The Kerry-Bush Health Care Proposals: A Characterization and Comparison of their Impacts on Connecticut (Full Report)

health care, connecticut, health insurance

The Kerry-Bush Health Care Proposals: A Characterization and Comparison of their Impacts on Connecticut (Executive Summary)

health care, connecticut, health insurance

The Kerry-Bush Health Care Proposals: A Characterization and Comparison of their Impacts on Connecticut (Technical Appendix)

health care, Connecticut, health insurance

Methyl 3,4-O-isopropyl­idene-2-O-[(methyl­sulfan­yl)thio­carbon­yl]-β-l-arabinoside

In the title compound, C11H18O5S2, the six- and five-membered rings adopt a chair and an approximately planar conformation, respectively

Crystal Structure Manipulation of the Exchange Bias in an Antiferromagnetic Film

Exchange bias is one of the most extensively studied phenomena in magnetism, since it exerts a unidirectional anisotropy to a ferromagnet (FM) when coupled to an antiferromagnet (AFM) and the control of the exchange bias is therefore very important for technological applications, such as magnetic random access memory and giant magnetoresistance sensors. In this letter, we report the crystal structure manipulation of the exchange bias in epitaxial hcp Cr2O3 films. By epitaxially growing twined (10-10) oriented Cr2O3 thin films, of which the c axis and spins of the Cr atoms lie in the film plane, we demonstrate that the exchange bias between Cr2O3 and an adjacent permalloy layer is tuned to in-plane from out-of-plane that has been observed in (0001) oriented Cr2O3 films. This is owing to the collinear exchange coupling between the spins of the Cr atoms and the adjacent FM layer. Such a highly anisotropic exchange bias phenomenon is not possible in polycrystalline films.Comment: To be published in Scientific Reports, 12 pages, 6 figure

Population genetic structure of Marbled Rockfish, Sebastiscus marmoratus (Cuvier, 1829), in the northwestern Pacific Ocean

Sebastiscus marmoratus is an ovoviviparous fish widely distributed in the northwestern Pacific. To examine the gene flow and test larval dispersal strategy of S. marmoratus in Chinese and Japanese coastal waters, 421 specimens were collected from 22 localities across its natural distribution. A 458 base-pair fragment of the mitochondrial DNA (mtDNA) control region was sequenced to examine genetic diversity and population structure. One-hundred-six variable sites defined 166 haplotypes. The populations of S. marmoratus showed high haplotype diversity with a range from 0.8587 to 0.9996, indicating a high level of intrapopulation genetic diversity. Low non-significant genetic differentiation was estimated among populations except those of Hyogo, Behai, and Niiigata, which showed significant genetic differences from the other populations. The demographic history examined by neutrality tests, mismatch distribution analysis, and Bayesian skyline analysis suggested a sudden population expansion dating to the late Pleistocene. Recent population expansion in the last glacial period, wide dispersal of larvae by coastal currents, and the homogeneity of the environment may have important influences on the population genetic pattern. Knowledge of genetic diversity and genetic structure will be crucial to establish appropriate fishery management of S. marmoratus

Functional Characterization of Target of Rapamycin Signaling in Verticillium dahliae

More than 200 plants have been suffering from Verticillium wilt caused by Verticillium dahliae (V. dahliae) across the world. The target of rapamycin (TOR) is a lethal gene and controls cell growth and development in various eukaryotes, but little is known about TOR signaling in V. dahliae. Here, we found that V. dahliae strain is hypersensitive to rapamycin in the presence of rapamycin binding protein VdFKBP12 while the deletion mutant aaavdfkbp12 is insensitive to rapamycin. Heterologous expressing VdFKBP12 in Arabidopsis conferred rapamycin sensitivity, indicating that VdFKBP12 can bridge the interaction between rapamycin and TOR across species. The key across species of TOR complex 1 (TORC1) and TORC2 have been identified in V. dahliae, suggesting that TOR signaling pathway is evolutionarily conserved in eukaryotic species. Furthermore, the RNA-seq analysis showed that ribosomal biogenesis, RNA polymerase II transcription factors and many metabolic processes were significantly suppressed in rapamycin treated cells of V. dahliae. Importantly, transcript levels of genes associated with cell wall degrading enzymes (CWEDs) were dramatically down-regulated in TOR-inhibited cells. Further infection assay showed that the pathogenicity of V. dahliae and occurrence of Verticillium wilt can be blocked in the presence of rapamycin. These observations suggested that VdTOR is a key target of V. dahliae for controlling and preventing Verticillium wilt in plants

