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Article in Chinese | WPRIM | ID: wpr-808825


Objective@#To investigate the molecular epidemiological characteristics of Human Calicivirus (HuCV) infection among children less than 5 years in Kunming city, Yunnan province, it might be provide effective evident for prevention and control the diarrhea related with HuCV infection.@*Methods@#Four sentinel hospitals were recruited in the study from Kunming city, Yunnan province, 850 diarrhea cases and 170 non-diarrhea subject were recruited in this study from 2014 to 2015. RT-PCR was performed to screen HuCV infection, and gene sequencing was used to ensure positive infection subtypes and genotypes.@*Results@#The positive rate of HuCV was higher in children with diarrhea than in non-diarrhea children (11.5%, 98/85; 4.7%, 8/170, χ2=7.083, P=0.008), and the positive rate of Norovirus (NoV) GII was higher in non-diarrhea children were (11.1%, 94/85; 4.7%, 8/170, χ2=6.353, P=0.012). There was no significant difference in the positive rate of NoV GI (0.1%, 1/850; 0.0%, 0/170, P=0.833) and Sappovirus (0.4%, 3/850; 0.0%, 0/170, P=0.578) in diarrhea children and non-diarrhea children. GII.P4 (10%, n=102) was the most important genotype of NoV GII detected in diarrhea and non-diarrhea individuals. Despite no significant difference in Norovirus GII infection between different age groups (χ2=0.038, P=0.846) and sex(χ2=0.620, P=0.733), infection rate of NoV GII varied with season (χ2=9.867, P=0.020), having close relationship with diarrhea in autumn (15.6%), primarily caused by GII.4 and GII.12 genotype (χ2=8.881, P=0.031; χ2=7.917, P=0.039).@*Conclusions@#NoV GII diarrhea had higher epidemic rate, which was caused by multiple genotypes, GII.P4 was a dominant genotype, and was a major pathogenic agent of diarrhea in infants f in Kunming city.

Article in Chinese | WPRIM | ID: wpr-312626


<p><b>OBJECTIVE</b>To analyze the biochemical and pathological changes in mice with type 2 diabetes mellitus (T2DM) induced by high-fat diet combined with low-dose streptozotocin (STZ) injections.</p><p><b>METHODS</b>C57BL/6J mice were divided randomly into normal control group (NC group), high-fat diet group (HC group) and high-fat diet plus STZ group (HC+STZ group). The mice were fed on normal chow or a high-fat diet for 1 month before two introperitoneal injections of STZ (40 mg/kg) or citrate buffer with an interval of 24 h as appropriate. Fasting blood glucose (FBG) was detected every week for 4 weeks, and oral glucose tolerance test (OGTT) was performed one month after the injections, after which the biochemical profiles, islet and liver were evaluated by immunohistochemical and pathological analysis.</p><p><b>RESULTS</b>In HC+STZ group, FBG was above the cutoff value (13.89 mmol/L) in 75% of the mice at 1 week after STZ injections and in all the mice at two weeks except for the death of 1 mouse, with a success rate of modeling of 91.3%. FBG in HC group, though slightly higher than that in NC group, remained normal (6.8 mmol/L). The body weight in HC+STZ and HC groups was significantly higher than that in NC group after feeding but without obvious increases after the injections (P<0.01). Blood glucose in HC+STZ group at 0.5 to 2 h after OGTT and the area under curve (AUC) were higher than those in NC and HC groups (P<0.01); the AUC in HC group was a also higher than that in NC group (P<0.05). Plasma creatinine was significantly higher in HC+STZ group than in NC (P<0.01) and HC (P<0.05) groups. Insulin secretion by the islets decreased obviously in HC+STZ and HC group. The mice in HC+STZ group showed atrophy, fibrosis, and vacuolization in the islets with mild fatty liver but no visible renal pathologies.</p><p><b>CONCLUSION</b>High-fat diet and low-dose STZ injections can induce T2DM in mice with very similar biochemical and pathological changes to human T2DM and with such complications as fatty liver.</p>

Animals , Blood Glucose , Body Weight , Diabetes Mellitus, Type 2 , Diet, High-Fat , Fatty Liver , Glucose Tolerance Test , Insulin , Insulin Resistance , Islets of Langerhans , Pathology , Kidney , Pathology , Mice , Mice, Inbred C57BL , Streptozocin
Article in Chinese | WPRIM | ID: wpr-319464


