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, 2010 Apr 30
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 - 2 of 2

1.	Nature. 2010 Mar 18;464(7287):367-73. Comparative genomics reveals mobile pathogenicity chromosomes in Fusarium. Ma LJ, van der Does HC, Borkovich KA, Coleman JJ, Daboussi MJ, Di Pietro A, Dufresne M, Freitag M, Grabherr M, Henrissat B, Houterman PM, Kang S, Shim WB, Woloshuk C, Xie X, Xu JR, Antoniw J, Baker SE, Bluhm BH, Breakspear A, Brown DW, Butchko RA, Chapman S, Coulson R, Coutinho PM, Danchin EG, Diener A, Gale LR, Gardiner DM, Goff S, Hammond-Kosack KE, Hilburn K, Hua-Van A, Jonkers W, Kazan K, Kodira CD, Koehrsen M, Kumar L, Lee YH, Li L, Manners JM, Miranda-Saavedra D, Mukherjee M, Park G, Park J, Park SY, Proctor RH, Regev A, Ruiz-Roldan MC, Sain D, Sakthikumar S, Sykes S, Schwartz DC, Turgeon BG, Wapinski I, Yoder O, Young S, Zeng Q, Zhou S, Galagan J, Cuomo CA, Kistler HC, Rep M. The Broad Institute, Cambridge, Massachusetts 02141, USA. Abstract Fusarium species are among the most important phytopathogenic and toxigenic fungi. To understand the molecular underpinnings of pathogenicity in the genus Fusarium, we compared the genomes of three phenotypically diverse species: Fusarium graminearum, Fusarium verticillioides and Fusarium oxysporum f. sp. lycopersici. Our analysis revealed lineage-specific (LS) genomic regions in F. oxysporum that include four entire chromosomes and account for more than one-quarter of the genome. LS regions are rich in transposons and genes with distinct evolutionary profiles but related to pathogenicity, indicative of horizontal acquisition. Experimentally, we demonstrate the transfer of two LS chromosomes between strains of F. oxysporum, converting a non-pathogenic strain into a pathogen. Transfer of LS chromosomes between otherwise genetically isolated strains explains the polyphyletic origin of host specificity and the emergence of new pathogenic lineages in F. oxysporum. These findings put the evolution of fungal pathogenicity into a new perspective.
	PMID: 20237561 [PubMed - indexed for MEDLINE]
	Related citations
	Publication Types: Comparative Study Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. MeSH Terms: Chromosomes, Fungal/genetics* Evolution, Molecular Fusarium/classification Fusarium/genetics* Fusarium/pathogenicity* Genome, Fungal/genetics* Genomics* Host-Parasite Interactions/genetics Multigene Family/genetics Phenotype Phylogeny Proteome/genetics Sequence Analysis, DNA Synteny/genetics Virulence/genetics Substances: Proteome

2.	Nature. 2010 Mar 18;464(7287):355. Q&A: Hervé This on flavour and perception. Interview by Michael White. This H.
	PMID: 20237550 [PubMed - indexed for MEDLINE]
	Related citations
	Publication Types: Interview MeSH Terms: Animals Cookery/instrumentation Cookery/methods* Flavoring Agents/isolation & purification Geography Humans Meat/analysis Molecular Biology/trends Odors/analysis Smell Taste* Temperature Turkeys Substances: Flavoring Agents

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 Wednesday, 2010 Apr 28
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

Item 1 of 1

1.	J Leukoc Biol. 2010 Apr;87(4):735-41. Epub 2009 Dec 22. Macrophages from BALB/c and CBA/Ca mice differ in their cellular responses to Streptococcus pneumoniae. Ripoll VM, Kadioglu A, Cox R, Hume DA, Denny P. Mammalian Genetics Unit, Medical Research Council, Harwell, Oxfordshire OX11 0RD, UK. v.ripoll@har.mrc.ac.uk Abstract In a mouse model of pneumonia caused by Streptococcus pneumoniae, differences in the timing and vigor of the host inflammatory response have been associated with susceptibility to invasive disease. BALB/c and CBA/Ca mice are known to be resistant and susceptible to acute pneumococcal disease, respectively. In this study, we have demonstrated that BMM from BALB/c and CBA/Ca mice differ in their expression and regulation of TLR9 in response to S. pneumoniae. We have also shown that BMM from CBA/Ca mice failed to fully activate p38, NF-kappaB, and ERK 1/2 signaling pathways, resulting in reduced secretion of TNF-alpha and CCL5 in response to this pathogen. In addition, we have established that S. pneumoniae induced significant cell death in BMM from CBA/Ca mice. These findings indicate that variations between the two strains are likely to reflect differences in macrophage responses to the pathogen.
	PMID: 20028774 [PubMed - indexed for MEDLINE]
	MeSH Terms: Acute Disease Animals Cell Death/immunology Chemokine CCL5/immunology Chemokine CCL5/metabolism Disease Models, Animal Inflammation/immunology Inflammation/metabolism MAP Kinase Signaling System/immunology* Macrophages/immunology* Macrophages/metabolism Male Mice Mice, Inbred BALB C Mitogen-Activated Protein Kinase 3/immunology Mitogen-Activated Protein Kinase 3/metabolism NF-kappa B/immunology NF-kappa B/metabolism Pneumonia, Pneumococcal/immunology* Pneumonia, Pneumococcal/metabolism Species Specificity Streptococcus pneumoniae/immunology* Streptococcus pneumoniae/metabolism Toll-Like Receptor 9/biosynthesis Toll-Like Receptor 9/immunology Tumor Necrosis Factor-alpha/immunology Tumor Necrosis Factor-alpha/secretion p38 Mitogen-Activated Protein Kinases/immunology p38 Mitogen-Activated Protein Kinases/metabolism Substances: Ccl5 protein, mouse Chemokine CCL5 NF-kappa B Tlr9 protein, mouse Toll-Like Receptor 9 Tumor Necrosis Factor-alpha Mitogen-Activated Protein Kinase 3 p38 Mitogen-Activated Protein Kinases

