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

Sent on Saturday, 2012 July 28
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 - 3 of 3

1.	N Engl J Med. 2012 Jul 12;367(2):115-23. Potassium channel KIR4.1 as an immune target in multiple sclerosis. Srivastava R, Aslam M, Kalluri SR, Schirmer L, Buck D, Tackenberg B, Rothhammer V, Chan A, Gold R, Berthele A, Bennett JL, Korn T, Hemmer B. Source Department of Neurology, Klinikum rechts der Isar, Technische Universität, Munich, Germany. Comment in Antibodies to potassium channels in multiple sclerosis. [N Engl J Med. 2012] Antibodies to potassium channels in multiple sclerosis.Cross AH, Waubant E. N Engl J Med. 2012 Jul 12; 367(2):172-4. Abstract BACKGROUND: Multiple sclerosis is a chronic inflammatory demyelinating disease of the central nervous system. Many findings suggest that the disease has an autoimmune pathogenesis; the target of the immune response is not yet known. METHODS: We screened serum IgG from persons with multiple sclerosis to identify antibodies that are capable of binding to brain tissue and observed specific binding of IgG to glial cells in a subgroup of patients. Using a proteomic approach focusing on membrane proteins, we identified the ATP-sensitive inward rectifying potassium channel KIR4.1 as the target of the IgG antibodies. We used a multifaceted validation strategy to confirm KIR4.1 as a target of the autoantibody response in multiple sclerosis and to show its potential pathogenicity in vivo. RESULTS: Serum levels of antibodies to KIR4.1 were higher in persons with multiple sclerosis than in persons with other neurologic diseases and healthy donors (P<0.001 for both comparisons). We replicated this finding in two independent groups of persons with multiple sclerosis or other neurologic diseases (P<0.001 for both comparisons). Analysis of the combined data sets indicated the presence of serum antibodies to KIR4.1 in 186 of 397 persons with multiple sclerosis (46.9%), in 3 of 329 persons with other neurologic diseases (0.9%), and in none of the 59 healthy donors. These antibodies bound to the first extracellular loop of KIR4.1. Injection of KIR4.1 serum IgG into the cisternae magnae of mice led to a profound loss of KIR4.1 expression, altered expression of glial fibrillary acidic protein in astrocytes, and activation of the complement cascade at sites of KIR4.1 expression in the cerebellum. CONCLUSIONS: KIR4.1 is a target of the autoantibody response in a subgroup of persons with multiple sclerosis. (Funded by the German Ministry for Education and Research and Deutsche Forschungsgemeinschaft.).
	PMID: 22784115 [PubMed - indexed for MEDLINE]
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2.	N Engl J Med. 2012 Jul 12;367(2):124-34. Epub 2012 Jun 27. Hydroxyethyl starch 130/0.42 versus Ringer's acetate in severe sepsis. Perner A, Haase N, Guttormsen AB, Tenhunen J, Klemenzson G, Åneman A, Madsen KR, Møller MH, Elkjær JM, Poulsen LM, Bendtsen A, Winding R, Steensen M, Berezowicz P, Søe-Jensen P, Bestle M, Strand K, Wiis J, White JO, Thornberg KJ, Quist L, Nielsen J, Andersen LH, Holst LB, Thormar K, Kjældgaard AL, Fabritius ML, Mondrup F, Pott FC, Møller TP, Winkel P, Wetterslev J; 6S Trial Group; Scandinavian Critical Care Trials Group. Collaborators: Perner A, Haase N, Guttormsen AB, Tenhunen J, Klemenzson G, Åneman A, Wetterslev J, Perner A, Haase N, Wetterslev J, Finfer S, Vercueil A, Rasmussen LS, Brunkhorst F, De Backer D, Dalgaard P, Rowan K, Perner A, Haase N, Wetterslev J, Perner A, Haase N, Kjær MN, Uhre KR, Knudsen V, Christiansen V, Schulze A, Wiis J, White JO, Thornberg K, Quist L, Sjøvall F, Wesche N, Reiter N, Jarnvig IL, Madsen KR, Kjældgaard A, Fabritius M, Mondrup F, Sommer KF, Pedersen L, Møller MH, Pott FC, Petersen JA, Lindhardt A, Møller K, Haraldson A, Pedersen C, Bülow HH, Elkjær JM, Møller T, Andersen LH, Holst LB, Schmidt JF, Nielsen ST, Treschow FP, Overgaard M, Ahlstrøm H, Grangaard S, Bruun JH, Larsen S, Poulsen LM, Madsen MV, Bang B, Bendtsen A, Winding R, Jepsen KV, Haubjerg S, Dey N, Hjørringsgaard J, Steensen M, Nielsen J, Albek C, Petersen S, Christensen A, Kristensen A, Berezowicz P, Søe-Jensen P, Tousi H, Bestle M, Nielsen K, Kold T, Grundahl K, Strand K, Larsen O, Iversen S, Schøidt O, Pawlowicz M, Kruse M, Rasmussen HS, Nielsen LO, Guttormsen