Friday, 22 April 2011

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, 2011 Apr 22
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 - 9 of 9

1. N Engl J Med. 2011 Apr 14;364(15):1477-8; author reply 1478-9.

Case 2-2011: a woman with shock after treatment of a furuncle.

Pollock AA.
PMID:
21488792
[PubMed - indexed for MEDLINE]
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2. N Engl J Med. 2011 Apr 14;364(15):1478; author reply 1478-9.

Case 2-2011: a woman with shock after treatment of a furuncle.

Milazzo L, Antinori S.
PMID:
21488791
[PubMed - indexed for MEDLINE]
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3. N Engl J Med. 2011 Apr 14;364(15):1472; author reply 1474-5.

Cholesterol efflux capacity and atherosclerosis.

Gupta A.
PMID:
21488784
[PubMed - indexed for MEDLINE]
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4. N Engl J Med. 2011 Apr 14;364(15):1472-3; author reply 1474-5.

Cholesterol efflux capacity and atherosclerosis.

Aeddula NR, Trivedi N, Pathireddy S.
PMID:
21488783
[PubMed - indexed for MEDLINE]
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5. Lancet. 2011 Apr 9;377(9773):1256-63.

Cytomegalovirus gly coprotein-B vaccine with MF59 adjuvant in transplant recipients: a phase 2 randomised placebo-controlled trial.

Griffiths PD, Stanton A, McCarrell E, Smith C, Osman M, Harber M, Davenport A, Jones G, Wheeler DC, O'Beirne J, Thorburn D, Patch D, Atkinson CE, Pichon S, Sweny P, Lanzman M, Woodford E, Rothwell E, Old N, Kinyanjui R, Haque T, Atabani S, Luck S, Prideaux S, Milne RS, Emery VC, Burroughs AK.

Source

Centre for Virology, UCL Medical School, London, UK. p.griffiths@medsch.ucl.ac.uk

Abstract

BACKGROUND:

Cytomegalovirus end-organ disease can be prevented by giving ganciclovir when viraemia is detected in allograft recipients. Values of viral load correlate with development of end-organ disease and are moderated by pre-existing natural immunity. Our aim was to determine whether vaccine-induced immunity could do likewise.

METHODS:

We undertook a phase-2 randomised placebo controlled trial in adults awaiting kidney or liver transplantation at the Royal Free Hospital, London, UK. Exclusion criteria were pregnancy, receipt of blood products (except albumin) in the previous 3 months, and simultaneous multiorgan transplantation. 70 patients seronegative and 70 seropositive for cytomegalovirus were randomly assigned from a scratch-off randomisation code in a 1:1 ratio to receive either cytomegalovirus glycoprotein-B vaccine with MF59 adjuvant or placebo, each given at baseline, 1 month and 6 months later. If a patient was transplanted, no further vaccinations were given and serial blood samples were tested for cytomegalovirus DNA by real-time quantitative PCR (rtqPCR). Any patient with one blood sample containing more than 3000 cytomegalovirus genomes per mL received ganciclovir until two consecutive undetectable cytomegalovirus DNA measurements. Safety and immunogenicity were coprimary endpoints and were assessed by intention to treat in patients who received at least one dose of vaccine or placebo. This trial is registered with ClinicalTrials.gov, NCT00299260.

FINDINGS:

67 patients received vaccine and 73 placebo, all of whom were evaluable. Glycoprotein-B antibody titres were significantly increased in both seronegative (geometric mean titre 12,537 (95% CI 6593-23,840) versus 86 (63-118) in recipients of placebo recipients; p<0.0001) and seropositive (118,395; 64,503-217,272) versus 24,682 (17,909-34,017); p<0.0001) recipients of vaccine. In those who developed viraemia after transplantation, glycoprotein-B antibody titres correlated inversely with duration of viraemia (p=0.0022). In the seronegative patients with seropositive donors, the duration of viraemia (p=0.0480) and number of days of ganciclovir treatment (p=0.0287) were reduced in vaccine recipients.

