Objective To investigate the expression of serum amyloid A (SAA) in patients adipose tissue with gestational diabetes mellitus (GDM) and the correlations between SAA and insulin resistance (IR) and body mass index (BMI).Methods A total of 60 single full-term pregnant women underwent cesarean section from June 2013 to December 2013 was enrolled in this study (GDM group,n =30;control group,n =30);serum SAA level was detected with Enzyme-Linked Immunosorbent Assay (ELISA);and mRNA expression of SAA1 in adipose tissue was determined by reverse transcription PCR (RT-PCR);SPSS software was used to compare these markers,and the correlations between SAA and HOMA-IR,BMI were analyzed with Pearson correlation method.Results SAA,mRNA expressions in omental and subcutaneous fat in GDM group (0.447 ± 0.069,0.291 ± 0.067) were significantly higher than those in control group (0.194 ± 0.070,0.231 ± 0.068,P ＜ 0.01).Serum SAA levels [(21.038 ± 6.648) mg/L] and homeostasis model assessment of insulin resistance(HOMA-IR) (4.168± 2.416) in GDM group were significantly higher than those in control group [(14.384 ± 12.770) mg/L,2.045 ± 1.008,P ＜ 0.05];SAA1 mRNA expression levels in omental and subcutaneous fat were positively correlated with serum SAA (r =0.353,0.342,P ＜ 0.01).SAA1 mRNA expression levels in omental were positively correlated to pregestational BMI,late gestational BMI,weight gain in pregnancy and HOMA-IR (r =0.543,0.644,0.340,0.473,P ＜ 0.01),and SAA1 mRNA expression levels in subcutaneous fat were positively correlated to pregestational BMI,late gestational BMI,and HOMA-IR (r =0.788,0.693,0.504,P ＜ 0.01),but was no correlation with weight gain in pregnancy(r =0.013,P ＞ 0.05).Conclusions SAA mRNA expressions in omental and subcutaneous fat in GDM group and serum SAA levels increase,which is positively correlated with BMI and the degree of insulin resistance,SAA may participate in the formation of GDM by increasing insulin resistance.SAA may be used as a new monitor of GDM.

Previous studies have shown that hepatitis E virus （HEV） infection in pregnancy can cause liver failure and adverse pregnancy outcomes such as miscarriage， stillbirth， and vertical transmission， especially in countries where HEV genotypes 1 and 2 are prevalent. In recent years， HEV infection in China is sporadic and is mainly caused by HEV genotype 4， and although studies have shown that most pregnant women with HEV infection in China have no signfinicant clinical symptoms， there is still a high incidence rate of adverse pregnancy outcomes. This article reviews the recent studies on HEV infection in pregnancy， including the advances in pathogenesis， epidemiology， prognosis， mechanism of severe exacerbation， treatment， and prognosis， and puts forward recommendations for the screening and evaluation of HEV infection in pregnancy.

OBJECTIVES: Bladder cancer is one of the most common urothelial tumors with high incidence and mortality rates. Although it has been reported that microRNA (miR)-133b can regulate tumorigenesis of bladder cancer, the mechanism remains unclear. Sex-determining region Y-box transcription factor 4 (SOX4) exhibits an important role in tumorigenesis, but it is unclear whether SOX4 and miR-133b are associated with regulation of pathogenesis of bladder cancer. This study aims to determine the expressions of SOX4 and miR-133b in bladder cancer tissues and cells, investigate their effects on the proliferation, colony formation, and invasion of bladder cancer cells, and to explore the association between miR-133b and SOX4 in regulating biological featurss of bladder cancer cells. METHODS: The bladder cancer and adjacent tissue samples of 10 patients who underwent surgical resection in the Second Xiangya Hospital of Central South Universty from Januray to June 2015 were obtained. The levels of miR-133b were tested by real-time PCR, and the protein levels of SOX4 were evaluated using Western blotting in bladder cancer tissues, matched adjacent tissues, and cell lines. The correlation between miR-133b expression and SOX4 expression in bladder cancer tissues was analyzed. Using the online database TargetScan, the relationship between SOX4 and miR-133b was predicted. MiR-133b mimics, miR-133b inhibitor, and short hairpin RNA (shRNA)-SOX4 were transfected into T24 cells by Lipofectamine 2000. The relationship between miR-133b and SOX4 was also verified by a dual-luciferase reporter assay. The proliferation of T24 cells cultured for 0, 12, 48, 72, and 96 h was evaluated by cell counting kit-8 (CCK-8) assay. The colony formation capacity of bladder cancer cells was tested after 14-day culture, and cell invasion capacity was evaluated with Transwell invasion assay. RESULTS: Bladder cancer tissue and bladder cancer cells had low level of miR-133b but high level of SOX4, compared with matched adjacent tissues and normal bladder epithelial cells. A negative correlation between miR-133b mRNA and SOX4 protein levels in bladder cancer tissues was also found (r=-0.84). The results of online database TargetScan showed that miR-133b targets at SOX4, and overexpression of miR-133b significantly attenuated the expression of SOX4 in T24 cells. Both overexpression of miR-133b and knockdown of SOX4 significantly inhibited the proliferation, colony formation, and invasion capacity of bladder cancer cells in vitro. SOX4 down-regulation restored the effects of miR-133b inhibitor on the proliferation, colony formation, and invasion capacity of T24 cells. CONCLUSIONS The up-regulation of SOX4 contributes to the progression of bladder cancer, and miR-133b can regulate the proliferation, colony formation, and invasion of bladder cancer cells via inhibiting SOX4.
Carcinogenesis/genetics* ; Cell Line, Tumor ; Cell Movement/genetics* ; Cell Proliferation/genetics* ; Epithelial Cells/metabolism* ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs/genetics* ; SOXC Transcription Factors/genetics* ; Urinary Bladder ; Urinary Bladder Neoplasms/genetics*