What's new for 'JKB_daily1' in PubMed

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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Saturday, 2010 Apr 24
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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1.	Nat Med. 2010 Apr;16(4):396-9. Endoplasmic reticulum stress and atherosclerosis. Hotamisligil GS. Department of Genetics, and the Broad Institute of Massachusetts Institute of Technology and Harvard, Harvard School of Public Health, Boston, Massachusetts, USA. ghotamis@hsph.harvard.edu Abstract Atherosclerosis and related cardiovascular diseases represent one of the greatest threats to human health worldwide. Despite important progress in prevention and treatment, these conditions still account for one third of all deaths annually. Often presented together with obesity, insulin resistance and type 2 diabetes, these chronic diseases are strongly influenced by pathways that lie at the interface of chronic inflammation and nutrient metabolism. Here I discuss recent advances in the study of endoplasmic reticulum stress as one mechanism that links immune response with nutrient sensing in the pathogenesis of atherosclerosis and its complications.
	PMID: 20376052 [PubMed - indexed for MEDLINE]
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	Publication Types: Research Support, N.I.H., Extramural MeSH Terms: Animals Apoptosis/physiology Atherosclerosis/etiology* Endoplasmic Reticulum/physiology* Humans Inflammation/physiopathology Lipid Metabolism/physiology Macrophages/physiology Stress, Physiological/physiology* Unfolded Protein Response/physiology

2.	Nat Med. 2010 Apr;16(4):452-9. Epub 2010 Mar 7. Programmed death-1-induced interleukin-10 production by monocytes impairs CD4+ T cell activation during HIV infection. Said EA, Dupuy FP, Trautmann L, Zhang Y, Shi Y, El-Far M, Hill BJ, Noto A, Ancuta P, Peretz Y, Fonseca SG, Van Grevenynghe J, Boulassel MR, Bruneau J, Shoukry NH, Routy JP, Douek DC, Haddad EK, Sekaly RP. Centre de Recherche du Centre hospitalier de l'Université de Montréal (CRCHUM), Hôpital St.-Luc, Montréal, Québec, Canada. Abstract Viral replication and microbial translocation from the gut to the blood during HIV infection lead to hyperimmune activation, which contributes to the decline in CD4+ T cell numbers during HIV infection. Programmed death-1 (PD-1) and interleukin-10 (IL-10) are both upregulated during HIV infection. Blocking interactions between PD-1 and programmed death ligand-1 (PD-L1) and between IL-10 and IL-10 receptor (IL-10R) results in viral clearance and improves T cell function in animal models of chronic viral infections. Here we show that high amounts of microbial products and inflammatory cytokines in the plasma of HIV-infected subjects lead to upregulation of PD-1 expression on monocytes that correlates with high plasma concentrations of IL-10. Triggering of PD-1 expressed on monocytes by PD-L1 expressed on various cell types induced IL-10 production and led to reversible CD4+ T cell dysfunction. We describe a new function for PD-1 whereby microbial products inhibit T cell expansion and function by upregulating PD-1 levels and IL-10 production by monocytes after binding of PD-1 by PD-L1.
	PMID: 20208540 [PubMed - indexed for MEDLINE]
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	Publication Types: Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't MeSH Terms: Antigens, CD/biosynthesis Antigens, CD/physiology* CD4-Positive T-Lymphocytes/immunology CD4-Positive T-Lymphocytes/physiology CD4-Positive T-Lymphocytes/virology* HIV Infections/immunology* HIV Infections/physiopathology Humans Interleukin-10/biosynthesis Interleukin-10/physiology* Lymphocyte Activation/immunology Lymphocyte Activation/physiology* Lymphocyte Subsets/immunology Lymphocyte Subsets/physiology Monocytes/immunology Monocytes/physiology* Phosphorylation Receptors, IgG/immunology Receptors, IgG/physiology STAT3 Transcription Factor/immunology STAT3 Transcription Factor/physiology Up-Regulation/physiology Viremia/immunology Viremia/physiopathology Substances: Antigens, CD CD274 protein, human Receptors, IgG STAT3 Transcription Factor STAT3 protein, human Interleukin-10