PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8883586-6 1996 In other studies we determined the effect of increasing concentrations of ZDV on production of granulocyte colony-stimulating factor (G-CSF) protein [enzyme-linked immunosorbent assay (ELISA)] and mRNA by fetal and maternal monocytes, and on production of erythropoietin protein (ELISA) and mRNA by Hep3B cells. Zidovudine 74-77 colony stimulating factor 3 Homo sapiens 95-132 8883586-6 1996 In other studies we determined the effect of increasing concentrations of ZDV on production of granulocyte colony-stimulating factor (G-CSF) protein [enzyme-linked immunosorbent assay (ELISA)] and mRNA by fetal and maternal monocytes, and on production of erythropoietin protein (ELISA) and mRNA by Hep3B cells. Zidovudine 74-77 colony stimulating factor 3 Homo sapiens 134-139 8680517-7 1996 Exciting new management strategies appear to be the use of granulocyte colony-stimulating factor to enhance neutrophilia and zidovudine to reduce vertical transmission of HIV infection. Zidovudine 125-135 colony stimulating factor 3 Homo sapiens 59-96 7511543-5 1993 These results suggest that combined therapy with granulocyte colony-stimulating factor and erythropoietin may improve leukopenia and anaemia, which is not zidovudine-related, in children who have AIDS. Zidovudine 155-165 colony stimulating factor 3 Homo sapiens 49-86 1281810-9 1992 G-CSF plays an important role in the treatment of patients with HIV-associated Kaposi sarcoma and enables combined treatment with zidovudine, interferon, and cytostatic drugs. Zidovudine 130-140 colony stimulating factor 3 Homo sapiens 0-5 1279153-2 1992 We evaluated the effect of subcutaneously administered granulocyte colony-stimulating factor (G-CSF) in pediatric patients whose absolute neutrophil count was less than 0.8 x 10(9)/L during AZT therapy despite dosage reductions to 120 mg/m2 every 6 hours. Zidovudine 190-193 colony stimulating factor 3 Homo sapiens 94-99 1279153-9 1992 With doses of G-CSF ranging from 1 to 20 micrograms/kg per day, 17 of 19 patients were able to tolerate AZT at a dose of 120 to 180 mg/m2 every 6 hours. Zidovudine 104-107 colony stimulating factor 3 Homo sapiens 14-19 1279153-10 1992 We conclude that G-CSF therapy enables patients who have had AZT-related neutropenia to receive therapeutic doses of AZT. Zidovudine 61-64 colony stimulating factor 3 Homo sapiens 17-22 1279153-10 1992 We conclude that G-CSF therapy enables patients who have had AZT-related neutropenia to receive therapeutic doses of AZT. Zidovudine 117-120 colony stimulating factor 3 Homo sapiens 17-22 2018046-3 1991 A combination of granulocyte colony-stimulating factor and erythropoietin has also been demonstrated to alleviate both neutropenia and anemia in patients with advanced AIDS or AIDS-related complex receiving zidovudine. Zidovudine 207-217 colony stimulating factor 3 Homo sapiens 17-54 1380256-9 1992 When erythropoietin was added to the regimen, combined G-CSF and EPO corrected both anemia and leukopenia and lessened subsequent zidovudine toxicity. Zidovudine 130-140 colony stimulating factor 3 Homo sapiens 55-60 1385275-0 1992 Efficacy of granulocyte colony-stimulating factor (G-CSF) on neutropenia in zidovudine-treated patients with AIDS and ARC: a preliminary report. Zidovudine 76-86 colony stimulating factor 3 Homo sapiens 12-49 1385275-0 1992 Efficacy of granulocyte colony-stimulating factor (G-CSF) on neutropenia in zidovudine-treated patients with AIDS and ARC: a preliminary report. Zidovudine 76-86 colony stimulating factor 3 Homo sapiens 51-56 1720567-5 1991 The combination of G-CSF and recombinant human erythropoietin completely reversed the zidovudine-induced neutropenia of AIDS patients but was only partially effective in reversing anemia. Zidovudine 86-96 colony stimulating factor 3 Homo sapiens 19-24 1714756-0 1991 Effects of recombinant human granulocyte colony-stimulating factor on leucopenia in zidovudine-treated patients with AIDS and AIDS related complex, a phase I/II study. Zidovudine 84-94 colony stimulating factor 3 Homo sapiens 29-66 1714756-13 1991 We conclude that G-CSF increases the number of circulating neutrophilic granulocytes in zidovudine-treated patients at relatively low doses and with few side-effects. Zidovudine 88-98 colony stimulating factor 3 Homo sapiens 17-22 1709368-0 1991 Combined therapy with recombinant granulocyte colony-stimulating factor and erythropoietin decreases