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

Sent on Tuesday, 2013 September 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. 2013 Jul;19(7):802. doi: 10.1038/nm0713-802. Straight talk with...Doris Meder and Geert Van Minnebruggen. Interview by Katharine Sanderson. Meder D, Van Minnebruggen G.
	PMID: 23836209 [PubMed - indexed for MEDLINE]

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, 2013 September 21
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.	Science. 2013 Sep 13;341(6151):1250-3. doi: 10.1126/science.1240988. Cytoplasmic LPS activates caspase-11: implications in TLR4-independent endotoxic shock. Hagar JA, Powell DA, Aachoui Y, Ernst RK, Miao EA. Department of Microbiology and Immunology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Comment in Immunology. Sensing endotoxins from within. [Science. 2013] Immunology. Sensing endotoxins from within.Kagan JC. Science. 2013 Sep 13; 341(6151):1184-5. Abstract Inflammatory caspases, such as caspase-1 and -11, mediate innate immune detection of pathogens. Caspase-11 induces pyroptosis, a form of programmed cell death, and specifically defends against bacterial pathogens that invade the cytosol. During endotoxemia, however, excessive caspase-11 activation causes shock. We report that contamination of the cytoplasm by lipopolysaccharide (LPS) is the signal that triggers caspase-11 activation in mice. Specifically, caspase-11 responds to penta- and hexa-acylated lipid A, whereas tetra-acylated lipid A is not detected, providing a mechanism of evasion for cytosol-invasive Francisella. Priming the caspase-11 pathway in vivo resulted in extreme sensitivity to subsequent LPS challenge in both wild-type and Tlr4-deficient mice, whereas Casp11-deficient mice were relatively resistant. Together, our data reveal a new pathway for detecting cytoplasmic LPS.
	PMID: 24031018 [PubMed - indexed for MEDLINE]
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2.	Science. 2013 Sep 13;341(6151):1239-42. doi: 10.1126/science.1239352. Marine taxa track local climate velocities. Pinsky ML, Worm B, Fogarty MJ, Sarmiento JL, Levin SA. Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ 08544, USA. malin.pinsky@rutgers.edu Abstract Organisms are expected to adapt or move in response to climate change, but observed distribution shifts span a wide range of directions and rates. Explanations often emphasize biological distinctions among species, but general mechanisms have been elusive. We tested an alternative hypothesis: that differences in climate velocity-the rate and direction that climate shifts across the landscape-can explain observed species shifts. We compiled a database of coastal surveys around North America from 1968 to 2011, sampling 128 million individuals across 360 marine taxa. Climate velocity explained the magnitude and direction of shifts in latitude and depth much more effectively than did species characteristics. Our results demonstrate that marine species shift at different rates and directions because they closely track the complex mosaic of local climate velocities.
	PMID: 24031017 [PubMed - indexed for MEDLINE]
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3.	Science. 2013 Sep 13;341(6151):1184-5. doi: 10.1126/science.1243939. Immunology. Sensing endotoxins from within. Kagan JC. Harvard Medical School and Division of Gastroenterology, Boston Children's Hospital, Boston, MA 02115, USA. jonathan.kagan@childrens.harvard.edu Comment on Cytoplasmic LPS activates caspase-11: implications in TLR4-independent endotoxic shock. [Science. 2013] Cytoplasmic LPS activates caspase-11: implications in TLR4-independent endotoxic shock.Hagar JA, Powell DA, Aachoui Y, Ernst RK, Miao EA. Science. 2013 Sep 13; 341(6151):1250-3. Noncanonical inflammasome activation by intracellular LPS independent of TLR4. [Science. 2013] Noncanonical inflammasome activation by intracellular LPS independent of TLR4.Kayagaki N, Wong MT, Stowe IB, Ramani SR, Gonzalez LC, Akashi-Takamura S, Miyake K, Zhang J, Lee WP, Muszyński A, et al. Science. 2013 Sep 13; 341(6151):1246-9. Epub 2013 Jul 25.
	PMID: 24031006 [PubMed - indexed for MEDLINE]
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4.	Science. 2013 Sep 13;341(6151):1163. doi: 10.1126/science.341.6151.1163. Genomics. Researchers to explore promise, risks of sequencing newborns' DNA. Kaiser J.
	PMID: 24030994 [PubMed - indexed for MEDLINE]
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5.	Science. 2013 Sep 13;341(6151):1182-4. doi: 10.1126/science.1240880. Epub 2013 Aug 29. Evolution. What, where, and when? Knapp S. Natural History Museum, London, UK. s.knapp@nhm.ac.uk
	PMID: 23989953 [PubMed - indexed for MEDLINE]
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6.	Science. 2013 Sep 13;341(6151):1246-9. doi: 10.1126/science.1240248. Epub 2013 Jul 25. Noncanonical inflammasome activation by intracellular LPS independent of TLR4. Kayagaki N, Wong MT, Stowe IB, Ramani SR, Gonzalez LC, Akashi-Takamura S, Miyake K, Zhang J, Lee WP, Muszyński A, Forsberg LS, Carlson RW, Dixit VM. Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA. kayagaki@gene.com Comment in Immunology. Sensing endotoxins from within. [Science. 2013] Immunology. Sensing endotoxins from within.Kagan JC. Science. 2013 Sep 13; 341(6151):1184-5. Abstract Gram-negative bacteria including Escherichia coli, Citrobacter rodentium, Salmonella typhimurium, and Shigella flexneri are sensed in an ill-defined manner by an intracellular inflammasome complex that activates caspase-11. We show that macrophages loaded with synthetic lipid A, E. coli lipopolysaccharide (LPS), or S. typhimurium LPS activate caspase-11 independently of the LPS receptor Toll-like receptor 4 (TLR4). Consistent with lipid A triggering the noncanonical inflammasome, LPS containing a divergent lipid A structure antagonized caspase-11 activation in response to E. coli LPS or Gram-negative bacteria. Moreover, LPS-mutant E. coli failed to activate caspase-11. Tlr4(-/-) mice primed with TLR3 agonist polyinosinic:polycytidylic acid [poly(I:C)] to induce pro-caspase-11 expression were as susceptible as wild-type mice were to sepsis induced by E. coli LPS. These data unveil a TLR4-independent mechanism for innate immune recognition of LPS.
	PMID: 23887873 [PubMed - indexed for MEDLINE]
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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, 2013 September 18
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.	Nature. 2013 Aug 29;500(7464):514. doi: 10.1038/500514a. African genes tracked back. Hayden EC.
	PMID: 23985853 [PubMed - indexed for MEDLINE]

