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  • 2015-2019  (544)
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Year
  • 1
    Publication Date: 2016-07-22
    Description: Activation of salt-inducible kinase 2 promotes the viability of peritoneal mesothelial cells exposed to stress of peritoneal dialysis Cell Death and Disease 7, e2298 (July 2016). doi:10.1038/cddis.2016.79 Authors: H-H Wang, C-Y Lin, S-H Su, C-T Chuang, Y-L Chang, T-Y Lee, S-C Lee & C-J Chang
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 2
    Publication Date: 2015-01-23
    Description: Intracellular annexin A2 regulates NF-κB signaling by binding to the p50 subunit: implications for gemcitabine resistance in pancreatic cancer Cell Death and Disease 6, e1606 (January 2015). doi:10.1038/cddis.2014.558 Authors: H Jung, J S Kim, W K Kim, K-J Oh, J-M Kim, H J Lee, B S Han, D S Kim, Y S Seo, S C Lee, S G Park & K-H Bae
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 3
    Publication Date: 2016-03-25
    Description: Crystal Growth & Design DOI: 10.1021/acs.cgd.5b01845
    Print ISSN: 1528-7483
    Electronic ISSN: 1528-7505
    Topics: Chemistry and Pharmacology , Geosciences , Physics
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  • 4
    Publication Date: 2016-06-04
    Description: Crystal Growth & Design DOI: 10.1021/acs.cgd.6b00111
    Print ISSN: 1528-7483
    Electronic ISSN: 1528-7505
    Topics: Chemistry and Pharmacology , Geosciences , Physics
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  • 5
    Publication Date: 2015-06-03
    Description: Chitinases are enzymes that cleave chitin, a component of the exoskeleton of many organisms including the house dust mite (HDM). Here we show that knockin mice expressing an enzymatically inactive acidic mammalian chitinase (AMCase), the dominant true chitinase in mouse lung, showed enhanced type 2 immune responses to inhaled HDM....
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 6
    Publication Date: 2015-12-09
    Description: The incorporation of In on the non-polar, piezoelectric-free (001) facet of cubic ( c -) GaN epitaxially grown over a Si(001) substrate by metal-organic vapor phase epitaxy is reported. Relying on a hexagonal ( h -) to c -phase transformation during epitaxy on an 800 nm-wide, Si(111)-faceted v-groove patterned into the substrate, the GaN epilayer at cross sectional view retains a triangular c -phase inside a chevron-shaped h -phase that results in a top surface bounded by a (001) facet parallel to Si(001) at the center and ( 1 1 ¯ 01 ) facets at both edges. A stack of five, ∼3 nm-thick, In x Ga 1−x N/GaN quantum wells (QWs) was deposited on the double-phased top surface. The c -phase region up to the QWs keeps extremely small misfit (∼0.002) to the fully relaxed h -GaN underneath it and is in tensile stress implying undefected by the h-c phase interface. The In incorporation on a strained non-polar (001) of c -GaN is comparable with that on totally relaxed semi-polar ( 1 1 ¯ 01 ) of h -GaN without noticeable adatom migration across the phase boundary, and sufficient to provide the room-temperature green emission at 496 nm from the c -In x Ga 1−x N/GaN QWs on Si(001) in photoluminescence.
    Print ISSN: 0003-6951
    Electronic ISSN: 1077-3118
    Topics: Physics
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  • 7
    Publication Date: 2016-05-25
    Description: Understanding how dynamical and aerosol inputs affect the temporal variability of hydrometeor formation in climate models will help to explain sources of model diversity in cloud forcing, to provide robust comparisons with data, and, ultimately, to reduce the uncertainty in estimates of the aerosol indirect effect. This variability attribution can...