hematologic toxicity from zidovudine. Zidovudine 127-137 colony stimulating factor 3 Homo sapiens 34-71 2022593-2 1991 Both G-CSF and GM-CSF have demonstrated the ability to correct leukopenia related to HIV infection and ameliorate the drug-related myelosuppressive effects of zidovudine, trimethoprim/sulfamethoxazole, ganciclovir, and, in the case of GM-CSF, alpha-interferon, and cancer chemotherapies. Zidovudine 159-169 colony stimulating factor 3 Homo sapiens 5-10 1713806-11 1991 Combined G-CSF and EPO treatment corrected both anemia and leukopenia and reduced zidovudine toxicity. Zidovudine 82-92 colony stimulating factor 3 Homo sapiens 9-14 9571329-10 1998 CONCLUSIONS: Gliclazide administration to NIDDM patients inhibits the increased adhesiveness of diabetic monocytes to endothelial cells and reduces the production of TNF-alpha by these cells. Gliclazide 13-23 tumor necrosis factor Homo sapiens 166-175 9517374-9 1998 RESULTS: In gliclazide-treated NIDDM patients, PDH activity in circulating lymphocytes recovered. Gliclazide 12-22 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 47-50 9517374-12 1998 CONCLUSIONS: This study suggests that free gliclazide concentrations determine recovery of PDH activity in circulating lymphocytes of treated patients through drug-mediated enhanced insulin control over PDH or through the drug alone. Gliclazide 43-53 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 91-94 9517374-12 1998 CONCLUSIONS: This study suggests that free gliclazide concentrations determine recovery of PDH activity in circulating lymphocytes of treated patients through drug-mediated enhanced insulin control over PDH or through the drug alone. Gliclazide 43-53 insulin Homo sapiens 182-189 9517374-12 1998 CONCLUSIONS: This study suggests that free gliclazide concentrations determine recovery of PDH activity in circulating lymphocytes of treated patients through drug-mediated enhanced insulin control over PDH or through the drug alone. Gliclazide 43-53 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 203-206 9498623-9 1998 These data indicate that gliclazide, aside from either a direct antioxidant action or an effect on insulin or glucose levels, may ameliorate diabetic endothelial cell dysfunction. Gliclazide 25-35 insulin Oryctolagus cuniculus 99-106 9439551-0 1997 The stimulation of insulin secretion in non-insulin-dependent diabetic patients by amino acids and gliclazide in the basal and hyperglycemic state. Gliclazide 99-109 insulin Homo sapiens 19-26 9439552-0 1997 Gliclazide treatment of streptozotocin diabetic rats restores GLUT4 protein content and basal glucose uptake in skeletal muscle. Gliclazide 0-10 solute carrier family 2 member 4 Rattus norvegicus 62-67 9439552-12 1997 In conclusion, gliclazide has a glucose-lowering effect in STZ-diabetic rats that could be attributed to an increase in muscle glucose clearance by a post-insulin receptor mechanism, probably related to a normalization of GLUT4 content. Gliclazide 15-25 insulin receptor Rattus norvegicus 155-171 9439552-12 1997 In conclusion, gliclazide has a glucose-lowering effect in STZ-diabetic rats that could be attributed to an increase in muscle glucose clearance by a post-insulin receptor mechanism, probably related to a normalization of GLUT4 content. Gliclazide 15-25 solute carrier family 2 member 4 Rattus norvegicus 222-227 9322798-6 1997 In addition, exposure of BAE cells to gliclazide (0 to 10 micrograms/mL) and native LDL (100 micrograms/mL) induced a dose-dependent diminution of the oxidized LDL-induced monocyte adhesion to BAE cells as measured by the myeloperoxidase (MPO) assay. Gliclazide 38-48 myeloperoxidase Bos taurus 222-237 9322798-6 1997 In addition, exposure of BAE cells to gliclazide (0 to 10 micrograms/mL) and native LDL (100 micrograms/mL) induced a dose-dependent diminution of the oxidized LDL-induced monocyte adhesion to BAE cells as measured by the myeloperoxidase (MPO) assay. Gliclazide 38-48 myeloperoxidase Bos taurus 239-242 8843172-0 1996 Gliclazide potentiates suppression of hepatic glucose production in non-insulin-dependent diabetic patients. Gliclazide 0-10 insulin Homo sapiens 72-79 8843172-9 1996 The increase in plasma insulin and C-peptide concentrations was similar with gliclazide and placebo, although the plasma insulin to glucose ratio was increased with gliclazide. Gliclazide 165-175 insulin Homo sapiens 121-128 8867904-2 1996 Having already shown positive