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  • American Association for the Advancement of Science (AAAS)  (13)
  • Nature Publishing Group (NPG)  (6)
  • American Institute of Physics
  • American Physical Society
  • 2020-2024
  • 2010-2014  (19)
  • 1980-1984
  • 1945-1949
  • 2014  (19)
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Verlag/Herausgeber
  • American Association for the Advancement of Science (AAAS)  (13)
  • Nature Publishing Group (NPG)  (6)
  • American Institute of Physics
  • American Physical Society
Erscheinungszeitraum
  • 2020-2024
  • 2010-2014  (19)
  • 1980-1984
  • 1945-1949
Jahr
  • 1
    Publikationsdatum: 2014-05-30
    Beschreibung: The availability of human genome sequence has transformed biomedical research over the past decade. However, an equivalent map for the human proteome with direct measurements of proteins and peptides does not exist yet. Here we present a draft map of the human proteome using high-resolution Fourier-transform mass spectrometry. In-depth proteomic profiling of 30 histologically normal human samples, including 17 adult tissues, 7 fetal tissues and 6 purified primary haematopoietic cells, resulted in identification of proteins encoded by 17,294 genes accounting for approximately 84% of the total annotated protein-coding genes in humans. A unique and comprehensive strategy for proteogenomic analysis enabled us to discover a number of novel protein-coding regions, which includes translated pseudogenes, non-coding RNAs and upstream open reading frames. This large human proteome catalogue (available as an interactive web-based resource at http://www.humanproteomemap.org) will complement available human genome and transcriptome data to accelerate biomedical research in health and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4403737/" 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/PMC4403737/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Min-Sik -- Pinto, Sneha M -- Getnet, Derese -- Nirujogi, Raja Sekhar -- Manda, Srikanth S -- Chaerkady, Raghothama -- Madugundu, Anil K -- Kelkar, Dhanashree S -- Isserlin, Ruth -- Jain, Shobhit -- Thomas, Joji K -- Muthusamy, Babylakshmi -- Leal-Rojas, Pamela -- Kumar, Praveen -- Sahasrabuddhe, Nandini A -- Balakrishnan, Lavanya -- Advani, Jayshree -- George, Bijesh -- Renuse, Santosh -- Selvan, Lakshmi Dhevi N -- Patil, Arun H -- Nanjappa, Vishalakshi -- Radhakrishnan, Aneesha -- Prasad, Samarjeet -- Subbannayya, Tejaswini -- Raju, Rajesh -- Kumar, Manish -- Sreenivasamurthy, Sreelakshmi K -- Marimuthu, Arivusudar -- Sathe, Gajanan J -- Chavan, Sandip -- Datta, Keshava K -- Subbannayya, Yashwanth -- Sahu, Apeksha -- Yelamanchi, Soujanya D -- Jayaram, Savita -- Rajagopalan, Pavithra -- Sharma, Jyoti -- Murthy, Krishna R -- Syed, Nazia -- Goel, Renu -- Khan, Aafaque A -- Ahmad, Sartaj -- Dey, Gourav -- Mudgal, Keshav -- Chatterjee, Aditi -- Huang, Tai-Chung -- Zhong, Jun -- Wu, Xinyan -- Shaw, Patrick G -- Freed, Donald -- Zahari, Muhammad S -- Mukherjee, Kanchan K -- Shankar, Subramanian -- Mahadevan, Anita -- Lam, Henry -- Mitchell, Christopher J -- Shankar, Susarla Krishna -- Satishchandra, Parthasarathy -- Schroeder, John T -- Sirdeshmukh, Ravi -- Maitra, Anirban -- Leach, Steven D -- Drake, Charles G -- Halushka, Marc K -- Prasad, T S Keshava -- Hruban, Ralph H -- Kerr, Candace L -- Bader, Gary D -- Iacobuzio-Donahue, Christine A -- Gowda, Harsha -- Pandey, Akhilesh -- HHSN268201000032C/HL/NHLBI NIH HHS/ -- HHSN268201000032C/PHS HHS/ -- P41 GM103504/GM/NIGMS NIH HHS/ -- P41GM103504/GM/NIGMS NIH HHS/ -- T32 GM007814/GM/NIGMS NIH HHS/ -- U24 CA160036/CA/NCI NIH HHS/ -- U24CA160036/CA/NCI NIH HHS/ -- U54 GM103520/GM/NIGMS NIH HHS/ -- U54GM103520/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 May 29;509(7502):575-81. doi: 10.1038/nature13302.