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The genesis and source of the H7N9 influenza viruses causing human infections in China
It is shown that H7 viruses probably transferred from domestic duck to chicken populations in China on at least two independent occasions and subsequently reassorted with enzootic H9N2 viruses to generate the H7N9 outbreak lineage, and a related previously unrecognized H7n7 lineage.
NAFLD causes selective CD4+ T lymphocyte loss and promotes hepatocarcinogenesis
It is shown that dysregulation of lipid metabolism in NAFLD causes a selective loss of intrahepatic CD4+ but not CD8+ T lymphocytes, leading to accelerated hepatocarcinogenesis, providing an unexpected link between lipid dysregulation and impaired anti-tumour surveillance.
Gut microbiome–mediated bile acid metabolism regulates liver cancer via NKT cells
The role of bile acids in immunosurveillance of tumors growing in the liver is focused on and altering commensal gut bacteria induced a liver-selective antitumor effect.
Opposing Effects of Sirtuins on Neuronal Survival: SIRT1-Mediated Neuroprotection Is Independent of Its Deacetylase Activity
This study represents the first analysis of SIRTs 3–7 in the regulation of neuronal survival and shows that neuroprotection by SIRT1 can be mediated by a novel, non-catalytic mechanism, and that subcellular localization may be an important determinant in the effect of SIRT5 on neuronal viability.
Dissemination, divergence and establishment of H7N9 influenza viruses in China
It is shown that H7N9 viruses have spread from eastern to southern China and become persistent in chickens, which has led to the establishment of multiple regionally distinct lineages with different reassortant genotypes.
The NKG2D ligand ULBP4 binds to TCRgamma9/delta2 and induces cytotoxicity to tumor cells through both TCRgammadelta and NKG2D.
The data suggest that ULBP4 functions as a ligand for both TCRgammadelta and NKG2D and may play a key role in immune surveillance of tumor development and clearance of viral infection.
Isoform-Specific Toxicity of Mecp2 in Postmitotic Neurons: Suppression of Neurotoxicity by FoxG1
It is reported that in cultured cerebellar granule neurons induced to die by low potassium treatment and in Aβ-treated cortical neurons, Mecp2-e2 expression is upregulated whereas expression of the Mec p3-e1 isoform is downregulated, and that elevated FoxG1 expression inhibits MeCP2- e2 neurotoxicity.