AB, Sjøbø B, Leivdal S, Ytrebø LM, Tenhunen J, Karlsson S, Kukkurainen A, Kortelainen S, Peltola ML, Varila S, Thormar K, Bådstøløkken PM, Klemenzson G, Karason S, Pettilä V, Kaukonen M, Pettilä L, Sutinen S, Carlson M, Lassen NH, Larsen UL, Jung KD, Kancir C, Rutanen J, Ruokonen E, Rissanen S, Kontra K, Klepstad P, Berthelsen RE, Bødker KD, Dilling B. Source Department of Intensive Care, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. anders.perner@rh.regionh.dk Abstract BACKGROUND: Hydroxyethyl starch (HES) 130/0.42 is widely used for fluid resuscitation in intensive care units (ICUs), but its safety and efficacy have not been established in patients with severe sepsis. METHODS: In this multicenter, parallel-group, blinded trial, we randomly assigned patients with severe sepsis to fluid resuscitation in the ICU with either 6% HES 130/0.42 (Tetraspan) or Ringer's acetate at a dose of up to 33 ml per kilogram of ideal body weight per day. The primary outcome measure was either death or end-stage kidney failure (dependence on dialysis) at 90 days after randomization. RESULTS: Of the 804 patients who underwent randomization, 798 were included in the modified intention-to-treat population. The two intervention groups had similar baseline characteristics. At 90 days after randomization, 201 of 398 patients (51%) assigned to HES 130/0.42 had died, as compared with 172 of 400 patients (43%) assigned to Ringer's acetate (relative risk, 1.17; 95% confidence interval [CI], 1.01 to 1.36; P=0.03); 1 patient in each group had end-stage kidney failure. In the 90-day period, 87 patients (22%) assigned to HES 130/0.42 were treated with renal-replacement therapy versus 65 patients (16%) assigned to Ringer's acetate (relative risk, 1.35; 95% CI, 1.01 to 1.80; P=0.04), and 38 patients (10%) and 25 patients (6%), respectively, had severe bleeding (relative risk, 1.52; 95% CI, 0.94 to 2.48; P=0.09). The results were supported by multivariate analyses, with adjustment for known risk factors for death or acute kidney injury at baseline. CONCLUSIONS: Patients with severe sepsis assigned to fluid resuscitation with HES 130/0.42 had an increased risk of death at day 90 and were more likely to require renal-replacement therapy, as compared with those receiving Ringer's acetate. (Funded by the Danish Research Council and others; 6S ClinicalTrials.gov number, NCT00962156.).
	PMID: 22738085 [PubMed - indexed for MEDLINE]
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3.	Nat Med. 2012 May;18(5):799-806. Lethal inflammasome activation by a multidrug-resistant pathobiont upon antibiotic disruption of the microbiota. Ayres JS, Trinidad NJ, Vance RE. Source Department of Molecular & Cell Biology, Division of Immunology & Pathogenesis, University of California, Berkeley, USA. jayres@berkeley.edu Comment in Germs gone wild. [Nat Med. 2012] Germs gone wild.Hoshi N, Medzhitov R. Nat Med. 2012 May 4; 18(5):654-6. Epub 2012 May 4. Mucosal immunology: Inflammasomes induce sepsis following community breakdown. [Nat Rev Immunol. 2012] Mucosal immunology: Inflammasomes induce sepsis following community breakdown.Bordon Y. Nat Rev Immunol. 2012 May 25; 12(6):400-1. Epub 2012 May 25. Abstract The mammalian intestine harbors a complex microbial community that provides numerous benefits to its host. However, the microbiota can also include potentially virulent species, termed pathobiont, which can cause disease when intestinal homeostasis is disrupted. The molecular mechanisms by which pathobionts cause disease remain poorly understood. Here we describe a sepsis-like disease that occurs upon gut injury in antibiotic-treated mice. Sepsis was associated with the systemic spread of a specific multidrug-resistant Escherichia coli pathobiont that expanded markedly in the microbiota of antibiotic-treated mice. Rapid sepsis-like death required a component of the innate immune system, the Naip5-Nlrc4 inflammasome. In accordance with Koch's postulates, we found the E. coli pathobiont was sufficient to activate Naip5-Nlrc4 and cause disease when injected intravenously into unmanipulated mice. These findings reveal how sepsis-like disease can result from recognition of pathobionts by the innate immune system.
	PMID: 22522562 [PubMed - indexed for MEDLINE]
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