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. ; Institute of Bioinformatics, International Tech Park, Bangalore 560066, India. ; 1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Adrienne Helis Malvin Medical Research Foundation, New Orleans, Louisiana 70130, USA. ; The Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada. ; 1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Department of Pathology, Universidad de La Frontera, Center of Genetic and Immunological Studies-Scientific and Technological Bioresource Nucleus, Temuco 4811230, Chile. ; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. ; School of Medicine, Imperial College London, South Kensington Campus, London SW7 2AZ, UK. ; Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. ; Department of Neurosurgery, Postgraduate Institute of Medical Education & Research, Chandigarh 160012, India. ; Department of Internal Medicine Armed Forces Medical College, Pune 411040, India. ; 1] Department of Neuropathology, National Institute of Mental Health and Neurosciences, Bangalore 560029, India [2] Human Brain Tissue Repository, Neurobiology Research Centre, National Institute of Mental Health and Neurosciences, Bangalore 560029, India. ; Department of Chemical and Biomolecular Engineering and Division of Biomedical Engineering, The Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong. ; Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore 560029, India. ; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224, USA. ; 1] The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [2] Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; 1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; 1] Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [2] Departments of Immunology and Urology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; 1] Department of Obstetrics and Gynecology, Johns Hopkins University School of Medicine Baltimore, Maryland 21205, USA [2] Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA. ; 1] The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [2] Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [3] Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA. ; 1] McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [3] Institute of Bioinformatics, International Tech Park, Bangalore 560066, India [4] Adrienne Helis Malvin Medical Research Foundation, New Orleans, Louisiana 70130, USA [5] The Sol Goldman Pancreatic Cancer Research Center, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [6] Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA [7] Diana Helis Henry Medical Research Foundation, New Orleans, Louisiana 70130, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24870542" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Cells, Cultured ; Databases, Protein ; Fetus/metabolism ; Fourier Analysis ; Gene Expression Profiling ; Genome, Human/genetics ; Hematopoietic Stem Cells/cytology/metabolism ; Humans ; Internet ; Mass Spectrometry ; Molecular Sequence Annotation ; Open Reading Frames/genetics ; Organ Specificity ; Protein Biosynthesis ; Protein Isoforms/analysis/genetics/metabolism ; Protein Sorting Signals ; Protein Transport ; Proteome/analysis/chemistry/genetics/*metabolism ; *Proteomics ; Pseudogenes/genetics ; RNA, Untranslated/genetics ; Reproducibility of Results ; Untranslated Regions/genetics
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Publikationsdatum: 2014-11-28
    Beschreibung: The development of human cancer is a multistep process characterized by the accumulation of genetic and epigenetic alterations that drive or reflect tumour progression. These changes distinguish cancer cells from their normal counterparts, allowing tumours to be recognized as foreign by the immune system. However, tumours are rarely rejected spontaneously, reflecting their ability to maintain an immunosuppressive microenvironment. Programmed death-ligand 1 (PD-L1; also called B7-H1 or CD274), which is expressed on many cancer and immune cells, plays an important part in blocking the 'cancer immunity cycle' by binding programmed death-1 (PD-1) and B7.1 (CD80), both of which are negative regulators of T-lymphocyte activation. Binding of PD-L1 to its receptors suppresses T-cell migration, proliferation and secretion of cytotoxic mediators, and