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  • Articles  (8)
  • Animals  (6)
  • Surface physics, nanoscale physics, low-dimensional systems  (2)
  • 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
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  • 2
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    Regulation of angiogenesis by a non-canonical Wnt-Flt1 pathway in myeloid cells (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-05-31
    Description: Myeloid cells are a feature of most tissues. Here we show that during development, retinal myeloid cells (RMCs) produce Wnt ligands to regulate blood vessel branching. In the mouse retina, where angiogenesis occurs postnatally, somatic deletion in RMCs of the Wnt ligand transporter Wntless results in increased angiogenesis in the deeper layers. We also show that mutation of Wnt5a and Wnt11 results in increased angiogenesis and that these ligands elicit RMC responses via a non-canonical Wnt pathway. Using cultured myeloid-like cells and RMC somatic deletion of Flt1, we show that an effector of Wnt-dependent suppression of angiogenesis by RMCs is Flt1, a naturally occurring inhibitor of vascular endothelial growth factor (VEGF). These findings indicate that resident myeloid cells can use a non-canonical, Wnt-Flt1 pathway to suppress angiogenic branching.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214992/" 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/PMC3214992/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stefater, James A 3rd -- Lewkowich, Ian -- Rao, Sujata -- Mariggi, Giovanni -- Carpenter, April C -- Burr, Adam R -- Fan, Jieqing -- Ajima, Rieko -- Molkentin, Jeffery D -- Williams, Bart O -- Wills-Karp, Marsha -- Pollard, Jeffrey W -- Yamaguchi, Terry -- Ferrara, Napoleone -- Gerhardt, Holger -- Lang, Richard A -- G1002033/Medical Research Council/United Kingdom -- R01 AR053293/AR/NIAMS NIH HHS/ -- R01 EY015766/EY/NEI NIH HHS/ -- R01 EY015766-05/EY/NEI NIH HHS/ -- Cancer Research UK/United Kingdom -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 May 29;474(7352):511-5. doi: 10.1038/nature10085.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Visual Systems Group, Division of Pediatric Ophthalmology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21623369" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/growth & development ; Endothelial Cells/metabolism ; Fibroblasts ; Intracellular Signaling Peptides and Proteins/genetics/metabolism ; LDL-Receptor Related Proteins/genetics/metabolism ; Ligands ; Low Density Lipoprotein Receptor-Related Protein-5 ; Mice ; Myeloid Cells/*metabolism ; Neovascularization, Physiologic/*physiology ; Receptors, G-Protein-Coupled ; Retina/*cytology ; *Signal Transduction ; Vascular Endothelial Growth Factor A/antagonists & inhibitors ; Vascular Endothelial Growth Factor ; Receptor-1/deficiency/genetics/*metabolism/secretion ; Wnt Proteins/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    A direct and melanopsin-dependent fetal light response regulates mouse eye development (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-01-22
    Description: Vascular patterning is critical for organ function. In the eye, there is simultaneous regression of embryonic hyaloid vasculature (important to clear the optical path) and formation of the retinal vasculature (important for the high metabolic demands of retinal neurons). These events occur postnatally in the mouse. Here we have identified a light-response pathway that regulates both processes. We show that when mice are mutated in the gene (Opn4) for the atypical opsin melanopsin, or are dark-reared from late gestation, the hyaloid vessels are persistent at 8 days post-partum and the retinal vasculature overgrows. We provide evidence that these vascular anomalies are explained by a light-response pathway that suppresses retinal neuron number, limits hypoxia and, as a consequence, holds local expression of vascular endothelial growth factor (VEGFA) in check. We also show that the light response for this pathway occurs in late gestation at about embryonic day 16 and requires the photopigment in the fetus and not the mother. Measurements show that visceral cavity photon flux is probably sufficient to activate melanopsin-expressing retinal ganglion cells in the mouse fetus. These data thus show that light--the stimulus for function of the mature eye--is also critical in preparing the eye for vision by regulating retinal neuron number and initiating a series of events that ultimately pattern the ocular blood vessels.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3746810/" 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/PMC3746810/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rao, Sujata -- Chun, Christina -- Fan, Jieqing -- Kofron, J Matthew -- Yang, Michael B -- Hegde, Rashmi S -- Ferrara, Napoleone -- Copenhagen, David R -- Lang, Richard A -- AR-47363/AR/NIAMS NIH HHS/ -- R01 EY001869/EY/NEI NIH HHS/ -- R01 EY014648/EY/NEI NIH HHS/ -- R01 EY021636/EY/NEI NIH HHS/ -- R01 EY022917/EY/NEI NIH HHS/ -- R01 EY023179/EY/NEI NIH HHS/ -- England -- Nature. 2013 Feb 14;494(7436):243-6. doi: 10.1038/nature11823. Epub 2013 Jan 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Visual Systems Group, Abrahamson Pediatric Eye Institute, Division of Pediatric Ophthalmology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23334418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Cell Hypoxia/radiation effects ; Eye/*blood supply/*growth & development/metabolism/radiation effects ; Female ; Fetus/cytology/embryology/metabolism/*radiation effects ; *Light ; Light Signal Transduction/*radiation effects ; Mice ; Mice, Inbred C57BL ; Neovascularization, Pathologic ; Neovascularization, Physiologic/radiation effects ; Photons ; Retinal Ganglion Cells/cytology/metabolism/radiation effects ; Retinal Neurons/cytology/metabolism/*radiation effects ; Rod Opsins/deficiency/genetics/*metabolism ; Vascular Endothelial Growth Factor A/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Quantitative flux analysis reveals folate-dependent NADPH production (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-05-09
