Saturday, 14 September 2013

What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

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

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]))

View complete results in PubMed (results may change over time).

Edit saved search settings, or unsubscribe from these e-mail updates.


PubMed Results
Items 1 - 3 of 3

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]
Related citations
Icon for Nature Publishing Group


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

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]
Related citations
Icon for Nature Publishing Group


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

PMID: 23883924 [PubMed - indexed for MEDLINE]
Related citations
Icon for Nature Publishing Group


0 Comments:

Post a Comment

Subscribe to Post Comments [Atom]

<< Home