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Sender's message: Sepsis or genomics or altitude: JKB_daily1
Sent on Wednesday, 2011 Nov 16Search (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 |
| 1. | Nature. 2011 Sep 28;477(7366):522-3. doi: 10.1038/477522a.Aboriginal genome analysis comes to grips with ethics.Callaway E.Comment in |
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| 2. | Lancet. 2011 Oct 22;378(9801):1493-500. Epub 2011 Sep 15.China's facility-based birth strategy and neonatal mortality: a population-based epidemiological study.Feng XL, Guo S, Hipgrave D, Zhu J, Zhang L, Song L, Yang Q, Guo Y, Ronsmans C.SourceDepartment of Health Policy and Administration, School of Public Health, Peking University, Beijing, China. Comment inAbstractBACKGROUND:China's success in improving the quality of and access to obstetric care in hospitals offers an opportunity to examine the effect of a large-scale facility-based strategy on neonatal mortality. We aimed to establish this effect by assessing how the institutional strategy of intrapartum care has affected neonatal mortality and its regional inequalities. METHODS:We did a population-based epidemiological study of China's National Maternal and Child Mortality Surveillance System from 1996 to 2008. We used data from 116 surveillance sites in China (37 urban districts and 79 rural counties) to examine neonatal mortality by cause, socioeconomic region, and place of birth, with Poisson regression to calculate relative risks. Rural counties were categorised into types 1-4, with type 4 being the least developed. We report attributable risks and preventable fractions for hospital births versus home births. FINDINGS:Neonatal mortality decreased by 62% between 1996 and 2008. The rate of neonatal mortality was much lower for hospital births than for home births in all regions, with relative risks (RR) ranging from 0·30 (95% CI 0·22-0·40) in type 2 rural counties, to 0·52 (0·33-0·83) in type 4 counties (p<0·0001). The proportion of neonatal deaths prevented by hospital birth ranged from 70% (95% CI 59·7-77·8) to 48% (16·9-67·3). Babies born in urban hospitals had a low rate of neonatal mortality (5·7 per 1000 livebirths); but those born in hospitals in type 4 rural counties were almost four times more likely to die than were children born in urban hospitals (RR 3·80, 2·53-5·72). INTERPRETATION:Other countries can learn from China's substantial progress in reducing neonatal mortality. The major effect of China's facility-based strategy on neonatal mortality is much greater than that reported for community-based interventions. Our findings will provide a great impetus for countries to increase demand for and quality of facility-based intrapartum care. FUNDING:China Medical Board, UNICEF China. Copyright © 2011 Elsevier Ltd. All rights reserved. |
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| 3. | Nature. 2011 Sep 14;477(7366):596-600. doi: 10.1038/nature10510.The NLRC4 inflammasome receptors for bacterial flagellin and type III secreti on apparatus.Zhao Y, Yang J, Shi J, Gong YN, Lu Q, Xu H, Liu L, Shao F.SourceGraduate Program in Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China. Comment inAbstractInflammasomes are large cytoplasmic complexes that sense microbial infections/danger molecules and induce caspase-1 activation-dependent cytokine production and macrophage inflammatory death. The inflammasome assembled by the NOD-like receptor (NLR) protein NLRC4 responds to bacterial flagellin and a conserved type III secretion system (TTSS) rod component. How the NLRC4 inflammasome detects the two bacterial products and the molecular mechanism of NLRC4 inflammasome activation are not understood. Here we show that NAIP5, a BIR-domain NLR protein required for Legionella pneumophila replication in mouse macrophages, is a universal component of the flagellin-NLRC4 pathway. NAIP5 directly and specifically interacted with flagellin, which determined the inflammasome-stimulation activities of different bacterial flagellins. NAIP5 engagement by flagellin promoted a physical NAIP5-NLRC4 association, rendering full reconstitution of a flagellin-responsive NLRC4 inflammasome in non-macrophage cells. The related NAIP2 functioned analogously to NAIP5, serving as a specific inflammasome receptor for TTSS rod proteins such as Salmonella PrgJ and Burkholderia BsaK. Genetic analysis of Chromobacterium violaceum infection revealed that the TTSS needle protein CprI can stimulate NLRC4 inflammasome activation in human macrophages. Similarly, CprI is specifically recognized by human NAIP, the sole NAIP family member in human. The finding that NAIP proteins are inflammasome receptors for bacterial flagellin and TTSS apparatus components further predicts that the remaining NAIP family members may recognize other unidentified microbial products to activate NLRC4 inflammasome-mediated innate immunity. © 2011 Macmillan Publishers Limited. All rights reserved |