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, 2010 Apr 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 - 2 of 2

1.	Nat Med. 2010 Apr;16(4):396-9. Endoplasmic reticulum stress and atherosclerosis. Hotamisligil GS. Department of Genetics, and the Broad Institute of Massachusetts Institute of Technology and Harvard, Harvard School of Public Health, Boston, Massachusetts, USA. ghotamis@hsph.harvard.edu Abstract Atherosclerosis and related cardiovascular diseases represent one of the greatest threats to human health worldwide. Despite important progress in prevention and treatment, these conditions still account for one third of all deaths annually. Often presented together with obesity, insulin resistance and type 2 diabetes, these chronic diseases are strongly influenced by pathways that lie at the interface of chronic inflammation and nutrient metabolism. Here I discuss recent advances in the study of endoplasmic reticulum stress as one mechanism that links immune response with nutrient sensing in the pathogenesis of atherosclerosis and its complications.
	PMID: 20376052 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Research Support, N.I.H., Extramural MeSH Terms: Animals Apoptosis/physiology Atherosclerosis/etiology* Endoplasmic Reticulum/physiology* Humans Inflammation/physiopathology Lipid Metabolism/physiology Macrophages/physiology Stress, Physiological/physiology* Unfolded Protein Response/physiology

2.	Nat Med. 2010 Apr;16(4):452-9. Epub 2010 Mar 7. Programmed death-1-induced interleukin-10 production by monocytes impairs CD4+ T cell activation during HIV infection. Said EA, Dupuy FP, Trautmann L, Zhang Y, Shi Y, El-Far M, Hill BJ, Noto A, Ancuta P, Peretz Y, Fonseca SG, Van Grevenynghe J, Boulassel MR, Bruneau J, Shoukry NH, Routy JP, Douek DC, Haddad EK, Sekaly RP. Centre de Recherche du Centre hospitalier de l'Université de Montréal (CRCHUM), Hôpital St.-Luc, Montréal, Québec, Canada. Abstract Viral replication and microbial translocation from the gut to the blood during HIV infection lead to hyperimmune activation, which contributes to the decline in CD4+ T cell numbers during HIV infection. Programmed death-1 (PD-1) and interleukin-10 (IL-10) are both upregulated during HIV infection. Blocking interactions between PD-1 and programmed death ligand-1 (PD-L1) and between IL-10 and IL-10 receptor (IL-10R) results in viral clearance and improves T cell function in animal models of chronic viral infections. Here we show that high amounts of microbial products and inflammatory cytokines in the plasma of HIV-infected subjects lead to upregulation of PD-1 expression on monocytes that correlates with high plasma concentrations of IL-10. Triggering of PD-1 expressed on monocytes by PD-L1 expressed on various cell types induced IL-10 production and led to reversible CD4+ T cell dysfunction. We describe a new function for PD-1 whereby microbial products inhibit T cell expansion and function by upregulating PD-1 levels and IL-10 production by monocytes after binding of PD-1 by PD-L1.
	PMID: 20208540 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't MeSH Terms: Antigens, CD/biosynthesis Antigens, CD/physiology* CD4-Positive T-Lymphocytes/immunology CD4-Positive T-Lymphocytes/physiology CD4-Positive T-Lymphocytes/virology* HIV Infections/immunology* HIV Infections/physiopathology Humans Interleukin-10/biosynthesis Interleukin-10/physiology* Lymphocyte Activation/immunology Lymphocyte Activation/physiology* Lymphocyte Subsets/immunology Lymphocyte Subsets/physiology Monocytes/immunology Monocytes/physiology* Phosphorylation Receptors, IgG/immunology Receptors, IgG/physiology STAT3 Transcription Factor/immunology STAT3 Transcription Factor/physiology Up-Regulation/physiology Viremia/immunology Viremia/physiopathology Substances: Antigens, CD CD274 protein, human Receptors, IgG STAT3 Transcription Factor STAT3 protein, human Interleukin-10

