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Objective:To evaluate the role of extracellular signal-regulated kinase 1/2 (ERK1/2)/cyclic adenosine monophosphate response element-binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling pathway in dexmedetomidine-induced inhibition of propofol-caused apoptosis in isolated hippocampal neurons of fetal rats.Methods:Pregnant Sprague-Dawley rats at 16 days of gestation were sacrificed, and the fetal rats were taken out, and hippocampal neurons of fetal rats were obtained and primarily cultured in vitro for 7 days.The neurons were divided into 9 groups ( n=12 each) using a random number table method: control group (group C), fat emulsion group (group I), dimethyl sulfoxide (DMSO) group, dexmedetomidine group (group D), propofol group (group P), propofol plus dexmedetomidine group (group PD), PD98059 plus propofol plus dexmedetomidine group (group PDP), MH89 plus propofol plus dexmedetomidine group (group HDP), and KG501 plus propofol plus dexmedetomidine group (group KDP). Group C received no treatment.In group I, 20% fat emulsion was added, and the neurons were incubated for 30 min, and 0.25% DMSO was added in group DMSO, and the neurons were incubated for 30 min.Dexmedetomidine at a final concentration of 10 μmol/L was added, and the neurons were incubated for 30 min in group D. Propofol at a final concentration of 100 μmol/L was added, and the neurons were incubated for 3 h in group P. In group PD, dexmedetomidine at a final concentration of 10 μmol/L was added, the neurons were incubated for 30 min, propofol at a final concentration of 100 μmol/L was added, and the neurons were incubated for 3 h. In PDP, HDP and KDP groups, 25 μmol PD98059 (p-ERK1/2 inhibitor), 10 μmol H89 (p-CREB inhibitor) and 25 μmol KG501 (CREB inhibitor) were added, respectively, the neurons were incubated for 30 min, dexmedetomidine at a final concentration of 10 μmol/L was added, the neurons were incubated for 30 min, and propofol at a final concentration of 100 μmol/L was added, and the neurons were incubated for 3 h. The cell ultrastructure was observed with the transmission electron microscope, the apoptosis in neurons was detected by flow cytometry, the expression of ERK1/2, CREB and BDNF mRNA was detected by quantitative real-time polymerase chain reaction, and the expression of p-ERK1/2, CREB, p-CREB, BDNF and cleaved caspase-3 was detected by Western blot. Results:Compared with group C, the apoptosis rate was significantly increased, the expression of p-ERK1/2 and p-CREB was down-regulated, and the expression of cleaved caspase-3 was up-regulated in P, PD, PDP, HDP and KDP groups, and the expression of BDNF was significantly down-regulated in P, PDP, HDP and KDP groups ( P<0.05). Compared with group P, the apoptosis rate was significantly decreased, the expression of p-ERK1/2, p-CREB and BDNF was up-regulated, and the expression of cleaved caspase-3 was down-regulated in group PD ( P<0.05). Compared with group PD, the apoptosis rate was significantly increased, the expression of p-ERK1/2, p-CREB and BDNF was down-regulated, and the expression of cleaved caspase-3 was up-regulated in PDP, HDP and KDP groups ( P<0.05). Conclusion:The ERK1/2/CREB/BDNF signaling pathway is involved in dexmedetomidine-induced inhibition of propofol-caused apoptosis in isolated hippocampal neurons of fetal rats.
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435 patients with type 2 diabetes were divided into 2 groups according to their fatty liver,then the relations between fatty liver and various parameters in two groups were observed and analyzed by statistical methods.Body mass index,HbA_1c and triglyceride were the risk factors for fatty liver.The prevalences of metabolic syndrome,hypertension and coronary heart disease in fatty liver group were significantly higher than those in the control group.
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Objective To study the clinical characteristics of Gitelman′s syndrome, and the differentiation of Gitelman′s syndrome from Bartter′s syndrome. Methods Clinical data of 2 patients diagnosed as Gitelman′s syndrome were retrospectively analysed. Results The symptoms of both patients appeared at adult age, their main manifestation included hypokalaemic alkalosis, hyperreninemia and juxtaglomerular apparatus hyperplasia with normal blood pressure, hypocalciuria and hypomagnesemia, then the diagnosis of Gitelman′s syndrome was established. Potassium and magnesium supplementation ameliorated one patient′s symptom. Another patient treated with indomethacin, serum potassium was recovered to normal level. Conclusion Gitelman′s syndrome and Bartter′s syndrome appear to be similar in the pathogenesis, clinical manifestation and prognosis, but still show some differences, Gitelman′s syndrome should be carefully differentiated from Bartter′s syndrome.
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This article reports the development of hyperosmolar hypernatremic hyperchloremic coma and acute renal failure in a male diabetic patient after recovery from hyperosmolar hypergly-cemic nonketonic coma, of which the cause is fluid retention in excess of urinary output due to the obstruction of lower urethra by diabetic neurogenic urinary bladder and hyper-plasia of prostate gland.By our experience each old diabetic man should be examined to confirm if he has neuro-genic urinary bladder and/or hyperplasia of prostate gland. Care should be taken to keep the balance of fluid intake and output provided that both of these conditions are present. The acute obstructive nephropathy can quickly ameliorate with release of the obstruction.