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 January 25
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 - 3 of 3

1.	Science. 2013 Jan 11;339(6116):161-6. doi: 10.1126/science.1230719. Leukocyte behavior in atherosclerosis, myocardial infarction, and heart failure. Swirski FK, Nahrendorf M. Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Simches Research Building, 185 Cambridge Street, Boston, MA 02114, USA. fswirski@mgh.harvard.edu Abstract Cardiovascular diseases claim more lives worldwide than any other. Etiologically, the dominant trajectory involves atherosclerosis, a chronic inflammatory process of lipid-rich lesion growth in the vascular wall that can cause life-threatening myocardial infarction (MI). Those who survive MI can develop congestive heart failure, a chronic condition of inadequate pump activity that is frequently fatal. Leukocytes (white blood cells) are important participants at the various stages of cardiovascular disease progression and complication. This Review will discuss leukocyte function in atherosclerosis, MI, and heart failure.
	PMID: 23307733 [PubMed - indexed for MEDLINE]
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2.	Science. 2013 Jan 11;339(6116):147-8. doi: 10.1126/science.1233223. Biomedicine. Improving metabolism by throwing out all the JNK. Ferrante AW Jr. Department of Medicine, Naomi Berrie Diabetes Center, Columbia University, 1150 Saint Nicholas Avenue, New York, NY 10032, USA. awf7@columbia.edu Comment on JNK expression by macrophages promotes obesity-induced insulin resistance and inflammation. [Science. 2013] JNK expression by macrophages promotes obesity-induced insulin resistance and inflammation.Han MS, Jung DY, Morel C, Lakhani SA, Kim JK, Flavell RA, Davis RJ. Science. 2013 Jan 11; 339(6116):218-22. Epub 2012 Dec 6.
	PMID: 23307726 [PubMed - indexed for MEDLINE]
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3.	Science. 2013 Jan 11;339(6116):218-22. doi: 10.1126/science.1227568. Epub 2012 Dec 6. JNK expression by macrophages promotes obesity-induced insulin resistance and inflammation. Han MS, Jung DY, Morel C, Lakhani SA, Kim JK, Flavell RA, Davis RJ. Howard Hughes Medical Institute, Worcester, MA 01605, USA. Comment in Biomedicine. Improving metabolism by throwing out all the JNK. [Science. 2013] Biomedicine. Improving metabolism by throwing out all the JNK.Ferrante AW Jr. Science. 2013 Jan 11; 339(6116):147-8. Abstract The cJun NH(2)-terminal kinase (JNK) signaling pathway contributes to inflammation and plays a key role in the metabolic response to obesity, including insulin resistance. Macrophages are implicated in this process. To test the role of JNK, we established mice with selective JNK deficiency in macrophages. We report that feeding a high-fat diet to control and JNK-deficient mice caused similar obesity, but only mice with JNK-deficient macrophages remained insulin-sensitive. The protection of mice with macrophage-specific JNK deficiency against insulin resistance was associated with reduced tissue infiltration by macrophages. Immunophenotyping demonstrated that JNK was required for pro-inflammatory macrophage polarization. These studies demonstrate that JNK in macrophages is required for the establishment of obesity-induced insulin resistance and inflammation.
	PMID: 23223452 [PubMed - indexed for MEDLINE]
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