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, 2010 Apr 20
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 - 7 of 7

1.	Nature. 2010 Mar 4;464(7285):104-7. Circulating mitochondrial DAMPs cause inflammatory responses to injury. Zhang Q, Raoof M, Chen Y, Sumi Y, Sursal T, Junger W, Brohi K, Itagaki K, Hauser CJ. Department of Surgery, Division of Trauma, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA. Comment in: Nature. 2010 Mar 4;464(7285):41-2. Abstract Injury causes a systemic inflammatory response syndrome (SIRS) that is clinically much like sepsis. Microbial pathogen-associated molecular patterns (PAMPs) activate innate immunocytes through pattern recognition receptors. Similarly, cellular injury can release endogenous 'damage'-associated molecular patterns (DAMPs) that activate innate immunity. Mitochondria are evolutionary endosymbionts that were derived from bacteria and so might bear bacterial molecular motifs. Here we show that injury releases mitochondrial DAMPs (MTDs) into the circulation with functionally important immune consequences. MTDs include formyl peptides and mitochondrial DNA. These activate human polymorphonuclear neutrophils (PMNs) through formyl peptide receptor-1 and Toll-like receptor (TLR) 9, respectively. MTDs promote PMN Ca(2+) flux and phosphorylation of mitogen-activated protein (MAP) kinases, thus leading to PMN migration and degranulation in vitro and in vivo. Circulating MTDs can elicit neutrophil-mediated organ injury. Cellular disruption by trauma releases mitochondrial DAMPs with evolutionarily conserved similarities to bacterial PAMPs into the circulation. These signal through innate immune pathways identical to those activated in sepsis to create a sepsis-like state. The release of such mitochondrial 'enemies within' by cellular injury is a key link between trauma, inflammation and SIRS. PMCID: PMC2843437 [Available on 2010/9/4]
	PMID: 20203610 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S. MeSH Terms: Acute Lung Injury/immunology Acute Lung Injury/pathology Animals Calcium Signaling Cells, Cultured CpG Islands/immunology DNA, Mitochondrial/blood DNA, Mitochondrial/immunology Femur/injuries Fractures, Bone/immunology Fractures, Bone/pathology Humans Immunity, Innate/immunology Liver/immunology Liver/injuries Liver/pathology Male Mitochondria/immunology* Mitochondria/secretion* Mitogen-Activated Protein Kinases/metabolism Muscle, Skeletal/immunology Muscle, Skeletal/pathology N-Formylmethionine Leucyl-Phenylalanine/immunology N-Formylmethionine Leucyl-Phenylalanine/metabolism Neutrophils/enzymology Neutrophils/immunology Neutrophils/metabolism Phosphorylation Rats Rats, Sprague-Dawley Receptors, Formyl Peptide/metabolism Sepsis/immunology Sepsis/metabolism Sepsis/microbiology Systemic Inflammatory Response Syndrome/blood Systemic Inflammatory Response Syndrome/complications* Systemic Inflammatory Response Syndrome/immunology* Systemic Inflammatory Response Syndrome/pathology Toll-Like Receptor 9/metabolism Wounds and Injuries/blood Wounds and Injuries/complications* Wounds and Injuries/immunology* Wounds and Injuries/pathology Substances: DNA, Mitochondrial Receptors, Formyl Peptide TLR9 protein, human Toll-Like Receptor 9 N-Formylmethionine Leucyl-Phenylalanine Mitogen-Activated Protein Kinases

2.	Nature. 2010 Mar 4;464(7285):59-65. A human gut microbial gene catalogue established by metagenomic sequencing. Qin J, Li R, Raes J, Arumugam M, Burgdorf KS, Manichanh C, Nielsen T, Pons N, Levenez F, Yamada T, Mende DR, Li J, Xu J, Li S, Li D, Cao J, Wang B, Liang H, Zheng H, Xie Y, Tap J, Lepage P, Bertalan M, Batto JM, Hansen T, Le Paslier D, Linneberg A, Nielsen HB, Pelletier E, Renault P, Sicheritz-Ponten T, Turner K, Zhu H, Yu C, Li S, Jian M, Zhou Y, Li Y, Zhang X, Li S, Qin N, Yang H, Wang J, Brunak S, Doré J, Guarner F, Kristiansen K, Pedersen O, Parkhill J, Weissenbach J; MetaHIT Consortium, Bork P, Ehrlich SD, Wang J. Collaborators: Antolin M, Artiguenave F, Blottiere H, Borruel N, Bruls T, Casellas F, Chervaux C, Cultrone A, Delorme C, Denariaz G, Dervyn R, Forte M, Friss C, van de Guchte M, Guedon E, Haimet F, Jamet A, Juste C, Kaci G, Kleerebezem M, Knol J, Kristensen M, Layec S, Le Roux K, Leclerc M, Maguin E, Minardi RM, Oozeer R, Rescigno M, Sanchez N, Tims S, Torrejon T, Varela E, de Vos W, Winogradsky Y, Zoetendal E. BGI-Shenzhen, Shenzhen 518083, China. Abstract To understand the impact of gut microbes on human health and well-being it is crucial to assess their genetic potential. Here we describe the Illumina-based metagenomic sequencing, assembly and characterization of 3.3 million non-redundant microbial genes, derived from 576.7 gigabases of sequence, from faecal samples of 124 European individuals. The gene set, approximately 150 times larger than the human gene complement, contains an overwhelming majority of the prevalent (more frequent) microbial genes of the cohort and probably includes a large proportion of the prevalent human intestinal microbial genes. The genes are largely shared among individuals of the cohort. Over 99% of the genes are bacterial, indicating that the entire cohort harbours between 1,000 and 1,150 prevalent bacterial species and each individual at least 160 such species, which are also largely shared. We define and describe the minimal gut metagenome and the minimal gut bacterial genome in terms of functions present in all individuals and most bacteria, respectively.
	PMID: 20203603 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Comparative Study Research Support, Non-U.S. Gov't MeSH Terms: Adult Bacteria/classification Bacteria/genetics Bacteria/isolation & purification Bacteria/metabolism Cohort Studies Contig Mapping Denmark Feces/microbiology Gastrointestinal Tract/microbiology* Genes, Bacterial/genetics Genes, Essential/genetics Genome, Bacterial/genetics Genomics* Health Humans Inflammatory Bowel Diseases/genetics Metagenome/genetics* Obesity/genetics Open Reading Frames/genetics Overweight/genetics Sequence Analysis, DNA Spain

