What's new for 'JKB_daily1' in PubMed

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

Sent on Wednesday, 2010 Jun 23
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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PubMed Results

Items 1 - 5 of 5

1.	N Engl J Med. 2010 Jun 17;362(24):2328; author reply 2330-1. Comparison of dopamine and norepinephrine in shock. Romero CM. Comment on: N Engl J Med. 2010 Mar 4;362(9):779-89.
	PMID: 20554990 [PubMed - indexed for MEDLINE]
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2.	Science. 2010 Jun 11;328(5984):1342. Human genetics. Who are the Jews? Genetic studies spark identity debate. Balter M.
	PMID: 20538924 [PubMed - indexed for MEDLINE]
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3.	Nat Med. 2010 Jun;16(6):638-9. Interleukin-33 safeguards neutrophils in sepsis. Roger T, Calandra T. Comment on: Nat Med. 2010 Jun;16(6):708-12.
	PMID: 20526314 [PubMed - indexed for MEDLINE]
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4.	Nat Med. 2010 Jun;16(6):708-12. Epub 2010 May 16. Interleukin-33 attenuates sepsis by enhancing neutrophil influx to the site of infection. Alves-Filho JC, Sônego F, Souto FO, Freitas A, Verri WA Jr, Auxiliadora-Martins M, Basile-Filho A, McKenzie AN, Xu D, Cunha FQ, Liew FY. Division of Immunology, Infection and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow, UK. Comment in: Nat Med. 2010 Jun;16(6):638-9. Abstract Sepsis is a systemic inflammatory condition following bacterial infection with a high mortality rate and limited therapeutic options. Here we show that interleukin-33 (IL-33) reduces mortality in mice with experimental sepsis from cecal ligation and puncture (CLP). IL-33-treated mice developed increased neutrophil influx into the peritoneal cavity and more efficient bacterial clearance than untreated mice. IL-33 reduced the systemic but not the local proinflammatory response, and it did not induce a T helper type 1 (T(H)1) to T(H)2 shift. The chemokine receptor CXCR2 is crucial for recruitment of neutrophils from the circulation to the site of infection. Activation of Toll-like receptors (TLRs) in neutrophils downregulates CXCR2 expression and impairs neutrophil migration. We show here that IL-33 prevents the downregulation of CXCR2 and inhibition of chemotaxis induced by the activation of TLR4 in mouse and human neutrophils. Furthermore, we show that IL-33 reverses the TLR4-induced reduction of CXCR2 expression in neutrophils via the inhibition of expression of G protein-coupled receptor kinase-2 (GRK2), a serine-threonine protein kinase that induces internalization of chemokine receptors. Finally, we find that individuals who did not recover from sepsis had significantly more soluble ST2 (sST2, the decoy receptor of IL-33) than those who did recover. Together, our results indicate a previously undescribed mechanism of action of IL-33 and suggest a therapeutic potential of IL-33 in sepsis.
	PMID: 20473304 [PubMed - indexed for MEDLINE]
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5.	Science. 2010 Jun 11;328(5984):1401-3. Lysosomal pathology and osteopetrosis upon loss of H+-driven lysosomal Cl- accumulation. Weinert S, Jabs S, Supanchart C, Schweizer M, Gimber N, Richter M, Rademann J, Stauber T, Kornak U, Jentsch TJ. Leibniz-Institut für Molekulare Pharmakologie (FMP), 13125 Berlin, Germany. Comment in: Science. 2010 Jun 11;328(5984):1364-5. Abstract During lysosomal acidification, proton-pump currents are thought to be shunted by a chloride ion (Cl-) channel, tentatively identified as ClC-7. Surprisingly, recent data suggest that ClC-7 instead mediates Cl-/proton (H+) exchange. We generated mice carrying a point mutation converting ClC-7 into an uncoupled (unc) Cl- conductor. Despite maintaining lysosomal conductance and normal lysosomal pH, these Clcn7(unc/unc) mice showed lysosomal storage disease like mice lacking ClC-7. However, their osteopetrosis was milder, and they lacked a coat color phenotype. Thus, only some roles of ClC-7 Cl-/H+ exchange can be taken over by a Cl- conductance. This conductance was even deleterious in Clcn7(+/unc) mice. Clcn7(-/-) and Clcn7(unc/unc) mice accumulated less Cl- in lysosomes than did wild-type mice. Thus, lowered lysosomal chloride may underlie their common phenotypes.
	PMID: 20430974 [PubMed - indexed for MEDLINE]
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