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  • 1
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    H7N9 influenza viruses are transmissible in ferrets by respiratory droplet (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-07-23
    Description: A newly emerged H7N9 virus has caused 132 human infections with 37 deaths in China since 18 February 2013. Control measures in H7N9 virus-positive live poultry markets have reduced the number of infections; however, the character of the virus, including its pandemic potential, remains largely unknown. We systematically analyzed H7N9 viruses isolated from birds and humans. The viruses were genetically closely related and bound to human airway receptors; some also maintained the ability to bind to avian airway receptors. The viruses isolated from birds were nonpathogenic in chickens, ducks, and mice; however, the viruses isolated from humans caused up to 30% body weight loss in mice. Most importantly, one virus isolated from humans was highly transmissible in ferrets by respiratory droplet. Our findings indicate nothing to reduce the concern that these viruses can transmit between humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Qianyi -- Shi, Jianzhong -- Deng, Guohua -- Guo, Jing -- Zeng, Xianying -- He, Xijun -- Kong, Huihui -- Gu, Chunyang -- Li, Xuyong -- Liu, Jinxiong -- Wang, Guojun -- Chen, Yan -- Liu, Liling -- Liang, Libin -- Li, Yuanyuan -- Fan, Jun -- Wang, Jinliang -- Li, Wenhui -- Guan, Lizheng -- Li, Qimeng -- Yang, Huanliang -- Chen, Pucheng -- Jiang, Li -- Guan, Yuntao -- Xin, Xiaoguang -- Jiang, Yongping -- Tian, Guobin -- Wang, Xiurong -- Qiao, Chuanling -- Li, Chengjun -- Bu, Zhigao -- Chen, Hualan -- New York, N.Y. -- Science. 2013 Jul 26;341(6144):410-4. doi: 10.1126/science.1240532. Epub 2013 Jul 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 150001, People's Republic of China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23868922" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chickens/virology ; Columbidae/virology ; Ducks/virology ; Ferrets/*virology ; Genes, Viral ; Hemagglutinin Glycoproteins, Influenza Virus/chemistry/genetics/metabolism ; Humans ; Influenza A virus/genetics/isolation & purification/*pathogenicity/physiology ; Influenza in Birds/virology ; Influenza, Human/*transmission/*virology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Mutation ; Orthomyxoviridae Infections/*transmission/*virology ; Receptors, Cell Surface/metabolism ; Receptors, Virus/metabolism ; Respiratory System/*virology ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Intestinal inflammation targets cancer-inducing activity of the microbiota (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-21
    Description: Inflammation alters host physiology to promote cancer, as seen in colitis-associated colorectal cancer (CRC). Here, we identify the intestinal microbiota as a target of inflammation that affects the progression of CRC. High-throughput sequencing revealed that inflammation modifies gut microbial composition in colitis-susceptible interleukin-10-deficient (Il10(-/-)) mice. Monocolonization with the commensal Escherichia coli NC101 promoted invasive carcinoma in azoxymethane (AOM)-treated Il10(-/-) mice. Deletion of the polyketide synthase (pks) genotoxic island from E. coli NC101 decreased tumor multiplicity and invasion in AOM/Il10(-/-) mice, without altering intestinal inflammation. Mucosa-associated pks(+) E. coli were found in a significantly high percentage of inflammatory bowel disease and CRC patients. This suggests that in mice, colitis can promote tumorigenesis by altering microbial composition and inducing the expansion of microorganisms with genotoxic capabilities.