effects of sulfonylreas in long-standing IDDM patients, we decided to try the association of gliclazide with insulin in newly diagnosed IDDM patients. Gliclazide 123-133 insulin Homo sapiens 139-146 9711995-2 1998 This study was designed to elucidate the effect of gliclazide, an oral hypoglycemic sulfonylurea, on diabetic neuropathy, because it has been indicated to be a free radical scavenger and TNF-alpha inhibitor. Gliclazide 51-61 tumor necrosis factor Rattus norvegicus 187-196 8920942-4 1996 Gastrocnemius muscles perfused with gliclazide had a significant increase (2.4-fold) in the GLUT4 content in plasma membranes compared to basal conditions (p < 0.05). Gliclazide 36-46 solute carrier family 2 member 4 Rattus norvegicus 92-97 8920942-6 1996 The effect of insulin on the glucose uptake and on the GLUT 4 translocation was significantly enhanced by gliclazide (3.4-fold and 3.7-fold vs basal, respectively). Gliclazide 106-116 solute carrier family 2 member 4 Rattus norvegicus 55-61 7829624-9 1995 In summary, the improvement in glycemic control and glucose disposal in NIDDM subjects receiving gliclazide therapy cannot be explained by increased expression of GLUT4 in muscle. Gliclazide 97-107 solute carrier family 2 (facilitated glucose transporter), member 4 Mus musculus 163-168 7750472-9 1995 We conclude that the stimulation of glucose uptake in L6 cells by gliclazide and glyburide is associated not with a redistribution but, rather, with an increase in the total membrane content and plasma membrane level of GLUT1, which is independent of protein synthesis. Gliclazide 66-76 solute carrier family 2 member 1 Homo sapiens 220-225 7988345-7 1994 The amount of administered somatostatin required for inhibiting glucagon secretion was higher than the maximal level obtained from endogenous secretion of somatostatin after gliclazide. Gliclazide 174-184 somatostatin Rattus norvegicus 27-39 7833494-3 1994 When five groups of type II diabetic patients were treated concurrently with five randomly allocated different sulfonylureas over 1 year, the percentage of patients achieving normal HbA1 levels was best with gliclazide (80%) and glibenclamide (74%), when compared with chlorpropamide (17%), glipizide (40%), and gliquidone (40%). Gliclazide 208-218 hemoglobin subunit alpha 1 Homo sapiens 182-186 7833497-1 1994 In circulating lymphocytes from patients with non-insulin-dependent diabetes mellitus (NIDDM) subnormal pyruvate dehydrogenase (PDH) activity returns to normal following patient treatment with sulfonylurea (gliclazide, 80 mg twice daily/5 weeks). Gliclazide 207-217 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 128-131 7833497-3 1994 Therefore, the low PDH activity in cells of NIDDM patients might be caused by defective insulin control on the enzyme and its recovery in gliclazide-treated patients by drug-mediated removal of the defect. Gliclazide 138-148 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 19-22 7833497-5 1994 In such conditions, the profile of PDH behavior in treated patients was no longer comparable to that in untreated patients but closer to that in euglycemic controls, thus supporting the view that the recovery of PDH activity in NIDDM patients following gliclazide treatment might be the expression of an additional effect that the drug would have in these patients, aimed to renew cell responsiveness to insulin. Gliclazide 253-263 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 35-38 7833497-5 1994 In such conditions, the profile of PDH behavior in treated patients was no longer comparable to that in untreated patients but closer to that in euglycemic controls, thus supporting the view that the recovery of PDH activity in NIDDM patients following gliclazide treatment might be the expression of an additional effect that the drug would have in these patients, aimed to renew cell responsiveness to insulin. Gliclazide 253-263 pyruvate dehydrogenase phosphatase catalytic subunit 1 Homo sapiens 212-215 7833497-5 1994 In such conditions, the profile of PDH behavior in treated patients was no longer comparable to that in untreated patients but closer to that in euglycemic controls, thus supporting the view that the recovery of PDH activity in NIDDM patients following gliclazide treatment might be the expression of an additional effect that the drug would have in these patients, aimed to renew cell responsiveness to insulin. Gliclazide 253-263 insulin Homo sapiens 404-411