BackgroundThe transmission of hemorrhagic fever with renal syndrome (HFRS) is influenced by climatic variables. However, few studies have examined the quantitative relationship between climate variation and HFRS transmission.ObjectiveWe examined the potential impact of climate variability on HFRS transmission and developed climate-based forecasting models for HFRS in northeastern China.MethodsWe obtained data on monthly counts of reported HFRS cases in Elunchun and Molidawahaner counties for 1997–2007 from the Inner Mongolia Center for Disease Control and Prevention and climate data from the Chinese Bureau of Meteorology. Cross-correlations assessed crude associations between climate variables, including rainfall, land surface temperature (LST), relative humidity (RH), and the multivariate El Niño Southern Oscillation (ENSO) index (MEI) and monthly HFRS cases over a range of lags. We used time-series Poisson regression models to examine the independent contribution of climatic variables to HFRS transmission.ResultsCross-correlation analyses showed that rainfall, LST, RH, and MEI were significantly associated with monthly HFRS cases with lags of 3–5 months in both study areas. The results of Poisson regression indicated that after controlling for the autocorrelation, seasonality, and long-term trend, rainfall, LST, RH, and MEI with lags of 3–5 months were associated with HFRS in both study areas. The final model had good accuracy in forecasting the occurrence of HFRS.ConclusionsClimate variability plays a significant role in HFRS transmission in northeastern China. The model developed in this study has implications for HFRS control and prevention.

The interferon-induced double-stranded RNA-activated protein kinase PKR is the prototype of a class of double-stranded (dsRNA)-binding proteins (DRBPs) which share a dsRNA-binding motif conserved from Drosophila to humans. Here we report the purification of DRBP76, a new human member of this class of proteins. Sequence from the amino terminus of DRBP76 matched that of the M phase-specific protein, MPP4. DRBP76 was also cloned by the yeast two-hybrid screening of a cDNA library using a mutant PKR as bait. Analysis of the cDNA sequence revealed that it is the fulllength version of MPP4, has a bipartite nuclear localization signal, two motifs that can mediate interactions with both dsRNA and PKR, five epitopes for potential M phase-specific phosphorylation, two potential sites for phosphorylation by cyclin-dependent kinases, a RG2 motif present in many RNA-binding proteins and predicts a protein of 76 kDa. DsRNA and PKR interactions of DRBP76 were confirmed by analysis of in vitro translated and purified native proteins. Cellular expression of an epitope-tagged DRBP76 demonstrated its nuclear localization, and its co-immunoprecipitation with PKR demonstrated that the two proteins interact in vivo. Finally, purified DRBP76 was shown to be a substrate of PKR in vitro, indicating that this protein's cellular activities may be regulated by PKR-mediated phosphorylation.

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Emerging evidence has identified that long non-coding RNAs (lncRNAs) may play an important role in the pathogenesis of many cancers, pancreatic cancer (PC) included. However, the role of linc00462 in PC remains unclear. The aim of our present study was to investigate the potential functions of linc00462 in PC and to identify the underlying mechanisms of action. CCK8 assay, transwell assay, cell cycle assay, cell apoptosis assay, EdU assay, western blot assay, cell adhesion assay, HE staining, IF staining, ELISA assay, vivo growth and metastasis assay, and colony formation assay were performed. We demonstrated that OSM mediated up-regulation of linc00462 promoted cell proliferation by accelerating cell cycle process and inhibiting cell apoptosis and adhesion in vitro, enhanced cell migration and invasion by accelerating EMT process, promoted tumor growth and matastasis in vivo and was associated with large tumor size, poor tumor differentiation, TNM stage and distant metastasis in patients of PC. In addition, we demonstrated that linc00462 was a target of miR-665. Linc00462 overexpression enhanced the expression levels of TGFBR1 and TGFBR2, and thus activated the SMAD2/3 pathway in PC cells. In conclusion, linc00462/miR-665/TGFBR1/2 regulatory network may shed light on tumorigenesis in PC.