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 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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PubMed Results

Items 1 - 6 of 6

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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