restricts tumour cell killing. The PD-L1-PD-1 axis protects the host from overactive T-effector cells not only in cancer but also during microbial infections. Blocking PD-L1 should therefore enhance anticancer immunity, but little is known about predictive factors of efficacy. This study was designed to evaluate the safety, activity and biomarkers of PD-L1 inhibition using the engineered humanized antibody MPDL3280A. Here we show that across multiple cancer types, responses (as evaluated by Response Evaluation Criteria in Solid Tumours, version 1.1) were observed in patients with tumours expressing high levels of PD-L1, especially when PD-L1 was expressed by tumour-infiltrating immune cells. Furthermore, responses were associated with T-helper type 1 (TH1) gene expression, CTLA4 expression and the absence of fractalkine (CX3CL1) in baseline tumour specimens. Together, these data suggest that MPDL3280A is most effective in patients in which pre-existing immunity is suppressed by PD-L1, and is re-invigorated on antibody treatment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herbst, Roy S -- Soria, Jean-Charles -- Kowanetz, Marcin -- Fine, Gregg D -- Hamid, Omid -- Gordon, Michael S -- Sosman, Jeffery A -- McDermott, David F -- Powderly, John D -- Gettinger, Scott N -- Kohrt, Holbrook E K -- Horn, Leora -- Lawrence, Donald P -- Rost, Sandra -- Leabman, Maya -- Xiao, Yuanyuan -- Mokatrin, Ahmad -- Koeppen, Hartmut -- Hegde, Priti S -- Mellman, Ira -- Chen, Daniel S -- Hodi, F Stephen -- 1R01CA155196/CA/NCI NIH HHS/ -- P30 CA 016359/CA/NCI NIH HHS/ -- P30 CA016359/CA/NCI NIH HHS/ -- R01 CA155196/CA/NCI NIH HHS/ -- England -- Nature. 2014 Nov 27;515(7528):563-7. doi: 10.1038/nature14011.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Yale Comprehensive Cancer Center, Yale School of Medicine, 333 Cedar Street, WWW221, New Haven, Connecticut 06520, USA. ; Gustave Roussy South-Paris University, 114 Rue Edouard Vaillant, 94805 Villefuij, Cedex, France. ; Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA. ; The Angeles Clinic and Research Institute, 11818 Wilshire Blvd, Los Angeles, California 90025, USA. ; Pinnacle Oncology Hematology, 9055 E Del Camino Dr 100, Scottsdale, Arizona 85258, USA. ; Vanderbilt-Ingram Cancer Center, 2220 Pierce Avenue, Nashville, Tennessee 37212, USA. ; Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Shapiro 9, Boston, Massachusetts 02215, USA. ; Carolina BioOncology Institute, 9801 W. Kincey Ave, Suite 145, Huntersville, North Carolina 28078, USA. ; Stanford University, CCSR Bldg Room 1110, Stanford, California 94305, USA. ; Vanderbilt-Ingram Cancer Center, 1301 Medical Center Dr, Suite 1710, Nashville, Tennessee 37212, USA. ; Massachusetts General Hospital, 55 Fruit Street, YAW 9E, Boston, Massachusetts 02114, USA. ; Dana-Farber/Brigham and Women's Cancer Center, 450 Brookline Avenue, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25428504" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Aged ; Aged, 80 and over ; Antibodies, Monoclonal/adverse effects/*therapeutic use ; Antigens, CD274/*antagonists & inhibitors/metabolism ; Biomarkers/blood ; CTLA-4 Antigen/metabolism ; Chemokine CX3CL1/metabolism ; Clinical Protocols ; Disease-Free Survival ; Female ; *Gene Expression Regulation, Neoplastic ; Humans ; *Immunotherapy/adverse effects ; Lymphocytes, Tumor-Infiltrating/immunology ; Male ; Middle Aged ; Neoplasms/diagnosis/*therapy ; Treatment Outcome ; Young Adult
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
    Publikationsdatum: 2014-09-13