3.	Nature. 2010 Mar 4;464(7285):44. Obituary: Marshall Nirenberg (1927-2010). Caskey CT.
	PMID: 20203601 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Biography Historical Article News Portraits MeSH Terms: Animals Genetic Code/genetics* History, 20th Century Molecular Biology/history* National Institutes of Health (U.S.) Nobel Prize Protein Biosynthesis United States Personal Name as Subject: Nirenberg M

4.	Nature. 2010 Mar 4;464(7285):41-2. Clinical immunology: Culprits with evolutionary ties. Calfee CS, Matthay MA. Comment on: Nature. 2010 Mar 4;464(7285):104-7.
	PMID: 20203598 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Comment News MeSH Terms: Acute Lung Injury/immunology Acute Lung Injury/pathology Animals DNA, Mitochondrial/blood DNA, Mitochondrial/immunology Humans Immunity, Innate/immunology* Mitochondria/immunology* Mitochondria/secretion* N-Formylmethionine Leucyl-Phenylalanine/immunology N-Formylmethionine Leucyl-Phenylalanine/metabolism Neutrophils/enzymology Neutrophils/immunology Sepsis/immunology Sepsis/metabolism Sepsis/microbiology Systemic Inflammatory Response Syndrome/blood Systemic Inflammatory Response Syndrome/complications* Systemic Inflammatory Response Syndrome/immunology* Systemic Inflammatory Response Syndrome/pathology Wounds and Injuries/blood Wounds and Injuries/complications* Wounds and Injuries/immunology* Wounds and Injuries/pathology Substances: DNA, Mitochondrial N-Formylmethionine Leucyl-Phenylalanine

5.	Nature. 2010 Mar 4;464(7285):22-4. Chinese bioscience: The sequence factory. Cyranoski D.
	PMID: 20203579 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: News MeSH Terms: Academies and Institutes/economics Academies and Institutes/trends* Animals Breeding/economics China Genomics/economics Genomics/instrumentation Genomics/trends* Human Genome Project Humans Outsourced Services/economics Sequence Analysis, DNA/economics Sequence Analysis, DNA/instrumentation Sequence Analysis, DNA/trends* Workload

6.	Nature. 2010 Mar 4;464(7285):7. Do scientists really need a PhD? [No authors listed]
	PMID: 20203559 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Editorial MeSH Terms: Age Factors China Education, Graduate/trends* Genomics/education Genomics/manpower Research/education* Research/manpower Research Personnel/education* Research Personnel/trends