<p><b>OBJECTIVE</b>To investigate AXIN1-related CSRNP1 gene expression and the mechanism of its transcriptional regulation in TGF-β1-induced tumor cells.</p><p><b>METHODS</b>Human lung carcinoma A549 cells or human prostate cancer PC3 cells were treated with TGF-β1 at different doses (0, 20, 40, and 80 ng/ml) or at 20 ng/ml for 0, 8, 12, or 24 h, and the dose and time effect of TGF-β1 on CSRNP1 mRNA expression in the tumor cells were evaluated with real-time RT-PCR. A549 cells were also treated with TGF-β1 and cycloheximide to clarify whether CSRNP1 expression induced by TGF-β1 required de novo protein synthesis. A549 cells transfected with pcDNA3.1, flag-SMAD3, or flag-SMAD3-mu, after serum starvation, were treated with or without TGF-β1 (20 ng/mL) for 24 h, and the overexpression of wild-type SMAD3 and dominant negative SMAD3-mu mutant were confirmed by Western blotting. The effect of SMAD3 or SMAD3-mu overexpression on CSRNP1 mRNA expression was also measured by real-time RT-PCR.</p><p><b>RESULTS</b>In both A549 and PC3 cells, TGF-β1 dose- and time-dependently stimulated CSRNP1 expression, which required de novo protein synthesis in A549 cells. Overexpression of wild-type SMAD3 significantly increased the expression of CSRNP1 mRNA induced by TGF-β1, while overexpression of dominant negative SMAD3 mutant remarkably reduced CSRNP1 mRNA expression in response to TGF-β1 in A549 cells.</p><p><b>CONCLUSION</b>TGF-β1 may contribute to CSRNP1 expression through SMAD3 activation and downstream signaling in tumor cells.</p>

Apoptosis Regulatory Proteins , Genetics , Metabolism , Axin Protein , Genetics , Metabolism , Cell Line, Tumor , Gene Expression Regulation, Neoplastic , Humans , RNA, Messenger , Genetics , Signal Transduction , Smad3 Protein , Genetics , Metabolism , Transfection , Transforming Growth Factor beta1 , Pharmacology
Article in Chinese | WPRIM | ID: wpr-322047


<p><b>OBJECTIVE</b>To explore the functional role of protein kinase D1 (PKD1) in the activation of nuclear factor-κB (NF-κB) signal pathway and NF-κB transcription mediated by Aspergillus fumigatus.</p><p><b>METHODS</b>A549 cells and HEK293 cells were transfected with green fluorescence protein (GFP) or GFP-PKD1 followed by treatment with 1×10(5) CFU/ml Aspergillus fumigatus conidia for different time lengths. The phosphorylation levels of PKD1, IκB and p65 (pS276) in the transfected cells were measured by Western blotting. A549 cells were transfected with GFP-PKD1 or siRNA-PKD1, and the phosphorylation of IκB and p65 (pS276) was examined. Finally, NF-κB-luc and renilla luciferase reporter pRL-SV40 were cotransfected into GFP- or GFP-PKD1-transfected A549 cells before exposure of the cells to Aspergillus fumigatus conidia for 24 h, and NF-κB transcriptional activity in the cells was determined using dual-luciferase reporter assay.</p><p><b>RESULTS</b>Overexpression of PKD1 significantly increased Aspergillus fumigatus conidia-stimulated phosphorylation of PKD1, IκB and p65 (pS276), whereas PKD1 knockdown by siRNA-PKD1 suppressed IκB and p65 (pS276) phosphorylation. Dual luciferase assay demonstrated that PKD1 overexpression markedly enhanced Aspergillus fumigatus-induced NF-κB transcription in A549 cells.</p><p><b>CONCLUSION</b>PKD1 may contribute to the activation of NF-κB signal pathway and NF-κB transcription induced by Aspergillus fumigatus.</p>

Aspergillus fumigatus , Cell Line, Tumor , HEK293 Cells , Humans , I-kappa B Kinase , Metabolism , NF-kappa B , Metabolism , Phosphorylation , Protein Kinase C , Metabolism , Signal Transduction , Transcription Factor RelA , Metabolism , Transcription, Genetic , Transfection