    Beschreibung: Cytotoxic T lymphocyte antigen-4 (CTLA-4) is an inhibitory receptor found on immune cells. The consequences of mutations in CTLA4 in humans are unknown. We identified germline heterozygous mutations in CTLA4 in subjects with severe immune dysregulation from four unrelated families. Whereas Ctla4 heterozygous mice have no obvious phenotype, human CTLA4 haploinsufficiency caused dysregulation of FoxP3(+) regulatory T (Treg) cells, hyperactivation of effector T cells, and lymphocytic infiltration of target organs. Patients also exhibited progressive loss of circulating B cells, associated with an increase of predominantly autoreactive CD21(lo) B cells and accumulation of B cells in nonlymphoid organs. Inherited human CTLA4 haploinsufficiency demonstrates a critical quantitative role for CTLA-4 in governing T and B lymphocyte homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4371526/" 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/PMC4371526/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuehn, Hye Sun -- Ouyang, Weiming -- Lo, Bernice -- Deenick, Elissa K -- Niemela, Julie E -- Avery, Danielle T -- Schickel, Jean-Nicolas -- Tran, Dat Q -- Stoddard, Jennifer -- Zhang, Yu -- Frucht, David M -- Dumitriu, Bogdan -- Scheinberg, Phillip -- Folio, Les R -- Frein, Cathleen A -- Price, Susan -- Koh, Christopher -- Heller, Theo -- Seroogy, Christine M -- Huttenlocher, Anna -- Rao, V Koneti -- Su, Helen C -- Kleiner, David -- Notarangelo, Luigi D -- Rampertaap, Yajesh -- Olivier, Kenneth N -- McElwee, Joshua -- Hughes, Jason -- Pittaluga, Stefania -- Oliveira, Joao B -- Meffre, Eric -- Fleisher, Thomas A -- Holland, Steven M -- Lenardo, Michael J -- Tangye, Stuart G -- Uzel, Gulbu -- 5R01HL113304-01/HL/NHLBI NIH HHS/ -- AI061093/AI/NIAID NIH HHS/ -- AI071087/AI/NIAID NIH HHS/ -- AI095848/AI/NIAID NIH HHS/ -- HHSN261200800001E/PHS HHS/ -- P01 AI061093/AI/NIAID NIH HHS/ -- R01 AI071087/AI/NIAID NIH HHS/ -- R01 HL113304/HL/NHLBI NIH HHS/ -- R21 AI095848/AI/NIAID NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 Sep 26;345(6204):1623-7. doi: 10.1126/science.1255904. Epub 2014 Sep 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, MD 20892, USA. tfleishe@cc.nih.gov lenardo@nih.gov guzel@niaid.nih.gov. ; Laboratory of Cell Biology, Division of Monoclonal Antibodies, Office of Biotechnology Products, Center for Drug Evaluation and Research, U.S. Food and Drug Administration, Bethesda, MD 20892, USA. tfleishe@cc.nih.gov lenardo@nih.gov guzel@niaid.nih.gov. ; Molecular Development of the Immune System Section, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. NIAID Clinical Genomics Program, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. tfleishe@cc.nih.gov lenardo@nih.gov guzel@niaid.nih.gov. ; Immunology and Immunodeficiency Group, Immunology Division, Garvan Institute of Medical Research, Sydney, NSW 2010, Australia. St. Vincent's Clinical School Faculty of Medicine, University of New South Wales, Sydney, NSW 2010, Australia. ; Department of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, MD 20892, USA. ; Immunology and Immunodeficiency Group, Immunology Division, Garvan Institute of Medical Research, Sydney, NSW 2010, Australia. ; Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06511, USA. ; Department of Pediatrics, University of Texas Medical School, Houston, TX 77030, USA. ; NIAID Clinical Genomics Program, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. Immunological Diseases Unit, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. ; Laboratory of Cell Biology, Division of Monoclonal Antibodies, Office of Biotechnology Products, Center for Drug Evaluation and Research, U.S. Food and Drug Administration, Bethesda, MD 20892, USA. ; Hematology Branch, National Heart, Lung and Blood Institute, Bethesda, MD 20892, USA. ; Radiology and Imaging and Sciences, Clinical Center, National Institutes of Health, Bethesda, MD 20892, USA. ; Clinical Research Directorate, Clinical Monitoring Research Program, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA. ; Molecular Development of the Immune System Section, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. NIAID Clinical Genomics Program, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. ; Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892, USA. ; Department of Pediatrics, University of Wisconsin, Madison, WI 53706, USA. ; Department of Pediatrics, University of Wisconsin, Madison, WI 53706, USA. Department of Medical Microbiology and Immunology, University of Wisconsin, Madison, WI 53706, USA. ; Laboratory