    Keywords: Sackler Colloquium on Improving Our Fundamental Understanding of the Role of Aerosol&ndash ; Cloud Int
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 8
    Publication Date: 2015-09-15
    Description: Bromodomain and extra terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a new therapeutic opportunity by directly targeting bromodomain proteins that bind acetylated chromatin marks. Early clinical trials have shown promise, especially in acute myeloid leukaemia, and therefore the evaluation of resistance mechanisms is crucial to optimize the clinical efficacy of these drugs. Here we use primary mouse haematopoietic stem and progenitor cells immortalized with the fusion protein MLL-AF9 to generate several single-cell clones that demonstrate resistance, in vitro and in vivo, to the prototypical BET inhibitor, I-BET. Resistance to I-BET confers cross-resistance to chemically distinct BET inhibitors such as JQ1, as well as resistance to genetic knockdown of BET proteins. Resistance is not mediated through increased drug efflux or metabolism, but is shown to emerge from leukaemia stem cells both ex vivo and in vivo. Chromatin-bound BRD4 is globally reduced in resistant cells, whereas the expression of key target genes such as Myc remains unaltered, highlighting the existence of alternative mechanisms to regulate transcription. We demonstrate that resistance to BET inhibitors, in human and mouse leukaemia cells, is in part a consequence of increased Wnt/beta-catenin signalling, and negative regulation of this pathway results in restoration of sensitivity to I-BET in vitro and in vivo. Together, these findings provide new insights into the biology of acute myeloid leukaemia, highlight potential therapeutic limitations of BET inhibitors, and identify strategies that may enhance the clinical utility of these unique targeted therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fong, Chun Yew -- Gilan, Omer -- Lam, Enid Y N -- Rubin, Alan F -- Ftouni, Sarah -- Tyler, Dean -- Stanley, Kym -- Sinha, Devbarna -- Yeh, Paul -- Morison, Jessica -- Giotopoulos, George -- Lugo, Dave -- Jeffrey, Philip -- Lee, Stanley Chun-Wei -- Carpenter, Christopher -- Gregory, Richard -- Ramsay, Robert G -- Lane, Steven W -- Abdel-Wahab, Omar -- Kouzarides, Tony -- Johnstone, Ricky W -- Dawson, Sarah-Jane -- Huntly, Brian J P -- Prinjha, Rab K -- Papenfuss, Anthony T -- Dawson, Mark A -- England -- Nature. 2015 Sep 24;525(7570):538-42. doi: 10.1038/nature14888. Epub 2015 Sep 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Division, Peter MacCallum Cancer Centre, East Melbourne, Victoria 3002, Australia. ; Sir Peter MacCallum Department of Oncology, The University of Melbourne, East Melbourne, Victoria 3002, Australia. ; Department of Haematology, Peter MacCallum Cancer Centre, East Melbourne, Victoria 3002, Australia. ; Bioinformatics Division, The Walter &Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia. ; Department of Medical Biology, University of Melbourne, Parkville, Victoria 3010, Australia. ; Department of Haematology, Cambridge Institute for Medical Research and Wellcome Trust-MRC Stem Cell Institute, Cambridge CB2 0XY, UK. ; Epinova DPU, Immuno-Inflammation Centre of Excellence for Drug Discovery, GlaxoSmithKline, Medicines Research Centre, Gunnels Wood Road, Stevenage SG1 2NY, UK. ; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Cancer Epigenetics DPU, Oncology R&D, GlaxoSmithKline, 1250 South Collegeville Road, Collegeville, Pennsylvania 19426, USA. ; QIMR Berghofer Medical Research Institute, University of Queensland, Brisbane, Queensland 4029, Australia. ; Gurdon Institute and Department of Pathology, Tennis Court Road, Cambridge CB2 1QN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26367796" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Azepines/pharmacology ; Benzodiazepines/*pharmacology ; Cell Line, Tumor ; Cells, Cultured ; Chromatin/metabolism ; Clone Cells/drug effects/metabolism/pathology ; Drug Resistance, Neoplasm/*drug effects/genetics ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic/drug effects ; Genes, myc/genetics ; Hematopoietic Stem Cells/cytology/drug effects/metabolism ; Humans ; Leukemia, Myeloid, Acute/*drug therapy/genetics/*metabolism/pathology ; Mice ; Molecular Targeted Therapy ; Neoplastic Stem Cells/*drug effects/metabolism/*pathology ; Nuclear Proteins/*antagonists & inhibitors/metabolism ; Transcription Factors/*antagonists & inhibitors/metabolism ; Transcription, Genetic/drug effects ; Triazoles/pharmacology ; Wnt Signaling Pathway/drug effects ; beta Catenin/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2015-11-28