INTERPRETATION:

Although cytomegalovirus disease occurs in the context of suppressed cell-mediated immunity post-transplantation, humoral immunity has a role in reduction of cytomegalovirus viraemia. Vaccines containing cytomegalovirus glycoprotein B merit further assessment in transplant recipients.

FUNDING:

National Institute of Allergy and Infectious Diseases, Grant R01AI051355 and Wellcome Trust, Grant 078332. Sponsor: University College London (UCL).

Copyright © 2011 Elsevier Ltd. All rights reserved.

PMID:
21481708
[PubMed - indexed for MEDLINE]
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6. Lancet. 2011 Apr 9;377(9773):1216-8.

A cytomegalovirus vaccine tames the troll of transplantation.

Schleiss MR.

Source

Center for Infectious Diseases and Microbiology Translational Research, Division of Pediatric Infectious Diseases, Department of Pediatrics, University of Minnesota Medical School, Minneapolis, MN 55455, USA. schleiss@umn.edu

PMID:
21481691
[PubMed - indexed for MEDLINE]
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7. Science. 2011 Apr 8;332(6026):186-7.

Immunology. Eosinophils forestall obesity.

Maizels RM, Allen JE.

Source

Centre for Immunity, Infection and Evolution and the Institute for Immunology and Infection Research, University of Edinburgh, Edinburgh EH9 3JT, UK. r.maizels@ed.ac.uk

PMID:
21474746
[PubMed - indexed for MEDLINE]
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8. Lancet. 2011 Apr 9;377(9773):1276-87. Epub 2011 Mar 28.

Osteoporosis: now and the future.

Rachner TD, Khosla S, Hofbauer LC.

Source

Division of Endocrinology, Diabetes, and Bone Diseases, Dresden Technical University Medical Centre, Dresden, Germany.

Abstract

Osteoporosis is a common disease characterised by a systemic impairment of bone mass and microarchitecture that results in fragility fractures. With an ageing population, the medical and socioeconomic effect of osteoporosis, particularly postmenopausal osteoporosis, will increase further. A detailed knowledge of bone biology with molecular insights into the communication between bone-forming osteoblasts and bone-resorbing osteoclasts and the orchestrating signalling network has led to the identification of novel therapeutic targets. Novel treatment strategies have been developed that aim to inhibit excessive bone resorption and increase bone formation. The most promising novel treatments include: denosumab, a monoclonal antibody for receptor activator of NF-κB ligand, a key osteoclast cytokine; odanacatib, a specific inhibitor of the osteoclast protease cathepsin K; and antibodies against the proteins sclerostin and dickkopf-1, two endogenous inhibitors of bone formation. This overview discusses these novel therapies and explains their underlying physiology.

Copyright © 2011 Elsevier Ltd. All rights reserved.

PMID:
21450337
[PubMed - indexed for MEDLINE]
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9. Science. 2011 Apr 8;332(6026):243-7. Epub 2011 Mar 24.

Eosinophils sustain adipose alternatively activated macrophages associated with glucos e homeostasis.

Wu D, Molofsky AB, Liang HE, Ricardo-Gonzalez RR, Jouihan HA, Bando JK, Chawla A, Locksley RM.

Source

Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143-0795, USA.

Abstract

Eosinophils are associated with helminth immunity and allergy, often in conjunction with alternatively activated macrophages (AAMs). Adipose tissue AAMs are necessary to maintain glucose homeostasis and are induced by the cytokine interleukin-4 (IL-4). Here, we show that eosinophils are the major IL-4-expressing cells in white adipose tissues of mice, and, in their absence, AAMs are greatly attenuated. Eosinophils migrate into adipose tissue by an integrin-dependent process and reconstitute AAMs through an IL-4- or IL-13-dependent process. Mice fed a high-fat diet develop increased body fat, impaired glucose tolerance, and insulin resistance in the absence of eosinophils, and helminth-induced adipose tissue eosinophilia enhances glucose tolerance. Our results suggest that eosinophils play an unexpected role in metabolic homeostasis through maintenance of adipose AAMs.

PMID:
21436399
[PubMed - indexed for MEDLINE]
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