Pubmed output: What's new for 'JKB

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

Sent on Wednesday, 2013 October 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 - 4 of 4

1.	N Engl J Med. 2013 Oct 17;369(16):1572. doi: 10.1056/NEJMc1311596. Metagenomic analysis of tuberculosis--current limitations. Hingley-Wilson SM. University of Surrey, Guildford, United Kingdom s.hingley-wilson@surrey.ac.uk. Comment on Metagenomic analysis of tuberculosis in a mummy. [N Engl J Med. 2013] Metagenomic analysis of tuberculosis in a mummy.Chan JZ, Sergeant MJ, Lee OY, Minnikin DE, Besra GS, Pap I, Spigelman M, Donoghue HD, Pallen MJ. N Engl J Med. 2013 Jul 18; 369(3):289-90.
	PMID: 24131193 [PubMed - indexed for MEDLINE]
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2.	N Engl J Med. 2013 Oct 3;369(14):1381-2. doi: 10.1056/NEJMc1301936. Primaquine failure and cytochrome P-450 2D6 in Plasmodium vivax malaria. Bennett JW, Pybus BS, Yadava A, Tosh D, Sousa JC, McCarthy WF, Deye G, Melendez V, Ockenhouse CF. Free Article
	PMID: 24088113 [PubMed - indexed for MEDLINE]
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3.	Science. 2013 Sep 6;341(6150):1078. doi: 10.1126/science.1244986. Retrospective. Tony Pawson (1952-2013). Hunter T. Salk Institute, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. hunter@salk.edu
	PMID: 24009385 [PubMed - indexed for MEDLINE]
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4.	Nat Med. 2012 Aug;18(8):1217-23. doi: 10.1038/nm.2843. Epub 2012 Jul 22. The pulmonary endothelial glycocalyx regulates neutrophil adhesion and lung injury during experimental sepsis. Schmidt EP, Yang Y, Janssen WJ, Gandjeva A, Perez MJ, Barthel L, Zemans RL, Bowman JC, Koyanagi DE, Yunt ZX, Smith LP, Cheng SS, Overdier KH, Thompson KR, Geraci MW, Douglas IS, Pearse DB, Tuder RM. Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, Program in Translational Lung Research, University of Colorado School of Medicine, Aurora, Colorado, USA; Denver Health Medical Center, Denver, Colorado, USA. eric.schmidt@ucdenver.edu Abstract Sepsis, a systemic inflammatory response to infection, commonly progresses to acute lung injury (ALI), an inflammatory lung disease with high morbidity. We postulated that sepsis-associated ALI is initiated by degradation of the pulmonary endothelial glycocalyx, leading to neutrophil adherence and inflammation. Using intravital microscopy, we found that endotoxemia in mice rapidly induced pulmonary microvascular glycocalyx degradation via tumor necrosis factor-α (TNF-α)-dependent mechanisms. Glycocalyx degradation involved the specific loss of heparan sulfate and coincided with activation of endothelial heparanase, a TNF-α-responsive, heparan sulfate-specific glucuronidase. Glycocalyx degradation increased the availability of endothelial surface adhesion molecules to circulating microspheres and contributed to neutrophil adhesion. Heparanase inhibition prevented endotoxemia-associated glycocalyx loss and neutrophil adhesion and, accordingly, attenuated sepsis-induced ALI and mortality in mice. These findings are potentially relevant to human disease, as sepsis-associated respiratory failure in humans was associated with higher plasma heparan sulfate degradation activity; moreover, heparanase content was higher in human lung biopsies showing diffuse alveolar damage than in normal human lung tissue. PMCID: PMC3723751 Free PMC Article
	PMID: 22820644 [PubMed - indexed for MEDLINE]
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