7.	Nature. 2010 Mar 4;464(7285):90-4. Epub 2010 Feb 21. Metabolic streamlining in an open-ocean nitrogen-fixing cyanobacterium. Tripp HJ, Bench SR, Turk KA, Foster RA, Desany BA, Niazi F, Affourtit JP, Zehr JP. Ocean Sciences Department, University of California, Santa Cruz, 1156 High Street, Santa Cruz, California 95064, USA. Abstract Nitrogen (N(2))-fixing marine cyanobacteria are an important source of fixed inorganic nitrogen that supports oceanic primary productivity and carbon dioxide removal from the atmosphere. A globally distributed, periodically abundant N(2)-fixing marine cyanobacterium, UCYN-A, was recently found to lack the oxygen-producing photosystem II complex of the photosynthetic apparatus, indicating a novel metabolism, but remains uncultivated. Here we show, from metabolic reconstructions inferred from the assembly of the complete UCYN-A genome using massively parallel pyrosequencing of paired-end reads, that UCYN-A has a photofermentative metabolism and is dependent on other organisms for essential compounds. We found that UCYN-A lacks a number of major metabolic pathways including the tricarboxylic acid cycle, but retains sufficient electron transport capacity to generate energy and reducing power from light. Unexpectedly, UCYN-A has a reduced genome (1.44 megabases) that is structurally similar to many chloroplasts and some bacteria, in that it contains inverted repeats of ribosomal RNA operons. The lack of biosynthetic pathways for several amino acids and purines suggests that this organism depends on other organisms, either in close association or in symbiosis, for critical nutrients. However, size fractionation experiments using natural populations have so far not provided evidence of a symbiotic association with another microorganism. The UCYN-A cyanobacterium is a paradox in evolution and adaptation to the marine environment, and is an example of the tight metabolic coupling between microorganisms in oligotrophic oceanic microbial communities.
	PMID: 20173737 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. MeSH Terms: Carbon/metabolism Chromosomes, Bacterial/genetics Cyanobacteria/classification Cyanobacteria/cytology Cyanobacteria/genetics* Cyanobacteria/metabolism* Electron Transport Genome, Bacterial/genetics* Genomics Marine Biology Molecular Sequence Data Nitrogen/metabolism* Nitrogen Fixation/genetics Nitrogen Fixation/physiology* Oceans and Seas Oxidoreductases/genetics Seawater/microbiology* Substances: Carbon Nitrogen Oxidoreductases nitrogenase reductase Secondary Source ID: GENBANK/CP001842

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, 2010 Apr 17
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

Item 1 of 1

1.	Nat Genet. 2010 Apr;42(4):277. Keeping the tires warm. [No authors listed]
	PMID: 20348959 [PubMed - indexed for MEDLINE]
	Publication Types: Editorial MeSH Terms: Genetics*/economics Genetics*/legislation & jurisprudence Middle East Policy Making Research/economics*

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, 2010 Apr 16
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 - 2 of 2

1.	Nat Genet. 2010 Mar;42(3):210-5. Epub 2010 Feb 7. Genome-wide association study of hematological and biochemical traits in a Japanese population. Kamatani Y, Matsuda K, Okada Y, Kubo M, Hosono N, Daigo Y, Nakamura Y, Kamatani N. Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, the University of Tokyo, Tokyo, Japan. Abstract We report genome-wide association studies for hematological and biochemical traits from approximately 14,700 Japanese individuals. We identified 60 associations for 8 hematological traits and 29 associations for 12 biochemical traits at genome-wide significance levels (P < 5 x 10(-8)). Of these, 46 associations were new to this study and 43 replicated previous reports. We compared these associated loci with those reported in similar GWAS in European populations. When the minor allele frequency was >10% in the Japanese population, 32 (94.1%) and 31 (91.2%) of the 34 hematological loci previously reported to be associated in a European population were replicated with P-values less than 0.05 and 0.01, respectively, and 31 (73.8%) and 27 (64.3%) of the 42 European biochemical loci were replicated.
	PMID: 20139978 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Research Support, Non-U.S. Gov't MeSH Terms: Asian Continental Ancestry Group/genetics* Biological Markers/analysis Biological Markers/blood* Blood Cell Count Blood Chemical Analysis Cohort Studies Erythrocytes/cytology Erythrocytes/pathology Gene Frequency Genetics, Population Genome-Wide Association Study* Hematologic Diseases/blood Hematologic Diseases/genetics Hematologic Diseases/pathology Hematologic Tests Humans Polymorphism, Single Nucleotide Quantitative Trait Loci* Uric Acid/blood Substances: Biological Markers Uric Acid

2.	Nat Genet. 2010 Mar;42(3):260-3. Epub 2010 Jan 24. Population resequencing reveals local adaptation of Arabidopsis lyrata to serpentine soils. Turner TL, Bourne EC, Von Wettberg EJ, Hu TT, Nuzhdin SV. Molecular and Computational Biology, University of Southern California, Los Angeles, California, USA. tturner@lifesci.ucsb.edu Abstract A powerful way to map functional genomic variation and reveal the genetic basis of local adaptation is to associate allele frequency across the genome with environmental conditions. Serpentine soils, characterized by high heavy-metal content and low calcium-to-magnesium ratios, are a classic context for studying adaptation of plants to local soil conditions. To investigate whether Arabidopsis lyrata is locally adapted to serpentine soil, and to map the polymorphisms responsible for such adaptation, we pooled DNA from individuals from serpentine and nonserpentine soils and sequenced each 'gene pool' with the Illumina Genome Analyzer. The polymorphisms that are most strongly associated with soil type are enriched at heavy-metal detoxification and calcium and magnesium transport loci, providing numerous candidate mutations for serpentine adaptation. Sequencing of three candidate loci in the European subspecies of A. lyrata indicates parallel differentiation of the same polymorphism at one locus, confirming ecological adaptation, and different polymorphisms at two other loci, which may indicate convergent evolution.
	PMID: 20101244 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. MeSH Terms: Adaptation, Biological/drug effects Adaptation, Biological/genetics* Arabidopsis/genetics* Arabidopsis/physiology Asbestos, Serpentine/pharmacology* DNA, Plant/analysis DNA, Plant/drug effects Evolution, Molecular Genes, Plant/drug effects Genetics, Population Genome, Plant/drug effects Geography Metals, Heavy/pharmacology Microsatellite Repeats/genetics Polymorphism, Genetic Sequence Analysis, DNA*/methods Soil* Substances: Asbestos, Serpentine DNA, Plant Metals, Heavy Soil Grant Support: RGM-076643/PHS HHS/United States

