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 Tuesday, 2012 January 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]))

Click here to view complete results in PubMed (Results may change over time.)
To unsubscribe from these e-mail updates click here.

PubMed Results

Items 1 - 6 of 6

1.	Nat Med. 2011 Nov 7;17(11):1344-6. doi: 10.1038/nm.2499. Targeting osteoclast-osteoblast communication. Cao X. Comment on Nat Med. 2011;17(11):1473-80.
	PMID: 22064408 [PubMed - indexed for MEDLINE]
	Related citations

2.	Nat Med. 2011 Nov 7;17(11):1329. doi: 10.1038/nm1111-1329a. Sequencing projects bring age-old wisdom to genomics. Borrell B.
	PMID: 22064397 [PubMed - indexed for MEDLINE]
	Related citations

3.	Nat Med. 2011 Nov 7;17(11):1327. doi: 10.1038/nm1111-1327. MS pipeline flowing, but niche remains for neuroprotection. Waters H.
	PMID: 22064394 [PubMed - indexed for MEDLINE]
	Related citations

4.	Nat Med. 2011 Nov 7;17(11):1323. doi: 10.1038/nm1111-1323. Preemptive genotyping trialed to prevent adverse drug reactions. Dolgin E.
	PMID: 22064389 [PubMed - indexed for MEDLINE]
	Related citations

5.	Nat Med. 2011 Oct 23;17(11):1473-80. doi: 10.1038/nm.2489. Suppression of bone formation by osteoclastic expression of semaphorin 4D. Negishi-Koga T, Shinohara M, Komatsu N, Bito H, Kodama T, Friedel RH, Takayanagi H. Source Department of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan. Comment in Nat Rev Rheumatol. 2011 Dec;7(12):681. Nat Med. 2011;17(11):1344-6. Abstract Most of the currently available drugs for osteoporosis inhibit osteoclastic bone resorption; only a few drugs promote osteoblastic bone formation. It is thus becoming increasingly necessary to identify the factors that regulate bone formation. We found that osteoclasts express semaphorin 4D (Sema4D), previously shown to be an axon guidance molecule, which potently inhibits bone formation. The binding of Sema4D to its receptor Plexin-B1 on osteoblasts resulted in the activation of the small GTPase RhoA, which inhibits bone formation by suppressing insulin-like growth factor-1 (IGF-1) signaling and by modulating osteoblast motility. Sema4d-/- mice, Plxnb1-/- mice and mice expressing a dominant-negative RhoA specifically in osteoblasts showed an osteosclerotic phenotype due to augmented bone formation. Notably, Sema4D-specific antibody treatment markedly prevented bone loss in a model of postmenopausal osteoporosis. Thus, Sema4D has emerged as a new therapeutic target for the discovery and development of bone-increasing drugs.
	PMID: 22019888 [PubMed - indexed for MEDLINE]
	Related citations

6.	Nat Med. 2011 Oct 23;17(11):1490-7. doi: 10.1038/nm.2461. Tissue factor-protease-activated receptor 2 signaling promotes diet-induced obesity and adipose inflammation. Badeanlou L, Furlan-Freguia C, Yang G, Ruf W, Samad F. Source Department of Cell Biology, Torrey Pines Institute for Molecular Studies, San Diego, California, USA. Comment in Nat Med. 2011;17(11):1343-4. Abstract Tissue factor, the initiator of the coagulation cascade, mediates coagulation factor VIIa-dependent activation of protease-activated receptor 2 (PAR2). Here we delineate a role for this signaling pathway in obesity and its complications. Mice lacking PAR2 (F2rl1) or the cytoplasmic domain of tissue factor were protected from weight gain and insulin resistance induced by a high-fat diet. In hematopoietic cells, genetic ablation of tissue factor-PAR2 signaling reduced adipose tissue macrophage inflammation, and specific pharmacological inhibition of macrophage tissue factor signaling rapidly ameliorated insulin resistance. In contrast, nonhematopoietic cell tissue factor-VIIa-PAR2 signaling specifically promoted obesity. Mechanistically, adipocyte tissue factor cytoplasmic domain-dependent VIIa signaling suppressed Akt phosphorylation with concordant adverse transcriptional changes of key regulators of obesity and metabolism. Pharmacological blockade of adipocyte tissue factor in vivo reversed these effects of tissue factor-VIIa signaling and rapidly increased energy expenditure. Thus, inhibition of tissue factor signaling is a potential therapeutic avenue for improving impaired metabolism and insulin resistance in obesity. PMCID: PMC3210891 [Available on 2012/4/23]
	PMID: 22019885 [PubMed - indexed for MEDLINE]
	Related citations