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| 4. | Nature. 2011 Aug 31;477(7366):587-91. doi: 10.1038/nature10390.The genome of the green anole lizard and a comparative analysis with birds and mammals.Alföldi J, Di Palma F, Grabherr M, Williams C, Kong L, Mauceli E, Russell P, Lowe CB, Glor RE, Jaffe JD, Ray DA, Boissinot S, Shedlock AM, Botka C, Castoe TA, Colbourne JK, Fujita MK, Moreno RG, ten Hallers BF, Haussler D, Heger A, Heiman D, Janes DE, Johnson J, de Jong PJ, Koriabine MY, Lara M, Novick PA, Organ CL, Peach SE, Poe S, Pollock DD, de Queiroz K, Sanger T, Searle S, Smith JD, Smith Z, Swofford R, Turner-Maier J, Wade J, Young S, Zadissa A, Edwards SV, Glenn TC, Schneider CJ, Losos JB, Lander ES, Breen M, Ponting CP, Lindblad-Toh K.SourceBroad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA. jalfoldi@broadinstitute.org AbstractThe evolution of the amniotic egg was one of the great evolutionary innovations in the history of life, freeing vertebrates from an obligatory connection to water and thus permitting the conquest of terrestrial environments. Among amniotes, genome sequences are available for mammals and birds, but not for non-avian reptiles. Here we report the genome sequence of the North American green anole lizard, Anolis carolinensis. We find that A. carolinensis microchromosomes are highly syntenic with chicken microchromosomes, yet do not exhibit the high GC and low repeat content that are characteristic of avian microchromosomes. Also, A. carolinensis mobile elements are very young and diverse-more so than in any other sequenced amniote genome. The GC content of this lizard genome is also unusual in its homogeneity, unlike the regionally variable GC content found in mammals and birds. We describe and assign sequence to the previously unknown A. carolinensis X chromosome. Comparative gene analysis shows that amniote egg proteins have evolved significantly more rapidly than other proteins. An anole phylogeny resolves basal branches to illuminate the history of their repeated adaptive radiations. © 2011 Macmillan Publishers Limited. All rights reserved |
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| 5. | Nature. 2011 Aug 28;477(7366):592-5. doi: 10.1038/nature10394.Innate immune recognition of bacterial ligands by NAIPs determines inflammasome specificity.Kofoed EM, Vance RE.SourceDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA. AbstractInflammasomes are a family of cytosolic multiprotein complexes that initiate innate immune responses to pathogenic microbes by activating the caspase 1 protease. Although genetic data support a critical role for inflammasomes in immune defence and inflammatory diseases, the molecular basis by which individual inflammasomes respond to specific stimuli remains poorly understood. The inflammasome that contains the NLRC4 (NLR family, CARD domain containing 4) protein was previously shown to be activated in response to two distinct bacterial proteins, flagellin and PrgJ, a conserved component of pathogen-associated type III secretion systems. However, direct binding between NLRC4 and flagellin or PrgJ has never been demonstrated. A homologue of NLRC4, NAIP5 (NLR family, apoptosis inhibitory protein 5), has been implicated in activation of NLRC4 (refs 7-11), but is widely assumed to have only an auxiliary role, as NAIP5 is often dispensable for NLRC4 activation. However, Naip5 is a member of a small multigene family, raising the possibility of redundancy and functional specialization among Naip genes. Here we show in mice that different NAIP paralogues determine the specificity of the NLRC4 inflammasome for distinct bacterial ligands. In particular, we found that activation of endogenous NLRC4 by bacterial PrgJ requires NAIP2, a previously uncharacterized member of the NAIP gene family, whereas NAIP5 and NAIP6 activate NLRC4 specifically in response to bacterial flagellin. We dissected the biochemical mechanism underlying the requirement for NAIP proteins by use of a reconstituted NLRC4 inflammasome system. We found that NAIP proteins control ligand-dependent oligomerization of NLRC4 and that the NAIP2-NLRC4 complex physically associates with PrgJ but not flagellin, whereas NAIP5-NLRC4 associates with flagellin but not PrgJ. Our results identify NAIPs as immune sensor proteins and provide biochemical evidence for a simple receptor-ligand model for activation of the NAIP-NLRC4 inflammasomes. © 2011 Macmillan Publishers Limited. All rights reserved |
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