ABSTRACT
Objective To investigate the role of glucose transporter ( GLUT ) 2 and 4 in hyperuricemia-induced insulin resistance. Methods Male uric acid oxidase gene knock-out spontaneous hyperuricemia mice ( KO) and wild-type mice ( WT) were fed with high-fat diet to establish an insulin resistance model. Then, some of KO mice were treated with allopurinol for lowering uric acid. Uric acid, fasting plasma glucose (FPG), and fasting insulin ( FINS) were detected. Intraperitoneal glucose tolerance test ( IPGTT ) and insulin tolerance test ( ITT ) were performed. Finally, the expression levels of Slc2a4 and Slc2a2 mRNA in tissues were determined by real-time PCR, while those of GLUT2 and GLUT4 proteins in tissues were analyzed by Western blot. Results There was no significant difference in FPG among various groups. The level of FINS in KO group was significantly higher than that in WT group [(0.636± 0.07) vs (0.456 ± 0.03) ng/ml, P<0.01], with decreased insulin sensitivity and impaired glucose tolerance. The uric acid level in the KO group remained at a high level [ ( 549. 68 ± 48. 7 ) vs ( 216. 61 ± 27. 5 )μmol/L] . After uric acid level in KO mice was reduced by allopurinol, insulin sensitivity and glucose metabolism were improved. Compared with WT group, the expression levels of Slc2a4 and GLUT4 in the gastrocnemius muscle were decreased while the expression levels of Slc2a2 and GLTU2 in liver were increased in KO group, which were reversed by allopurinol-mediated uric acid reduction. Conclusion Uric acid may induce insulin resistance via decreasing Slc2a4/GLUT4 expressions in skeletal muscle, and increasing Slc2a2/GLTU2 expressions in liver.
ABSTRACT
Objective:To explore the influence of new labor standards on the indications in the birth process and the prognosis of mothers and infants.Methods:186 cases treated in our hospital from January,2015 to January,2016 were divided into the observation group (85 cases) and the control group (101 cases),the observation group received new labor standards,the control group adopt Friedman labor standards.The clinical indications,pregnant complications,pregnant outcome,neonatal-perinatal outcome were compared between two groups.Results:The cesarean delivery rate,number of using oxytocin,forceps delivery rate of observation group were significantly lower than those of the control group(P＜0.05);the duration time of both first and second stage of labor were obviously longer than those of the control group (P＜0.05);the duration time of active phase,bleeding volume in birth process in both groups showed no statistical difference (P＞0.05);there was no adverse maternal and infant events in both groups;the incidence rate of pregnancy complications,fetal distress in uterus,asphyxia neonatorum and neonatal body weight were of no statistical difference (P＞0.05).Conclusion:The new labor standards prolong the duration time of birth and give women fully trial opportunities,could effectively reduce the rate of cesarean section,reduce the over intervention production.
ABSTRACT
<p><b>BACKGROUND AND OBJECTIVE</b>Several reports demonstrated that the ubiquitin C terminal hydrolase-L1 (UCH-L1) has been found to be an oncogene in malignant tumors such as esophageal carcinoma, lung cancer and breast cancer. The aim of this study is to explore the effects of liposomal transfection of UCH-L1 siRNA on the proliferation and apoptosis of lung adenocarcinoma cell lines H157.</p><p><b>METHODS</b>UCH-L1 siRNA was synthesized and transfected into H157 cell by liposome. Cell morphological change was observed with microscope, and cell proliferation and apoptosis index detected by flow cytometry, UCH-L1 mRNA expression was determined by RT-PCR and protein level of UCH-L1 was determined by Western blot.</p><p><b>RESULTS</b>For the H157 cell transfected with siRNA, cell proliferation was inhibited significantly, cell apoptosis appeared obviously, the expression of UCH-L1 mRNA and protein level of UCH-L1 significantly decreased.</p><p><b>CONCLUSION</b>UCH-L1 siRNA is able to inhibit the proliferation of lung adenocarcinoma cell lines H157 and induce the apoptosis. UCH-L1 might become a new target for lung carcinoma gene therapy.</p>