinase 8 Homo sapiens 71-74 24812029-7 2014 Pretreatment with the JNK inhibitor, SP600125, suppressed DMAC-induced JNK phosphorylation, which was accompanied by a reversal of Bcl-XL expression. dimethylacetamide 58-62 BCL2 like 1 Homo sapiens 131-137 24174393-0 2014 Evaluation of effects of busulfan and DMA on SOS in pediatric stem cell recipients. dimethylacetamide 38-41 xylosyltransferase 2 Homo sapiens 45-48 24174393-5 2014 METHODS: In a two-centre study Bu and DMA AUC (area under the curve) were correlated in pediatric stem cell recipients to the risk of developing SOS and to the clinical outcome. dimethylacetamide 38-41 xylosyltransferase 2 Homo sapiens 145-148 24174393-9 2014 To identify subgroups (e.g., infants), in which Bu or DMA might be risk factors for the induction of SOS, larger cohorts have to be evaluated. dimethylacetamide 54-57 xylosyltransferase 2 Homo sapiens 101-104 23770347-7 2013 Furthermore, immunoblotting analysis of placental tissue harvested from our murine models revealed DMA-mediated regulation of expression of the proinflammatory cytokines IL-1beta, tumor necrosis factor alpha, and IL-6, and increased expression of the regulatory inflammatory cytokine IL-10. dimethylacetamide 99-102 interleukin 1 beta Mus musculus 170-178 23770347-7 2013 Furthermore, immunoblotting analysis of placental tissue harvested from our murine models revealed DMA-mediated regulation of expression of the proinflammatory cytokines IL-1beta, tumor necrosis factor alpha, and IL-6, and increased expression of the regulatory inflammatory cytokine IL-10. dimethylacetamide 99-102 tumor necrosis factor Mus musculus 180-207 23770347-7 2013 Furthermore, immunoblotting analysis of placental tissue harvested from our murine models revealed DMA-mediated regulation of expression of the proinflammatory cytokines IL-1beta, tumor necrosis factor alpha, and IL-6, and increased expression of the regulatory inflammatory cytokine IL-10. dimethylacetamide 99-102 interleukin 6 Mus musculus 213-217 23770347-7 2013 Furthermore, immunoblotting analysis of placental tissue harvested from our murine models revealed DMA-mediated regulation of expression of the proinflammatory cytokines IL-1beta, tumor necrosis factor alpha, and IL-6, and increased expression of the regulatory inflammatory cytokine IL-10. dimethylacetamide 99-102 interleukin 10 Mus musculus 284-289 23681561-8 2013 However, the use of chloroalkylaluminium reagents, such as dimethylaluminium chloride (DMAC) and methylaluminium dichloride (MADC), as co-catalysts in the presence of the reactivator ethyl trichloroacetate (ETA) generated thermally stable catalysts with, in the case of niobium, catalytic activities that were two orders of magnitude higher than those previously observed. dimethylacetamide 87-91 endothelin receptor type A Homo sapiens 207-210 23218259-5 2013 B-CDA-acetone/DMAc solution is a shear-thinning fluid. dimethylacetamide 14-18 cytidine deaminase Homo sapiens 2-5 22724013-12 2012 Cryoprotectants, 8% methanol and 10% dimethylacetamide (DMA), reduced the motility over the control value (P<0.5), whereas 10% dimethylformamide (DMF) with or without CAT did not (P>0.05). dimethylacetamide 56-59 catalase Danio rerio 170-173 21789295-1 2011 The excited state crystal structure of the ionic complex (Nd(DMA)(4)(H(2)O)(4)-Fe(CN)(6) 3H(2)O (DMA = dimethylacetamide) has been determined at 15 K upon UV illumination by single crystal X-ray diffraction. dimethylacetamide 103-120 major histocompatibility complex, class II, DM alpha Homo sapiens 61-64 21789295-1 2011 The excited state crystal structure of the ionic complex (Nd(DMA)(4)(H(2)O)(4)-Fe(CN)(6) 3H(2)O (DMA = dimethylacetamide) has been determined at 15 K upon UV illumination by single crystal X-ray diffraction. dimethylacetamide 103-120 major histocompatibility complex, class II, DM alpha Homo sapiens 97-100 21819779-1 2011 The interaction of N,N-dimethyl formamide (DMF) and N,N-dimethyl acetamide (DMA) with methanol in solution mixtures was studied using Fourier transform infrared-attenuated total reflection (FT-IR/ATR) spectroscopy. dimethylacetamide 52-74 ATR serine/threonine kinase Homo sapiens 190-199 21819779-1 2011 The interaction of N,N-dimethyl formamide (DMF) and N,N-dimethyl acetamide (DMA) with methanol in solution mixtures was studied using Fourier transform infrared-attenuated total reflection (FT-IR/ATR) spectroscopy. dimethylacetamide 76-79 ATR serine/threonine kinase Homo sapiens 190-199 19813714-1 2009 Zn(2+) ions react with 3,5-pyridinedicarboxylate (pydc) to form a new metal-organic framework (MOF), [Zn(pydc)(dma)] (dma = N,N"-dimethylacetamide), based on a noninterpenetrating (10,3)-a topology. dimethylacetamide 124-146 lysine acetyltransferase 8 Homo sapiens 70-100 19338350-5 2009 Mark-Houwink exponents were determined: they were lower than that for cellulose dissolved in LiCl/N,N-dimethylacetamide at 30 degrees C and close to theta-value. dimethylacetamide 100-119 microtubule affinity regulating kinase 1 Homo sapiens 0-4