    Description: ATP is the dominant energy source in animals for mechanical and electrical work (for example, muscle contraction or neuronal firing). For chemical work, there is an equally important role for NADPH, which powers redox defence and reductive biosynthesis. The most direct route to produce NADPH from glucose is the oxidative pentose phosphate pathway, with malic enzyme sometimes also important. Although the relative contribution of glycolysis and oxidative phosphorylation to ATP production has been extensively analysed, similar analysis of NADPH metabolism has been lacking. Here we demonstrate the ability to directly track, by liquid chromatography-mass spectrometry, the passage of deuterium from labelled substrates into NADPH, and combine this approach with carbon labelling and mathematical modelling to measure NADPH fluxes. In proliferating cells, the largest contributor to cytosolic NADPH is the oxidative pentose phosphate pathway. Surprisingly, a nearly comparable contribution comes from serine-driven one-carbon metabolism, in which oxidation of methylene tetrahydrofolate to 10-formyl-tetrahydrofolate is coupled to reduction of NADP(+) to NADPH. Moreover, tracing of mitochondrial one-carbon metabolism revealed complete oxidation of 10-formyl-tetrahydrofolate to make NADPH. As folate metabolism has not previously been considered an NADPH producer, confirmation of its functional significance was undertaken through knockdown of methylenetetrahydrofolate dehydrogenase (MTHFD) genes. Depletion of either the cytosolic or mitochondrial MTHFD isozyme resulted in decreased cellular NADPH/NADP(+) and reduced/oxidized glutathione ratios (GSH/GSSG) and increased cell sensitivity to oxidative stress. Thus, although the importance of folate metabolism for proliferating cells has been long recognized and attributed to its function of producing one-carbon units for nucleic acid synthesis, another crucial function of this pathway is generating reducing power.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104482/" 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/PMC4104482/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fan, Jing -- Ye, Jiangbin -- Kamphorst, Jurre J -- Shlomi, Tomer -- Thompson, Craig B -- Rabinowitz, Joshua D -- P01 CA104838/CA/NCI NIH HHS/ -- P30 CA072720/CA/NCI NIH HHS/ -- P50 GM071508/GM/NIGMS NIH HHS/ -- R01 AI097382/AI/NIAID NIH HHS/ -- R01 CA105463/CA/NCI NIH HHS/ -- R01 CA163591/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Jun 12;510(7504):298-302. doi: 10.1038/nature13236. Epub 2014 May 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Chemistry and Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08540, USA [2]. ; 1] Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA [2]. ; Department of Chemistry and Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08540, USA. ; 1] Department of Chemistry and Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08540, USA [2] Department of Computer Science, Technion - Israel Institute of Technology, Haifa 32000, Israel. ; Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24805240" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon/metabolism ; Cell Line ; Cell Line, Tumor ; Cytosol/enzymology/metabolism ; Folic Acid/*metabolism ; Glutathione/metabolism ; Glycine/metabolism ; HEK293 Cells ; Humans ; Isoenzymes/deficiency/genetics/metabolism ; Leucovorin/analogs & derivatives/metabolism ; Methylenetetrahydrofolate Dehydrogenase (NADP)/deficiency/genetics/metabolism ; Mice ; Mitochondria/enzymology/metabolism ; NADP/*biosynthesis/metabolism ; Oxidation-Reduction ; Oxidative Stress ; Pentose Phosphate Pathway ; Serine/metabolism ; Tetrahydrofolates/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Intestinal inflammation targets cancer-inducing activity of the microbiota (2012)
    American Association for the Advancement of Science (AAAS)
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    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
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  • 6
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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
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  • 7
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    Anomalous Raman spectra and thickness-dependent electronic properties of WSe_{2} (2013)
    American Physical Society (APS)
    Details
    Publication Date: 2013-04-06
    Description: Author(s): H. Sahin, S. Tongay, S. Horzum, W. Fan, J. Zhou, J. Li, J. Wu, and F. M. Peeters Typical Raman spectra of transition-metal dichalcogenides (TMDs) display two prominent peaks, E 2 g and A 1 g , that are well separated from each other. We find that these modes are degenerate in bulk WSe 2 yielding one single Raman peak in contrast to other TMDs. As the dimensionality is lowered, the obs... [Phys. Rev. B 87, 165409] Published Fri Apr 05, 2013
    Keywords: Surface physics, nanoscale physics, low-dimensional systems
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
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  • 8
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    Time-resolved magnetophotoluminescence studies of magnetic polaron dynamics in type-II quantum dots (2015)
    American Physical Society (APS)
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    Publication Date: 2015-07-25
    Description: Author(s): B. Barman, R. Oszwałdowski, L. Schweidenback, A. H. Russ, J. M. Pientka, Y. Tsai, W-C. Chou, W. C. Fan, J. R. Murphy, A. N. Cartwright, I. R. Sellers, A. G. Petukhov, I. Žutić, B. D. McCombe, and A. Petrou We used continuous wave photoluminescence (cw-PL) and time-resolved photoluminescence (TR-PL) spectroscopy to compare the properties of magnetic polarons (MP) in two related spatially indirect II-VI epitaxially grown quantum dot systems. In the ZnTe / ( Zn , Mn ) Se system the holes are confined in the non… [Phys. Rev. B 92, 035430] Published Fri Jul 24, 2015
    Keywords: Surface physics, nanoscale physics, low-dimensional systems
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
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