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 Wednesday, 2010 Apr 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]))
Click here to view complete results in PubMed. (Results may change over time.)
To unsubscribe from these e-mail updates click here.

PubMed Results

Item 1 of 1

1.	Science. 2010 Mar 26;327(5973):1580-1. Medicine. The future of psychiatric research: genomes and neural circuits. Akil H, Brenner S, Kandel E, Kendler KS, King MC, Scolnick E, Watson JD, Zoghbi HY. Molecular and Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, MI 48109, USA. akil@umich.edu
	PMID: 20339051 [PubMed - indexed for MEDLINE]
	Publication Types: Research Support, Non-U.S. Gov't MeSH Terms: Animals Brain/pathology* Brain/physiopathology* Forecasting Genetic Predisposition to Disease Genome, Human Genomics Humans Mental Disorders/genetics* Mental Disorders/pathology Mental Disorders/physiopathology Neural Pathways/pathology Neural Pathways/physiopathology Sequence Analysis, DNA/economics Grant Support: Howard Hughes Medical Institute/United States

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, 2010 Apr 09
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 - 3 of 3

1.	Nature. 2010 Mar 25;464(7288):487; author reply 487. Issues raised by use of ethnic-group names in genome study. Schlebusch C. Comment on: Nature. 2010 Feb 18;463(7283):943-7.
	PMID: 20336115 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Comment Letter MeSH Terms: Ethnic Groups* Human Genome Project Humans Terminology as Topic*

2.	Nature. 2010 Mar 25;464(7288):487. Questions over the scientific basis of epigenome project. Ptashne M, Hobert O, Davidson E. Comment on: Nature. 2010 Feb 4;463(7281):587.
	PMID: 20336114 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Comment Letter MeSH Terms: Animals Biodiversity Epigenesis, Genetic/genetics* Gene Expression Regulation/genetics Genetic Research/ethics Genome/genetics* Humans

3.	Nature. 2010 Mar 25;464(7288):624-7. Epub 2010 Mar 7. Transcription-independent ARF regulation in oncogenic stress-mediated p53 responses. Chen D, Shan J, Zhu WG, Qin J, Gu W. Institute for Cancer Genetics, and Department of Pathology and Cell Biology College of Physicians & Surgeons, Columbia University, 1130 St Nicholas Avenue, New York, New York 10032, USA. Abstract The tumour suppressor ARF is specifically required for p53 activation under oncogenic stress. Recent studies showed that p53 activation mediated by ARF, but not that induced by DNA damage, acts as a major protection against tumorigenesis in vivo under certain biological settings, suggesting that the ARF-p53 axis has more fundamental functions in tumour suppression than originally thought. Because ARF is a very stable protein in most human cell lines, it has been widely assumed that ARF induction is mediated mainly at the transcriptional level and that activation of the ARF-p53 pathway by oncogenes is a much slower and largely irreversible process by comparison with p53 activation after DNA damage. Here we report that ARF is very unstable in normal human cells but that its degradation is inhibited in cancerous cells. Through biochemical purification, we identified a specific ubiquitin ligase for ARF and named it ULF. ULF interacts with ARF both in vitro and in vivo and promotes the lysine-independent ubiquitylation and degradation of ARF. ULF knockdown stabilizes ARF in normal human cells, triggering ARF-dependent, p53-mediated growth arrest. Moreover, nucleophosmin (NPM) and c-Myc, both of which are commonly overexpressed in cancer cells, are capable of abrogating ULF-mediated ARF ubiquitylation through distinct mechanisms, and thereby promote ARF stabilization in cancer cells. These findings reveal the dynamic feature of the ARF-p53 pathway and suggest that transcription-independent mechanisms are critically involved in ARF regulation during responses to oncogenic stress.
	PMID: 20208519 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't MeSH Terms: ADP-Ribosylation Factors/metabolism* Cell Line Fibroblasts/metabolism Gene Expression Regulation* Humans Molecular Sequence Data Nuclear Proteins/metabolism Proto-Oncogene Proteins c-myc/metabolism Stress, Physiological/physiology* Tumor Suppressor Protein p53/metabolism* U937 Cells Ubiquitin-Protein Ligases/metabolism Ubiquitination Substances: MYC protein, human Nuclear Proteins Proto-Oncogene Proteins c-myc Tumor Suppressor Protein p53 nucleophosmin ADP-Ribosylation Factors Ubiquitin-Protein Ligases Secondary Source ID: GENBANK/EU489742