of Pathology, National Cancer Institute, Bethesda, MD 20892, USA. ; Division of Immunology and Manton Center for Orphan Disease Research, Children's Hospital, Harvard Medical School, Boston, MA 10217, USA. ; Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. ; Merck Research Laboratories, Merck & Co., Boston, MA 02130, USA. ; Instituto de Medicina Integral Prof. Fernando Figueira-IMIP, 50070 Recife-PE, Brazil. ; NIAID Clinical Genomics Program, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. ; Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. tfleishe@cc.nih.gov lenardo@nih.gov guzel@niaid.nih.gov.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25213377" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Animals ; B-Lymphocytes/immunology ; CTLA-4 Antigen/*genetics ; Female ; Forkhead Transcription Factors/immunology ; *Germ-Line Mutation ; *Haploinsufficiency ; Humans ; Immune System Diseases/*genetics ; Immunity/*genetics ; Male ; Mice ; Mice, Mutant Strains ; Pedigree ; T-Lymphocytes, Regulatory/immunology ; Young Adult
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
    Publikationsdatum: 2014-07-06
    Beschreibung: In 11 studies, we found that participants typically did not enjoy spending 6 to 15 minutes in a room by themselves with nothing to do but think, that they enjoyed doing mundane external activities much more, and that many preferred to administer electric shocks to themselves instead of being left alone with their thoughts. Most people seem to prefer to be doing something rather than nothing, even if that something is negative.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4330241/" 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/PMC4330241/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, Timothy D -- Reinhard, David A -- Westgate, Erin C -- Gilbert, Daniel T -- Ellerbeck, Nicole -- Hahn, Cheryl -- Brown, Casey L -- Shaked, Adi -- T32 MH020006/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2014 Jul 4;345(6192):75-7. doi: 10.1126/science.1250830.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Virginia, Charlottesville, VA, USA. tdw@virginia.edu. ; Department of Psychology, University of Virginia, Charlottesville, VA, USA. ; Department of Psychology, Harvard University, Cambridge, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24994650" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adolescent ; Adult ; Aged ; Attention ; Electroshock/psychology ; Humans ; Loneliness/*psychology ; Middle Aged ; *Pleasure ; *Thinking ; Young Adult
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
    Publikationsdatum: 2014-05-24
    Beschreibung: Novel vaccines are urgently needed to reduce the burden of severe malaria. Using a differential whole-proteome screening method, we identified Plasmodium falciparum schizont egress antigen-1 (PfSEA-1), a 244-kilodalton parasite antigen expressed in schizont-infected red blood cells (RBCs). Antibodies to PfSEA-1 decreased parasite replication by arresting schizont rupture, and conditional disruption of PfSEA-1 resulted in a profound parasite replication defect. Vaccination of mice with recombinant Plasmodium berghei PbSEA-1 significantly reduced parasitemia and delayed mortality after lethal challenge with the Plasmodium berghei strain ANKA. Tanzanian children with antibodies to recombinant PfSEA-1A (rPfSEA-1A) did not experience severe malaria, and Kenyan adolescents and adults with antibodies to rPfSEA-1A had significantly lower parasite densities than individuals without these antibodies. By blocking schizont egress, PfSEA-1 may synergize with other vaccines targeting hepatocyte and RBC invasion.