Herpes Simplex Virus Type 2 Immediate Early Protein ICP27 Inhibits IFN-β Production in Mucosal Epithelial Cells by Antagonizing IRF3 Activation.

Herpes simplex virus type 2 (HSV-2) is the main cause of genital herpes and infections are common in the lower genital tract. Although neuronal and immune cells can be infected, epithelial cells, and keratinocytes are the primary HSV-2 target cells. HSV-2 establishes latency by evading the host immune system and its infection can also increase the risk of HIV-1 sexual transmission. Our pervious study found that HSV-2 immediate early protein ICP22, inhibited IFN-β production by interfering with the IRF3 pathway. However, ICP22-null HSV-2 did not completely lose the capability of suppressing IFN-β induction, suggesting the involvement of other viral components in the process. In this study, by using an ex vivo cervical explant model, we first demonstrated that HSV-2 can indeed inhibit IFN-β induction in human mucosal tissues. We further identified HSV-2 immediate early protein ICP27 as a potent IFN-β antagonist. ICP27 significantly suppresses the Sendai virus or polyinosinic-polycytidylic acid-induced IFN-β production in human mucosal epithelial cells, showing that ICP27 inhibits the IFN-β promoter activation, and IFN-β production at both mRNA and protein levels. Additional studies revealed that ICP27 directly associates with IRF3 and inhibits its phosphorylation and nuclear translocation, resulting in the inhibition of IFN-β induction. Our findings provide insights into the molecular mechanism underlying HSV-2 mucosal immune evasion, and information for the design of HSV-2 mucosal vaccines

(Bis{2-[3-(2,4,6-trimethyl­benz­yl)imid­azolin-2-yliden-1-yl-κC 2]-4-methyl­phenyl}amido-κN)chloridopalladium(II)

The coordination geometry about the Pd centre in the title compound, [Pd(C40H42N5)Cl], is approximately square-planar. The CNC pincer-type N-heterocyclic carbene ligand binds to the Pd atom in a tridentate fashion by the amido N atom and the two carbene atoms and generates two six-membered chelate rings, completing the coordination

NETSTARS 模式加入橋墩沖刷功能之研究─以八掌溪為例

This study applies NETSTARS V3.0 by adding the calculation functions of eighteen pier scour formulas based on a comprehensive literature review to demonstrate local scour mechanisms. The study area is a reach of the Pachang Creek from the Housheng Bridge to the Chukou Bridge. We do not set the structures and weirs in the river to be scoured. Simulations are conducted by setting boundary conditions and importing information about nineteen bridges, and validations are separated into two steps as: general scouring and bridge local scouring. The best parameters are qualified by computing error evaluated parameter to fit the changing tendencies of the Pachang Creek. Finally, long-term riverbed evolution is simulated. The results show that there are 5 bridges with erosion trends. The results can be used as a reference for one-dimensional numerical models with pier scouring functions.本研究以NETSTARS V3.0 功能為基礎，根據橋墩沖刷研究，撰寫橋墩沖刷功能並新增18 個常用的橋墩沖刷公式於模式中。研究區域為八掌溪厚生橋至觸口橋河段。在輸砂模式建置上，將結構物設定為不可沖刷，並輸入邊界條件與現有19 座橋樑資訊，完成一般沖刷與局部沖刷階段之參數檢定，並利用誤差評估參數檢視最佳參數以反應八掌溪流域河床變遷趨勢。最後對未來十年河床沖淤進行預測，推測有沖刷趨勢的橋樑共5 座，研究成果可作為一維數值模式新增橋墩沖刷功能之參考

Chromatic interferometry with small frequency differences

By developing a `two-crystal' method for color erasure, we can broaden the scope of chromatic interferometry to include optical photons whose frequency difference falls outside of the 400 nm to 4500 nm wavelength range, which is the passband of a PPLN crystal. We demonstrate this possibility experimentally, by observing interference patterns between sources at 1064.4 nm and 1063.6 nm, corresponding to a frequency difference of about 200 GHz.Comment: 5 pages, 3 figure

Corrigendum to: The TianQin project: current progress on science and technology

In the originally published version, this manuscript included an error related to indicating the corresponding author within the author list. This has now been corrected online to reflect the fact that author Jun Luo is the corresponding author of the article

Nucleosomes Correlate with In Vivo Progression Pattern of De Novo Methylation of p16 CpG Islands in Human Gastric Carcinogenesis

BACKGROUND: The exact relationship between nucleosome positioning and methylation of CpG islands in human pathogenesis is unknown. METHODOLOGY/PRINCIPAL FINDINGS: In the present study, we characterized the nucleosome position within the p16 CpG island and established a seeding methylation-specific PCR (sMSP) assay based on bisulfite modification to enrich the p16 alleles containing methylated-CpG at the methylation "seeding" sites within its intron-1 in gastric carcinogenesis. The sMSP-positive rate in primary gastric carcinoma (GC) samples (36/40) was significantly higher than that observed in gastritis (19/45) or normal samples (7/13) (P<0.01). Extensive clone sequencing of these sMSP products showed that the density of methylated-CpGs in p16 CpG islands increased gradually along with the severity of pathological changes in gastric tissues. In gastritis lesions the methylation was frequently observed in the region corresponding to the exon-1 coding-nucleosome and the 5'UTR-nucleosome; the methylation was further extended to the region corresponding to the promoter-nucleosome in GC samples. Only few methylated-CpG sites were randomly detected within p16 CpG islands in normal tissues. The significantly inversed relationship between the p16 exon-1 methylation and its transcription was observed in GC samples. An exact p16 promoter-specific 83 bp-MSP assay confirms the result of sMSP (33/55 vs. 1/6, P<0.01). In addition, p16 methylation in chronic gastritis lesions significantly correlated with H. pylori infection; however, such correlation was not observed in GC specimens. CONCLUSIONS/SIGNIFICANCE: It was determined that de novo methylation was initiated in the coding region of p16 exon-1 in gastritis, then progressed to its 5'UTR, and ultimately to the proximal promoter in GCs. Nucleosomes may function as the basic extension/progression unit of de novo methylation of p16 CpG islands in vivo