    Description: Two-dimensional (2D) transition metal dichalcogenides have emerged as a promising material system for optoelectronic applications, but their primary figure of merit, the room-temperature photoluminescence quantum yield (QY), is extremely low. The prototypical 2D material molybdenum disulfide (MoS2) is reported to have a maximum QY of 0.6%, which indicates a considerable defect density. Here we report on an air-stable, solution-based chemical treatment by an organic superacid, which uniformly enhances the photoluminescence and minority carrier lifetime of MoS2 monolayers by more than two orders of magnitude. The treatment eliminates defect-mediated nonradiative recombination, thus resulting in a final QY of more than 95%, with a longest-observed lifetime of 10.8 +/- 0.6 nanoseconds. Our ability to obtain optoelectronic monolayers with near-perfect properties opens the door for the development of highly efficient light-emitting diodes, lasers, and solar cells based on 2D materials.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amani, Matin -- Lien, Der-Hsien -- Kiriya, Daisuke -- Xiao, Jun -- Azcatl, Angelica -- Noh, Jiyoung -- Madhvapathy, Surabhi R -- Addou, Rafik -- KC, Santosh -- Dubey, Madan -- Cho, Kyeongjae -- Wallace, Robert M -- Lee, Si-Chen -- He, Jr-Hau -- Ager, Joel W 3rd -- Zhang, Xiang -- Yablonovitch, Eli -- Javey, Ali -- New York, N.Y. -- Science. 2015 Nov 27;350(6264):1065-8. doi: 10.1126/science.aad2114.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Electrical Engineering and Computer Sciences, University of California, Berkeley, Berkeley, CA 94720, USA. Materials Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA. ; Electrical Engineering and Computer Sciences, University of California, Berkeley, Berkeley, CA 94720, USA. Materials Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA. Computer, Electrical and Mathematical Sciences and Engineering Division, King Abdullah University of Science and Technology (KAUST), Thuwal 23955-6900, Saudi Arabia. Department of Electrical Engineering, Institute of Electronics Engineering, National Taiwan University, Taipei 10617, Taiwan, Republic of China. ; National Science Foundation Nanoscale Science and Engineering Center, University of California, Berkeley, Berkeley, CA 94720, USA. Materials Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA. ; Department of Materials Science and Engineering, University of Texas, Dallas, Richardson, TX 75080, USA. ; Sensors and Electron Devices Directorate, U.S. Army Research Laboratory, Adelphi, MD 20723, USA. ; Department of Electrical Engineering, Institute of Electronics Engineering, National Taiwan University, Taipei 10617, Taiwan, Republic of China. ; Computer, Electrical and Mathematical Sciences and Engineering Division, King Abdullah University of Science and Technology (KAUST), Thuwal 23955-6900, Saudi Arabia. ; Materials Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA. ; National Science Foundation Nanoscale Science and Engineering Center, University of California, Berkeley, Berkeley, CA 94720, USA. Materials Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA. Department of Physics, King Abdulaziz University, Jeddah 21589, Saudi Arabia. ; Electrical Engineering and Computer Sciences, University of California, Berkeley, Berkeley, CA 94720, USA. Materials Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA. ajavey@eecs.berkeley.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26612948" target="_blank"〉PubMed〈/a〉
    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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  • 10
    Publication Date: 2016-04-16
