The role of arecoline on hepatic insulin resistance in type 2 diabetes rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To explore the effects of arecoline on hepatic insulin resistance in type 2 diabetes rats and to elucidate its possible mechanism.</p><p><b>METHODS</b>Forty five Wistar rats were fed with high fructose diet for 12 weeks to induce type 2 diabetic rat model. rats were randomly divided into 5 groups (n = 8): control group, model group and model group were treated with different dose (0, 0.5, 1, 5 mg/kg) of arecoline. After 4 weeks, the fasting blood glucose, blood lipid and insulin level measured , mRNA expression of liver constitutive androstane receptor (CAR), pregnane X receptor (PXR), glucose-6-phosphatase (G6Pase), phosphoenolpyruvate carboxykinase (PEPCK), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were detected by reverse transcription polymerase chain reaction (RT-PCR), the protein expression of p-AKT and glucose transporter4 (GLUT4) were detected by Western blot.</p><p><b>RESULTS</b>1.5 mg/kg arecoline could significantly decrease the level of fasting blood glucose, blood lipid, blood insulin level and liver G6Pase, PEPCK, IL-6, TNF-alpha mRNA level in type 2 diabetes rats. 1.5 mg/kg arecoline also could significantly increase CAR, PXR mRNA level and p-AKT and GLUT4 protein expression.</p><p><b>CONCLUSION</b>Arecoline improved hepatic insulin resistance in type 2 diabetes rats by increasing the mRNA levels of CAR and PXR leading to the creased glucose metabolism and inflammation related genes expression.</p>

miRNA expression change of differentiation of mice marrow mesenchymal stem cells into adipocytes / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To explore miRNA expression change of differentiation of mice marrow mesenchymal stem cells (MSCs) into adipocytes, which lay the foundation for further studies on molecular mechanism of miRNA regulating the differentiation of MSCs into adipocytes.</p><p><b>METHODS</b>C57BL/6 mice MSCs were isolated, cultured through the whole bone marrow method, amplified by the differential adherent method. Cell growth was observed by morphology and the expression of superficial antigen CD29, CD44, CD34 were detected through immunohistochemistry. MSCs was induced to differentiation into adipocytes with adipocyte differentiation medium, and adipogenic differentiation of MSCs was analyzed by oil Red O staining. MicroRNA microarray was used to investigate the differentially expressed miRNAs in MSCs and adipocytes.</p><p><b>RESULTS</b>(1) The fifth passage of MSCs had high purity under an inverted m icroscope. Immunohistochemistry staining showed that CD29, CD44 were positive and CD34 was negative in more than 90% MSCs. There were a large number of lipid droplets in cytoplasm after MSCs were induced with adipocyte differentiation medium, Oil O staining was positive. (2) The microarray experiment showed that 75 differentially expressed miRNAs were obtained in adipocytes compared with MSCs, 20 up-regulated and 55 down-regulated miRNAs were observed among them.</p><p><b>CONCLUSION</b>There was a expression change of miRNA of differentiation of MSCs into adipocytes, some miRNAs might play important roles in MSCs adipogenic differentiation.</p>

The emergence of candidate pathogenicity island 89K DNA sequence of Streptococcus suis isolated from sporadic patients in Zhejiang province / 中华流行病学杂志

Objective To identify the presence of candidate pathogenicity island 89K DNA sequence of Streptococcus suis serotype 2 (SS2) strains isolated from patient in Zhejiang province. Methods Genes and DNA fragments were amplified by PCR, using specific primers, and three amplified fragments of the89K sequence were directly sequenced. The results were analyzed using software related to bioinformaties and epidemiology. Results 8 strains of SS2 all contained 89K sequence, cps2J and mrp virulent genes, and species-specific 16S rDNA. 3 amplified fragments of 89K candidate pathogenicity island of SS2 ZJ0501 were above 99% similar to SS2 strain identified from outbreaks in Jiangsu in 1998, and the gene fragment of coding DNA recombinant protein in the 89K sequence was highly homological with that of S. dysgalactiae and S. agalactiae. Conclusion In recent years SS2 strains isolaed from patients with clinical symptoms in Zhejiang province had been detected to have contained candidate pathogenicy 89K DNA fragment.

Involvement of TRAIL up-regulation of CD4+, CD8+ T cells in liver injury in chronic hepatitis B / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To describe a novel mechanism for TRAIL up-regulation of CD4+, CD8+ T cells to participate in the pathophysiological process in patients with chronic hepatitis B (CHB).</p><p><b>METHODS</b>The serum levels of soluble TRAIL (sTRAIL), IFN-gamma and membrane bound TRAIL expression on peripheral leucocytes from 58 CHB patients were examined by ELISA and flow cytometry respectively. The levels of TRAIL were compared with the baseline levels of 15 healthy controls, and correlation analysis were performed between ALT, TBil and PT, morphological change in hepatic tissues.</p><p><b>RESULTS</b>The results showed that TRAIL levels on membranes of CD4+, CD8+ T cells in CHB patients were much higher than the healthy controls (P < 0.001), which of CD4+ T cells positively correlated with serum TBil (r=0.354, P = 0.008), Serum IFN-gamma level (r=0.302, P = 0.011) and which of CD8+ T cells positively correlated with serum TBil (r=0.522, P = 0.000), ALT (r=0.393, P = 0.003), PT (r=0.385, P = 0.004), serum IFN-gamma level (r=0.307, P = 0.009). The serum levels of soluble TRAIL only correlated with serum HBeAg expression (r=0.695, P = 0.001).</p><p><b>CONCLUSION</b>These findings suggest that the expression of TRAIL on the membranes of lymphocytes was up-regulated, which may take part in the immunopathogenesis in CHB patients. TRAIL expression can be induced either by virus-specific protein expression or by inflammation cytokine IFN-gamma</p>

Effects of hyperthermia on brainstem auditory evoked potentials and middle latency response in rats / 中国应用生理学杂志

<p><b>AIM</b>To study the effects of hyperthermia on brainstem auditory evoked potentials (BAEP) and middle latency response (MLR) in rats.</p><p><b>METHODS</b>BAEP and MLR were recorded at the skull surface of rats. The body temperature of anesthetized rats increased gradually with a physical method and was detected by a digital thermometer inserted into the rectum. The peak latency (PL), interpeak latency (IPL), wave amplitude and the critical body temperature at which BAEP and MLR completely lost had been observed.</p><p><b>RESULTS</b>All PL and I - II, I - III and I -IV IPL of BAEP shortened more and more as the body temperature increased step by step from 37 degrees C to 41.5 degrees C. But all PL and I - II and I -IV IPL did not shortened further and prolonged a little contrary as the body temperature at 42 degrees C and over 42 degrees C. All PL and P1-P3 and P2-P3 IPL of MLR also shortened as the body temperature increased from 37 degrees C to 43 degrees C. The wave amplitudes of BAEP and MLR decreased as the body temperature increased, especially as the body temperature over 42 degrees C. BAEP and MLR lost completely and synchronously at the body temperature (43.1 +/- 0.5) degrees C, which was not reversed as the body temperature returning to normal by cooling.</p><p><b>CONCLUSION</b>There were obvious effects of hyperthermia on both BAEP and MLR in rats, and irreversible impairments appeared at a critical body temperature.</p>