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 Wednesday, 2010 Apr 07
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 - 2 of 2

1.	Science. 2010 Mar 19;327(5972):1463-5. Neuroscience. AMPA receptors--another twist? Farrant M, Cull-Candy SG. Department of Neuroscience, Physiology, and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK. m.farrant@ucl.ac.uk Comment on: Science. 2010 Mar 19;327(5972):1518-22.
	PMID: 20299582 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Comment Research Support, Non-U.S. Gov't MeSH Terms: Animals CA1 Region, Hippocampal/cytology CA1 Region, Hippocampal/metabolism* Dendritic Spines/metabolism Dentate Gyrus/cytology Dentate Gyrus/metabolism* Excitatory Postsynaptic Potentials Membrane Proteins/metabolism Mice Miniature Postsynaptic Potentials Nerve Tissue Proteins/chemistry Nerve Tissue Proteins/metabolism* Neuronal Plasticity* Neurons/metabolism* Protein Interaction Domains and Motifs Protein Structure, Tertiary Proteomics Pyramidal Cells/metabolism Receptors, AMPA/chemistry Receptors, AMPA/metabolism* Synapses/physiology* Synaptic Transmission* Substances: CKAMP44 protein, mouse Membrane Proteins Nerve Tissue Proteins Receptors, AMPA Grant Support: Wellcome Trust/United Kingdom

2.	Science. 2010 Mar 19;327(5972):1518-22. Epub 2010 Feb 25. CKAMP44: a brain-specific protein attenuating short-term synaptic plasticity in the dentate gyrus. von Engelhardt J, Mack V, Sprengel R, Kavenstock N, Li KW, Stern-Bach Y, Smit AB, Seeburg PH, Monyer H. Department of Clinical Neurobiology, University of Heidelberg, 6910 Heidelberg, Germany. Comment in: Science. 2010 Mar 19;327(5972):1463-5. Abstract CKAMP44, identified here by a proteomic approach, is a brain-specific type I transmembrane protein that associates with AMPA receptors in synaptic spines. CKAMP44 expressed in Xenopus oocytes reduced GluA1- and A2-mediated steady-state currents, but did not affect kainate- or N-methyl-D-aspartate (NMDA) receptor-mediated currents. Mouse hippocampal CA1 pyramidal neurons expressed CKAMP44 at low abundance, and overexpression of CKAMP44 led to stronger and faster AMPA receptor desensitization, slower recovery from desensitization, and a reduction in the paired-pulse ratio of AMPA currents. By contrast, dentate gyrus granule cells exhibited strong CKAMP44 expression, and CKAMP44 knockout increased the paired-pulse ratio of AMPA currents in lateral and medial perforant path-granule cell synapses. CKAMP44 thus modulates short-term plasticity at specific excitatory synapses.
	PMID: 20185686 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Research Support, Non-U.S. Gov't MeSH Terms: Animals CA1 Region, Hippocampal/metabolism Calcium Channels/metabolism Dendritic Spines/metabolism Dentate Gyrus/cytology Dentate Gyrus/metabolism* Excitatory Postsynaptic Potentials Glutamic Acid/metabolism Intracellular Signaling Peptides and Proteins/metabolism Membrane Proteins/metabolism Mice Mice, Knockout Miniature Postsynaptic Potentials Molecular Sequence Data Nerve Tissue Proteins/chemistry Nerve Tissue Proteins/genetics Nerve Tissue Proteins/metabolism* Neural Inhibition Neuronal Plasticity* Neurons/metabolism* Oocytes/metabolism Patch-Clamp Techniques Perforant Pathway Protein Interaction Domains and Motifs Protein Isoforms/genetics Protein Isoforms/metabolism Proteomics Pyramidal Cells/metabolism Receptors, AMPA/chemistry Receptors, AMPA/metabolism* Recombinant Fusion Proteins/metabolism Reverse Transcriptase Polymerase Chain Reaction Synapses/physiology* Synaptic Transmission* Xenopus laevis Substances: CKAMP44 protein, mouse Cacng2 protein, mouse Calcium Channels Dlgh4 protein, mouse Intracellular Signaling Peptides and Proteins Membrane Proteins Nerve Tissue Proteins Protein Isoforms Receptors, AMPA Recombinant Fusion Proteins Glutamic Acid Secondary Source ID: GENBANK/GU479981 GENBANK/GU479982

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, 2010 Apr 02
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 - 2 of 2