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3645302/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3645302/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arthur, Janelle C -- Perez-Chanona, Ernesto -- Muhlbauer, Marcus -- Tomkovich, Sarah -- Uronis, Joshua M -- Fan, Ting-Jia -- Campbell, Barry J -- Abujamel, Turki -- Dogan, Belgin -- Rogers, Arlin B -- Rhodes, Jonathan M -- Stintzi, Alain -- Simpson, Kenneth W -- Hansen, Jonathan J -- Keku, Temitope O -- Fodor, Anthony A -- Jobin, Christian -- MOP114872/Canadian Institutes of Health Research/Canada -- P30 CA016086/CA/NCI NIH HHS/ -- P30 DK034987/DK/NIDDK NIH HHS/ -- P40 R018603/PHS HHS/ -- R01 CA136887/CA/NCI NIH HHS/ -- R01 DK047700/DK/NIDDK NIH HHS/ -- R01 DK073338/DK/NIDDK NIH HHS/ -- R01 DK47700/DK/NIDDK NIH HHS/ -- R01 DK53347-11/DK/NIDDK NIH HHS/ -- R01 DK73338/DK/NIDDK NIH HHS/ -- T32 DK007737/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 5;338(6103):120-3. doi: 10.1126/science.1224820. Epub 2012 Aug 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Pharmacology and Immunology-Microbiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22903521" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Azoxymethane/toxicity ; Carcinogens/toxicity ; Carcinoma/chemically induced/*microbiology/pathology ; Cell Transformation, Neoplastic/genetics/pathology ; Colitis/*complications/genetics ; Colorectal Neoplasms/chemically induced/*microbiology/pathology ; *DNA Damage ; Escherichia coli/genetics/pathogenicity ; Interleukin-10/genetics ; Intestines/*microbiology/pathology ; Metagenome/genetics/*physiology ; Mice ; Mice, Mutant Strains ; Polyketide Synthases/genetics ; Sequence Deletion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    METABOLISM. S-Nitrosylation links obesity-associated inflammation to endoplasmic reticulum dysfunction (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-08-01
    Description: The association between inflammation and endoplasmic reticulum (ER) stress has been observed in many diseases. However, if and how chronic inflammation regulates the unfolded protein response (UPR) and alters ER homeostasis in general, or in the context of chronic disease, remains unknown. Here, we show that, in the setting of obesity, inflammatory input through increased inducible nitric oxide synthase (iNOS) activity causes S-nitrosylation of a key UPR regulator, IRE1alpha, which leads to a progressive decline in hepatic IRE1alpha-mediated XBP1 splicing activity in both genetic (ob/ob) and dietary (high-fat diet-induced) models of obesity. Finally, in obese mice with liver-specific IRE1alpha deficiency, reconstitution of IRE1alpha expression with a nitrosylation-resistant variant restored IRE1alpha-mediated XBP1 splicing and improved glucose homeostasis in vivo. Taken together, these data describe a mechanism by which inflammatory pathways compromise UPR function through iNOS-mediated S-nitrosylation of IRE1alpha, which contributes to defective IRE1alpha activity, impaired ER function, and prolonged ER stress in obesity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573582/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573582/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Ling -- Calay, Ediz S -- Fan, Jason -- Arduini, Alessandro -- Kunz, Ryan C -- Gygi, Steven P -- Yalcin, Abdullah -- Fu, Suneng -- Hotamisligil, Gokhan S -- DK052539/DK/NIDDK NIH HHS/ -- R01 DK052539/DK/NIDDK NIH HHS/ -- T32 GM007367/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2015 Jul 31;349(6247):500-6. doi: 10.1126/science.aaa0079.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Complex Diseases and Sabri Ulker Center, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA. ; Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. ; Department of Genetics and Complex Diseases and Sabri Ulker Center, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA. Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA. ghotamis@hsph.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26228140" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA-Binding Proteins/*genetics ; Diet, High-Fat ; Disease Models, Animal ; Endoplasmic Reticulum/*metabolism ; *Endoplasmic Reticulum Stress ; Endoribonucleases/*metabolism ; Glucose/metabolism ; Homeostasis ; Inflammation/metabolism ; Liver/metabolism ; Mice ; Mice, Obese ; Nitric Oxide Synthase Type II/metabolism ; Nitrogen Oxides/*metabolism ; Obesity/*metabolism/*pathology ; Protein-Serine-Threonine Kinases/*metabolism ; *RNA Splicing ; RNA, Messenger/metabolism ; Transcription Factors/*genetics ; Unfolded Protein Response
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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