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Sent on Tuesday, 2013 September 17
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.	Lancet. 2013 Aug 31;382(9894):758. Funding: new NIH grants aim to improve clinical use of genomics. Arnold C.
	PMID: 24003449 [PubMed - indexed for MEDLINE]

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Sent on Saturday, 2013 September 14
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.	Nature. 2013 Aug 1;500(7460):20-2. doi: 10.1038/500020a. Archaeology: The milk revolution. Curry A.
	PMID: 23903732 [PubMed - indexed for MEDLINE]
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2.	Nature. 2013 Aug 1;500(7460):45-50. doi: 10.1038/nature12415. Epub 2013 Jul 24. Integrative genomics identifies APOE ε4 effectors in Alzheimer's disease. Rhinn H, Fujita R, Qiang L, Cheng R, Lee JH, Abeliovich A. Department of Pathology, Columbia University, 650 W. 168th Street, New York, New York 10032, USA. Comment in Alzheimer's disease: From big data to mechanism. [Nature. 2013] Alzheimer's disease: From big data to mechanism.Swarup V, Geschwind DH. Nature. 2013 Aug 1; 500(7460):34-5. Epub 2013 Jul 24. Abstract Late-onset Alzheimer's disease (LOAD) risk is strongly influenced by genetic factors such as the presence of the apolipoprotein E ε4 allele (referred to here as APOE4), as well as non-genetic determinants including ageing. To pursue mechanisms by which these affect human brain physiology and modify LOAD risk, we initially analysed whole-transcriptome cerebral cortex gene expression data in unaffected APOE4 carriers and LOAD patients. APOE4 carrier status was associated with a consistent transcriptomic shift that broadly resembled the LOAD profile. Differential co-expression correlation network analysis of the APOE4 and LOAD transcriptomic changes identified a set of candidate core regulatory mediators. Several of these--including APBA2, FYN, RNF219 and SV2A--encode known or novel modulators of LOAD associated amyloid beta A4 precursor protein (APP) endocytosis and metabolism. Furthermore, a genetic variant within RNF219 was found to affect amyloid deposition in human brain and LOAD age-of-onset. These data implicate an APOE4 associated molecular pathway that promotes LOAD.
	PMID: 23883936 [PubMed - indexed for MEDLINE]
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3.	Nature. 2013 Aug 1;500(7460):34-5. doi: 10.1038/nature12457. Epub 2013 Jul 24. Alzheimer's disease: From big data to mechanism. Swarup V, Geschwind DH. Comment on Integrative genomics identifies APOE ε4 effectors in Alzheimer's disease. [Nature. 2013] Integrative genomics identifies APOE ε4 effectors in Alzheimer's disease.Rhinn H, Fujita R, Qiang L, Cheng R, Lee JH, Abeliovich A. Nature. 2013 Aug 1; 500(7460):45-50. Epub 2013 Jul 24.
	PMID: 23883924 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