1.	Nat Med. 2010 Mar;16(3):279-85. Epub 2010 Feb 28. Kynurenine is an endothelium-derived relaxing factor produced during inflammation. Wang Y, Liu H, McKenzie G, Witting PK, Stasch JP, Hahn M, Changsirivathanathamrong D, Wu BJ, Ball HJ, Thomas SR, Kapoor V, Celermajer DS, Mellor AL, Keaney JF Jr, Hunt NH, Stocker R. Centre for Vascular Research, School of Medical Sciences (Pathology) and Bosch Institute, Faculty of Medicine, University of Sydney, Sydney, Australia. Comment in: Nat Med. 2010 Mar;16(3):265-7. Control of blood vessel tone is central to vascular homeostasis. Here we show that metabolism of tryptophan to kynurenine by indoleamine 2,3-dioxygenase (Ido) expressed in endothelial cells contributes to arterial vessel relaxation and the control of blood pressure. Infection of mice with malarial parasites (Plasmodium berghei) or induction of endotoxemia in mice led to endothelial expression of Ido, decreased plasma tryptophan concentration, increased kynurenine concentration and hypotension. Pharmacological inhibition of Ido increased blood pressure in systemically inflamed mice but not in mice deficient in Ido or interferon-gamma, which is required for Ido induction. Both tryptophan and kynurenine dilated preconstricted porcine coronary arteries; the dilating effect of tryptophan required the presence of active Ido and an intact endothelium, whereas the effect of kynurenine was endothelium independent. The arterial relaxation induced by kynurenine was mediated by activation of the adenylate and soluble guanylate cyclase pathways. Kynurenine administration decreased blood pressure in a dose-dependent manner in spontaneously hypertensive rats. Our results identify tryptophan metabolism by Ido as a new pathway contributing to the regulation of vascular tone.
	PMID: 20190767 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Research Support, Non-U.S. Gov't MeSH Terms: Adenylate Cyclase/metabolism Animals Blood Pressure/drug effects Blood Pressure/physiology Coronary Vessels/drug effects Coronary Vessels/physiopathology Dose-Response Relationship, Drug Endothelium, Vascular/enzymology Endothelium, Vascular/physiology Endothelium, Vascular/physiopathology Endothelium-Dependent Relaxing Factors/physiology* Endotoxemia/physiopathology Enzyme Activation/physiology Guanylate Cyclase/metabolism Guanylate Cyclase/physiology Indoleamine-Pyrrole 2,3,-Dioxygenase/antagonists & inhibitors Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism Indoleamine-Pyrrole 2,3,-Dioxygenase/physiology Inflammation/physiopathology* Interferon-gamma/physiology Kynurenine/biosynthesis Kynurenine/pharmacology Kynurenine/physiology* Malaria/physiopathology Mice Mice, Inbred C57BL Muscle, Smooth, Vascular/drug effects Muscle, Smooth, Vascular/physiology Plasmodium berghei Rats Rats, Inbred SHR Tryptophan/blood Tryptophan/pharmacology Tryptophan/physiology Substances: Endothelium-Dependent Relaxing Factors Kynurenine Tryptophan Interferon-gamma Indoleamine-Pyrrole 2,3,-Dioxygenase Adenylate Cyclase Guanylate Cyclase

2.	Nat Med. 2010 Mar;16(3):334-8. Epub 2010 Jan 28. A virus-like particle vaccine for epidemic Chikungunya virus protects nonhuman primates against infection. Akahata W, Yang ZY, Andersen H, Sun S, Holdaway HA, Kong WP, Lewis MG, Higgs S, Rossmann MG, Rao S, Nabel GJ. Vaccine Research Center, National Institute of Allergy and Infectious Diseases, US National Institutes of Health, Bethesda, Maryland, USA. Chikungunya virus (CHIKV) has infected millions of people in Africa, Europe and Asia since this alphavirus reemerged from Kenya in 2004. The severity of the disease and the spread of this epidemic virus present a serious public health threat in the absence of vaccines or antiviral therapies. Here, we describe a new vaccine that protects against CHIKV infection of nonhuman primates. We show that selective expression of viral structural proteins gives rise to virus-like particles (VLPs) in vitro that resemble replication-competent alphaviruses. Immunization with these VLPs elicited neutralizing antibodies against envelope proteins from alternative CHIKV strains. Monkeys immunized with VLPs produced high-titer neutralizing antibodies that protected against viremia after high-dose challenge. We transferred these antibodies into immunodeficient mice, where they protected against subsequent lethal CHIKV challenge, indicating a humoral mechanism of protection. Immunization with alphavirus VLP vaccines represents a strategy to contain the spread of CHIKV and related pathogenic viruses in humans. PMCID: PMC2834826 [Available on 2010/9/1]
	PMID: 20111039 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Research Support, N.I.H., Extramural MeSH Terms: Alphavirus Infections/immunology Alphavirus Infections/prevention & control* Animals Antibodies, Viral/immunology Antibody Formation/immunology Cells, Cultured Chikungunya virus/immunology* Female Humans Immunoglobulin G/immunology Macaca mulatta/immunology Macaca mulatta/virology Mice Mice, Inbred BALB C Viral Envelope Proteins/immunology Viral Vaccines/immunology Viral Vaccines/therapeutic use* Viremia/immunology Viremia/prevention & control Substances: Antibodies, Viral Immunoglobulin G Viral Envelope Proteins Viral Vaccines