ABSTRACT
Objective:To investigate the changes and clinical significance of neuron specific enolase (NSE) and S-100β protein levels in cerebrospinal fluid of children with viral encephalitis and meningitis.Methods:Sixty children with viral encephalitis and meningitis admitted to The Second Hospital of Jiaxing from February 2018 to December 2020 were included in the observation group. An additional 30 children without central nervous system diseases who concurrently received treatment in the same hospital were included in the control group. The value of NSE and S-100β protein levels in the diagnosis and treatment of viral encephalitis and meningitis in chiblren were analyzed.Results:NSE and S-100β protein levels in the observation group were (17.683 ± 1.321) μg/L and (1.755 ± 0.129) μg/L, respectively, which were significantly higher than (5.267 ± 0.907) μg/L and (0.827 ± 0.172) μg/L in the control group ( t = 46.25, 28.65, both P < 0.001). NSE and S-100β protein levels in children with mild viral encephalitis and meningitis were (15.219 ± 0.870) μg/L and (1.456 ± 0.113) μg/L, respectively, which were significantly lower than (19.893 ± 1.066) μg/L and (2.014 ± 0.085) μg/L in children with severe viral encephalitis and meningitis ( t = -18.69, -21.32, both P < 0.001). In children with viral encephalitis and meningitis, NSE and S-100β protein levels during the acute phase were (17.250 ± 1.188) μg/L and (1.683 ± 0.096) μg/L, respectively, which were significantly higher than (11.150 ± 0.971) μg/L and (1.147 ± 0.098) μg/L during the convalescence phase ( t = 30.79, 30.27, both P < 0.001). Conclusion:NSE and S-100β protein levels in cerebrospinal fluid of children with viral encephalitis and meningitis can help evaluate the severity of viral encephalitis and meningitis in children, providing important clinical application value for judging the development and prognosis of viral encephalitis and meningitis.
ABSTRACT
Insulin resistance in insulin sensitive organ results in metabolic disorder such as hyperglycemia, hyperinsulinemia and hyper triglyceridemia which are common features of type 2 diabetes.Insulin resistance in liver cells mainly causes impaired glycogen synthesis, failed to suppress glucose production which is the major contribution to hyperglycemia.FGF-21 as a new metabolic regulator can control fasting blood glucose.The mechanism of FGF-21 effects on regulating plasma glucose has little to known.In order to establish an in vitro insulin resistant model of liver cells and evaluate the effects and mechanism of FGF-21 on glucose metabolism in the cell model, HepG2 cells were incubated with 10-7 mol/L insulin for 24 h to build insulin-resistant cell model.To evaluate the cells for insulin resistance, the cells were stimulated with fresh insulin for 24 h and the glucose uptake by these cells was carried out.The insulin-resistant cells were treated with different concentrations of FGF-21 for 24 h and insulin-treated cells were used as a control.The glucose uptake by the cells was detected by the method of glucose oxidizes/peroxides(GOD-POD);the synergy between insulin and FGF-21 was evaluated.The mRNA expression of GLUT1 in the insulin-resistant cells was detected by the real-time PCR.Glycogen synthesis of the cells was examined by the anthrone method.The results showed that HepG2 cells treated with 10-7 mol/L insulin for 24 h became resistant to insulin and the insulin resistance status was maintained for 48 h without change of cell morphology.FGF-21 could stimulate glucose consumption of the insulin-resistant model in a dose-dependent manner.The glucose consumption and glycogen synthesis of the insulin-resistant model were significantly improved by FGF-21 treatment.FGF-21 showed strong synergy with insulin in glucose uptake and glycogen synthesis of the model cells.While the cells became resistant to insulin, FGF-21 could increase the mRNA expression of GLUT1.Thus, It is concluded that FGF-21 stimulates glucose uptake in insulin resistant HepG2 cells through GLUT1 expression, stimulates glycogen synthesis and improves the glucose metabolism in the insulin resistant liver cell model.