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 Friday, 2014 May 23
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.

To make a comment in PubMed, invite an author to comment, or rate the helpfulness of others' comments, join PubMed Commons. PubMed Commons is open to all authors of publications in PubMed.

PubMed Results

Items 1 - 2 of 2

1.	N Engl J Med. 2014 May 8;370(19):1799-808. doi: 10.1056/NEJMoa1303944. Parasite burden and severity of malaria in Tanzanian children. Gonçalves BP1, Huang CY, Morrison R, Holte S, Kabyemela E, Prevots DR, Fried M, Duffy PE. Author information: 1From the Laboratory of Malaria Immunology and Vaccinology (B.P.G., M.F., P.E.D.), Laboratory of Clinical Infectious Diseases-Epidemiology Unit (B.P.G., D.R.P.), and Biostatistics Research Branch (C.-Y.H.), National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Rockville, MD; the Seattle Biomedical Research Institute (R.M., M.F., P.E.D.) and the Fred Hutchinson Cancer Research Center (S.H.) - both in Seattle; and the Mother-Offspring Malaria Studies Project, Muheza Designated District Hospital, Muheza, Tanzania (E.K., M.F., P.E.D.). Abstract BACKGROUND: Severe Plasmodium falciparum malaria is a major cause of death in children. The contribution of the parasite burden to the pathogenesis of severe malaria has been controversial. METHODS: We documented P. falciparum infection and disease in Tanzanian children followed from birth for an average of 2 years and for as long as 4 years. RESULTS: Of the 882 children in our study, 102 had severe malaria, but only 3 had more than two episodes. More than half of first episodes of severe malaria occurred after a second infection. Although parasite levels were higher on average when children had severe rather than mild disease, most children (67 of 102) had high-density infection (>2500 parasites per 200 white cells) with only mild symptoms before severe malaria, after severe malaria, or both. The incidence of severe malaria decreased considerably after infancy, whereas the incidence of high-density infection was similar among all age groups. Infections before and after episodes of severe malaria were associated with similar parasite densities. Nonuse of bed nets, placental malaria at the time of a woman's second or subsequent delivery, high-transmission season, and absence of the sickle cell trait increased severe-malaria risk and parasite density during infections. CONCLUSIONS: Resistance to severe malaria was not acquired after one or two mild infections. Although the parasite burden was higher on average during episodes of severe malaria, a high parasite burden was often insufficient to cause severe malaria even in children who later were susceptible. The diverging rates of severe disease and high-density infection after infancy, as well as the similar parasite burdens before and after severe malaria, indicate that naturally acquired resistance to severe malaria is not explained by improved control of parasite density. (Funded by the National Institute of Allergy and Infectious Diseases and others.). Free Article
	PMID: 24806160 [PubMed - indexed for MEDLINE]
	Related citations

2.	Science. 2014 May 9;344(6184):645-8. doi: 10.1126/science.1251414. Epub 2014 Apr 24. The transcription factor Gata6 links tissue macrophage phenotype and proliferative renewal. Rosas M1, Davies LC, Giles PJ, Liao CT, Kharfan B, Stone TC, O'Donnell VB, Fraser DJ, Jones SA, Taylor PR. Author information: 1Cardiff Institute of Infection and Immunity, Cardiff University School of Medicine, Heath Park, Cardiff CF14 4XN, UK. Abstract Tissue-resident macrophages are heterogeneous as a consequence of anatomical niche-specific functions. Many populations self-renew independently of bone marrow in the adult, but the molecular mechanisms of this are poorly understood. We determined a transcriptional profile for the major self-renewing population of peritoneal macrophages in mice. These cells specifically expressed the transcription factor Gata6. Selective deficiency of Gata6 in myeloid cells caused substantial alterations in the transcriptome of peritoneal macrophages. Gata6 deficiency also resulted in dysregulated peritoneal macrophage proliferative renewal during homeostasis and in response to inflammation, which was associated with delays in the resolution of inflammation. Our investigations reveal that the tissue macrophage phenotype is under discrete tissue-selective transcriptional control and that this is fundamentally linked to the regulation of their proliferation renewal.
	PMID: 24762537 [PubMed - indexed for MEDLINE]
	Related citations