    Description: Increasing incidence of inflammatory bowel diseases, such as Crohn's disease, in developed nations is associated with changes to the microbial environment, such as decreased prevalence of helminth colonization and alterations to the gut microbiota. We find that helminth infection protects mice deficient in the Crohn's disease susceptibility gene Nod2 from intestinal abnormalities by inhibiting colonization by an inflammatory Bacteroides species. Resistance to Bacteroides colonization was dependent on type 2 immunity, which promoted the establishment of a protective microbiota enriched in Clostridiales. Additionally, we show that individuals from helminth-endemic regions harbor a similar protective microbiota and that deworming treatment reduced levels of Clostridiales and increased Bacteroidales. These results support a model of the hygiene hypothesis in which certain individuals are genetically susceptible to the consequences of a changing microbial environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramanan, Deepshika -- Bowcutt, Rowann -- Lee, Soo Ching -- Tang, Mei San -- Kurtz, Zachary D -- Ding, Yi -- Honda, Kenya -- Gause, William C -- Blaser, Martin J -- Bonneau, Richard A -- Lim, Yvonne A L -- Loke, P'ng -- Cadwell, Ken -- AI007180/AI/NIAID NIH HHS/ -- AI093811/AI/NIAID NIH HHS/ -- AI107588/AI/NIAID NIH HHS/ -- DK090989/DK/NIDDK NIH HHS/ -- DK093668/DK/NIDDK NIH HHS/ -- DK103788/DK/NIDDK NIH HHS/ -- HL123340/HL/NHLBI NIH HHS/ -- P30CA016087/CA/NCI NIH HHS/ -- UL1 TR000038/TR/NCATS NIH HHS/ -- UL1 TR00038/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):608-12. doi: 10.1126/science.aaf3229. Epub 2016 Apr 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kimmel Center for Biology and Medicine at the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA. Sackler Institute of Graduate Biomedical Sciences, New York University School of Medicine, New York, NY 10016, USA. ; Departments of Microbiology and Medicine, New York University School of Medicine, New York, NY 10016, USA. ; Department of Parasitology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. ; Sackler Institute of Graduate Biomedical Sciences, New York University School of Medicine, New York, NY 10016, USA. Departments of Microbiology and Medicine, New York University School of Medicine, New York, NY 10016, USA. ; Department of Pathology, New York University Langone Medical Center, New York, NY 10016, USA. ; RIKEN Center for Integrative Medical Sciences (IMS), Yokohama, Kanagawa 230-0045, Japan. Japan Agency for Medical Research and Development (AMED)-Core Research for Evolutional Science and Technology (CREST), Tokyo 100-0004, Japan. ; Center for Immunity and Inflammation, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ 07101, USA. ; Department of Biology, Center for Genomics and Systems Biology, New York University, New York, NY 10003, USA. Courant Institute of Mathematical Sciences, New York University, New York, NY 10012, USA. Simons Center for Data Analysis, Simons Foundation, New York, NY 10011, USA. ; Department of Parasitology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. ken.cadwell@med.nyu.edu png.loke@nyumc.org limailian@um.edu.my. ; Departments of Microbiology and Medicine, New York University School of Medicine, New York, NY 10016, USA. ken.cadwell@med.nyu.edu png.loke@nyumc.org limailian@um.edu.my. ; Kimmel Center for Biology and Medicine at the Skirball Institute, New York University School of Medicine, New York, NY 10016, USA. Departments of Microbiology and Medicine, New York University School of Medicine, New York, NY 10016, USA. ken.cadwell@med.nyu.edu png.loke@nyumc.org limailian@um.edu.my.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27080105" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteroides/*immunology ; Bacteroides Infections/*immunology ; Clostridiales/immunology ; Clostridium Infections/immunology ; Crohn Disease/*genetics/immunology ; Gastrointestinal Microbiome/*immunology ; Genetic Predisposition to Disease ; Hygiene Hypothesis ; Intestines/*immunology/microbiology/parasitology ; Mice ; Mice, Mutant Strains ; Nod2 Signaling Adaptor Protein/*genetics ; Trichuriasis/*immunology ; Trichuris/*immunology
    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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