Hepatitis B virus–induced imbalance of inflammatory and antiviral signaling by differential phosphorylation of STAT1 in human monocytes

It is not clear how hepatitis B virus (HBV) modulates host immunity during chronic infection. In addition to the key mediators of inflammatory response in viral infection, monocytes also express a high-level IFN-stimulated gene, CH25H, upon response to IFN-a exerting an antiviral effect. In this study, the mechanism by which HBV manipulates IFN signaling in human monocytes was investigated. We observed that monocytes from chronic hepatitis B patients express lower levels of IFN signaling/stimulated genes and higher levels of inflammatory cytokines compared with healthy donors. HBV induces monocyte production of inflammatory cytokines via TLR2/MyD88/NF-kB signaling and STAT1-Ser727 phosphorylation and inhibits IFN-a–induced stat1, stat2, and ch25h expression through the inhibition of STAT1-Tyr701 phosphorylation and in an IL-10–dependent, partially autocrine manner. Further, we found that enhancement of STAT1 activity with a small molecule (2-NP) rescued HBV-mediated inhibition of IFN signaling and counteracted the induction of inflammatory cytokines. In conclusion, HBV contributes to the monocyte inflammatory response but inhibits their IFN-a/b responsiveness to impair antiviral innate immunity. These effects are mediated via differential phosphorylation of Tyr701 and Ser727 of STAT1

Hepatitis C virus core protein triggers expansion and activation of CD4+CD25+ regulatory T cells in chronic hepatitis C patients

CD4+CD25+FoxP3+ regulatory T cells (Tregs) are increased in patients with chronic hepatitis C, which may contribute to the sustained suppression of hepatitis C virus (HCV)-specific T-cell responses and viral persistence in HCV-infected individuals. We postulated that HCV core protein (HCVc) directly contributes to the expansion of Tregs in HCV-infected patients, and we provide evidence to support this hypothesis in the report. Peripheral blood mononuclear cells (PBMCs) and sera were collected from 87 treatment-naïve chronic HCV-infected patients, CD4+CD25+ Tregs were measured by flow cytometry, and HCV RNA and HCVc levels were detected using qPCR and enzyme-linked immunosorbent assay (ELISA), respectively. CD4+, CD8+, CD4+CD25+ and CD4+CD25− T cells were purified from healthy donors and cultured with recombinant HCVc and Toll-like receptor (TLR) ligands. Flow cytometry was used to analyze cell proliferation, and ELISA was performed to measure cytokine production. In the 87 chronic HCV-infected patients, HCVc showed a significant correlation with HCV RNA and CD4+CD25+ Tregs. Mechanistic studies showed that HCVc, together with anti-CD3 antibody, augmented CD4+CD25+ Treg proliferation, but inhibited CD4+CD25− T-cell proliferation and IFN-γ production, in a dose-dependent and Treg-dependent manner. Moreover, unlike the TLR3 ligand (poly I:C) and the TLR4 ligand (lipopolysaccharide, LPS), the TLR2 ligand (lipoteichoic acid, LTA) and HCVc both inhibited TCR-induced CD4+ T-cell proliferation and IFN-γ secretion in a Treg-dependent manner. These data indicate that HCVc, like other TLR2 ligands, triggers CD4+CD25+ Treg activation and expansion to inhibit host immune responses, which may play a critical role in viral persistence in HCV-infected patients