OBJECTIVETo investigate the association between neck circumference and central obesity, overweight, and metabolic syndrome in Chinese individuals with type 2 diabetes.RESEARCH DESIGN AND METHODSA total of 3,182 diabetic subjects (aged 20–80 years) were recruited from 15 community health centers in Beijing using a multistage random sampling approach.RESULTSReceiver operating characteristic analysis showed that the area under the curve for neck circumference and central obesity was 0.77 for men and 0.75 for women (P < 0.001). Furthermore, a neck circumference of ≥38 cm for men and ≥35 cm for women was the best cutoff point for determining overweight subjects. A neck circumference of ≥39 cm for men and ≥35 cm for women was the best cutoff point to determine subjects with metabolic syndrome.CONCLUSIONSIn the present study, neck circumference is positively related with BMI, waist circumference, and metabolic syndrome in Chinese individuals with type 2 diabetes.

Sclerotinia sclerotiorum causes a highly destructive disease in oilseed rape (Brassica napus) resulting in significant economic losses. Studies on the Arabidopsis thaliana MPK4 loss-of-function mutant have implicated that AtMPK4 is involved in plant defense regulation, and its effect on disease resistance varies in different plant-pathogen interactions. In this study, we isolated a B. napus mitogen-activated protein kinase, BnMPK4, and found that BnMPK4 along with PDF1.2 are inducible in resistant line Zhongshuang9 but both are consistently suppressed in susceptible line 84039 after inoculation with S. sclerotiorum. Transgenic oilseed rape overexpressing BnMPK4 markedly enhances resistance to S. sclerotiorum and Botrytis cinerea. Further experiments showed that transgenic plants inhibited growth of S. sclerotiorum and constitutively activated PDF1.2 but decreased H2O2 production and constitutively suppressed PR-1 expression. Treatment of roots of the transgenic plants with H2O2 solution resulted in enhanced susceptibility to the two pathogens. Our results support the idea that MPK4 positively regulates jasmonic acid-mediated defense response, which might play an important role in resistance to S. sclerotiorum in oilseed rape.

It has been verified that long noncoding RNAs (lncRNAs) have great effects on various biological behaviors of human diseases. Although more and more lncRNAs have been studied in human cancers, countless lncRNAs still need to be excavated. This study aims to investigate the impacts of lncRNA SNHG16 on proliferation and metastasis of human hemangioma endothelial cell (HemECs). qRT‐PCR analysis was carried out to explore the expression pattern of SNHG16, miR‐520d‐3p, and STAT3. The effect of SNHG16 on cell proliferation was detected by MTT and colony formation assay. Flow cytometry analysis was performed to test the apoptosis of HemECs cells. Migration and invasion of HemECs cells were determined and examined by transwell assays. Tube formation assay helped to observe the influence of SNHG16 expression on the vasoformation of HemECs cells. The correlations among SNHG16, miR‐520d‐3p, and STAT3 were certified by bioinformatics analysis, pull‐down assay, and dual‐luciferase reporter assay. Finally, rescue assays were conducted to demonstrate the effects of SNHG16‐miR‐520d‐3p‐STAT3 axis on biological behaviors of HemECs cell. SNHG16 was strongly expressed in proliferating phase hemangioma tissues and HemECs cells. Silenced SNHG16 negatively affected proliferation, migration, and invasion of HemECs cell. LncRNA SNHG16 acted as a ceRNA to upregulate STAT3 through binding with miR‐520d‐3p in HemECs cell. LncRNA SNHG16 acted as a ceRNA to drive proliferation, vasoformation, migration, and invasion of HemECs cells through modulating miR‐520d‐3p/STAT3 axis.

MicroRNAs may function to promote or suppress tumor development, depending on the cellular context. The important role of microRNAs in regulating molecular pathways underlying tumorigenesis has been emphasized in hepatocellular carcinoma (HCC). MicroRNAs regulate gene expression via post-transcriptional mechanisms by inhibiting translation or by degrading mRNA. In this study, we show that microRNA-1 (miR-1) and microRNA-499 (miR-499) are capable of repressing the expression of the ets1 proto-oncogene, which plays a fundamental role in the extracellular matrix (ECM) degradation, a process required for tumor cell invasion and migration. We used luciferase reporter assays to demonstrate that miR-1 and miR-499 target the 3' untranslated region (UTR) of ets1. Overexpression of miR-1 and miR-499 in HepG2 cells led to downregulation of ets1 mRNA and protein as assessed by quantitative reverse transcription PCR and western blot analysis. Furthermore, overexpression of miR-1 and miR-499 inhibited the invasion and migration of HepG2 cells in matrigel invasion and transwell migration assays, respectively. These results suggest that miR-1 and miR-499 may play an important role in the pathogenesis of HCC by regulating ets1.