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

Sent on Friday, 2013 September 13
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.	N Engl J Med. 2013 Aug 29;369(9):852. doi: 10.1056/NEJMicm1213758. Images in clinical medicine. Staphylococcal toxic shock syndrome. Chan BC, Maurice P. Christchurch Hospital, Christchurch, New Zealand. chanchoyui@gmail.com Free Article
	PMID: 23984732 [PubMed - indexed for MEDLINE]
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2.	N Engl J Med. 2013 Aug 29;369(9):840-51. doi: 10.1056/NEJMra1208623. Severe sepsis and septic shock. Angus DC, van der Poll T. CRISMA (Clinical Research, Investigation, and Systems Modeling of Acute Illness) Center, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA. angusdc@upmc.edu Free Article
	PMID: 23984731 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

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Sent on Wednesday, 2013 September 11
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.	Science. 2013 Aug 30;341(6149):1016-20. doi: 10.1126/science.1240729. βCaMKII in lateral habenula mediates core symptoms of depression. Li K, Zhou T, Liao L, Yang Z, Wong C, Henn F, Malinow R, Yates JR 3rd, Hu H. Institute of Neuroscience and State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, P R China. Abstract The lateral habenula (LHb) has recently emerged as a key brain region in the pathophysiology of depression. However, the molecular mechanism by which LHb becomes hyperactive in depression remains unknown. Through a quantitative proteomic screen, we found that expression of the β form of calcium/calmodulin-dependent protein kinase type II (βCaMΚΙΙ) was significantly up-regulated in the LHb of animal models of depression and down-regulated by antidepressants. Increasing β-, but not α-, CaMKII in the LHb strongly enhanced the synaptic efficacy and spike output of LHb neurons and was sufficient to produce profound depressive symptoms, including anhedonia and behavioral despair. Down-regulation of βCaMKII levels, blocking its activity or its target molecule the glutamate receptor GluR1 reversed the depressive symptoms. These results identify βCaMKII as a powerful regulator of LHb neuron function and a key molecular determinant of depression.
	PMID: 23990563 [PubMed - indexed for MEDLINE]
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2.	Science. 2013 Aug 30;341(6149):959. doi: 10.1126/science.341.6149.959-a. Data disclosure crucial after DNA patent verdict. de Costa A.
	PMID: 23990544 [PubMed - indexed for MEDLINE]
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3.	Science. 2013 Aug 30;341(6149):958-9. doi: 10.1126/science.341.6149.958-b. Call for prudence in whole-genome testing. van El CG, Dondorp WJ, de Wert GM, Cornel MC. Comment on Point-counterpoint. Patient autonomy and incidental findings in clinical genomics. [Science. 2013] Point-counterpoint. Patient autonomy and incidental findings in clinical genomics.Wolf SM, Annas GJ, Elias S. Science. 2013 May 31; 340(6136):1049-50. Epub 2013 May 16.
	PMID: 23990543 [PubMed - indexed for MEDLINE]
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4.	Nat Genet. 2013 Jul;45(7):716. doi: 10.1038/ng.2679. David R. Cox 1946-2013. Barsh GS, Myers RM. HudsonAlpha Institute for Biotechnology, Huntsville, AL, USA. gbarsh@hudsonalpha.org
	PMID: 23800862 [PubMed - indexed for MEDLINE]
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5.	Nat Genet. 2013 Jul;45(7):715. doi: 10.1038/ng.2688. EconOmics. [No authors listed]
	PMID: 23800861 [PubMed - indexed for MEDLINE]
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6.	Nat Genet. 2013 Jul;45(7):818-21. doi: 10.1038/ng.2636. Epub 2013 May 26. A genome-wide association study identifies two risk loci for congenital heart malformations in Han Chinese populations. Hu Z, Shi Y, Mo X, Xu J, Zhao B, Lin Y, Yang S, Xu Z, Dai J, Pan S, Da M, Wang X, Qian B, Wen Y, Wen J, Xing J, Guo X, Xia Y, Ma H, Jin G, Yu S, Liu J, Zhou Z, Wang X, Chen Y, Sha J, Shen H. State Key Laboratory of Reproductive Medicine, School of Public Health, Nanjing Medical University, Nanjing, China. zhibin_hu@njmu.edu.cn Abstract Congenital heart malformation (CHM) is the most common form of congenital human birth anomaly and is the leading cause of infant mortality. Although some causative genes have been identified, little progress has been made in identifying genes in which low-penetrance susceptibility variants occur in the majority of sporadic CHM cases. To identify common genetic variants associated with sporadic non-syndromic CHM in Han Chinese populations, we performed a multistage genome-wide association study (GWAS) in a total of 4,225 CHM cases and 5,112 non-CHM controls. The GWAS stage included 945 cases and 1,246 controls and was followed by 2-stage validation with 2,160 cases and 3,866 controls. The combined analyses identified significant associations (P < 5.0 × 10⁻⁸) at 1p12 (rs2474937 near TBX15; odds ratio (OR) = 1.40; P = 8.44 × 10⁻¹⁰) and 4q31.1 (rs1531070 in MAML3; OR = 1.40; P = 4.99 × 10⁻¹²). These results extend current knowledge of genetic contributions to CHM in Han Chinese populations.
	PMID: 23708190 [PubMed - indexed for MEDLINE]
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