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4184151/" 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/PMC4184151/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raj, Dipak K -- Nixon, Christian P -- Nixon, Christina E -- Dvorin, Jeffrey D -- DiPetrillo, Christen G -- Pond-Tor, Sunthorn -- Wu, Hai-Wei -- Jolly, Grant -- Pischel, Lauren -- Lu, Ailin -- Michelow, Ian C -- Cheng, Ling -- Conteh, Solomon -- McDonald, Emily A -- Absalon, Sabrina -- Holte, Sarah E -- Friedman, Jennifer F -- Fried, Michal -- Duffy, Patrick E -- Kurtis, Jonathan D -- 1K08AI100997-01A1/AI/NIAID NIH HHS/ -- DP2 AI112219/AI/NIAID NIH HHS/ -- DP2-AI112219/AI/NIAID NIH HHS/ -- K08 AI100997/AI/NIAID NIH HHS/ -- P20GM103421/GM/NIGMS NIH HHS/ -- P30 AI042853/AI/NIAID NIH HHS/ -- P30AI042853/AI/NIAID NIH HHS/ -- R01 AI102907/AI/NIAID NIH HHS/ -- R01-AI076353/AI/NIAID NIH HHS/ -- R01-AI102907/AI/NIAID NIH HHS/ -- R01-AI52059/AI/NIAID NIH HHS/ -- T32-DA013911/DA/NIDA NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 May 23;344(6186):871-7. doi: 10.1126/science.1254417.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for International Health Research, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. ; Division of Infectious Diseases, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115, USA. ; Center for International Health Research, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. Department of Pediatrics, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. ; Department of Pathology and Laboratory Medicine, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02906, USA. ; Laboratory of Malaria Immunology and Vaccinology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20892, USA. ; Fred Hutchinson Cancer Research Center Program in Biostatistics and Biomathematics, Department of Biostatistics and Global Health, University of Washington, Seattle, WA 98109, USA. ; Center for International Health Research, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. Department of Pathology and Laboratory Medicine, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02906, USA. jonathan_kurtis@brown.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24855263" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adolescent ; Adult ; Animals ; Antibodies, Protozoan/blood/*immunology ; Antigens, Protozoan/*immunology ; Child ; Erythrocytes/*parasitology ; Hepatocytes/immunology/parasitology ; Humans ; Immunoglobulin G/blood/immunology ; Kenya ; Malaria/prevention & control ; Malaria Vaccines/*immunology ; Malaria, Falciparum/*prevention & control ; Mice ; Plasmodium berghei/immunology ; Plasmodium falciparum/*growth & development/immunology ; Protozoan Proteins/*immunology ; Recombinant Proteins/immunology ; Schizonts/*growth & development ; Young Adult
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
    Publikationsdatum: 2014-11-28
    Beschreibung: There have been no major advances for the treatment of metastatic urothelial bladder cancer (UBC) in the last 30 years. Chemotherapy is still the standard of care. Patient outcomes, especially for those in whom chemotherapy is not effective or is poorly tolerated, remain poor. One hallmark of UBC is the presence of high rates of somatic mutations. These alterations may enhance the ability of the host immune system to recognize tumour cells as foreign owing to an increased number of antigens. However, these cancers may also elude immune surveillance and eradication through the expression of programmed death-ligand 1 (PD-L1; also called CD274 or B7-H1) in the tumour microenvironment. Therefore, we examined the anti-PD-L1 antibody MPDL3280A, a systemic cancer immunotherapy, for the treatment of metastatic UBC. MPDL3280A is a high-affinity engineered human anti-PD-L1 monoclonal immunoglobulin-G1 antibody that inhibits the interaction of PD-L1 with PD-1 (PDCD1) and B7.1 (CD80). Because PD-L1 is expressed on activated T cells, MPDL3280A was engineered with a modification in the Fc domain that eliminates antibody-dependent cellular cytotoxicity at clinically relevant doses to prevent the depletion of T cells expressing PD-L1. Here we show that MPDL3280A has noteworthy activity in metastatic UBC. Responses were often rapid, with many occurring at the time of the first response assessment (6 weeks) and nearly all were ongoing at the data cutoff. This phase I expansion study, with an adaptive design that allowed for biomarker-positive enriched cohorts, demonstrated that tumours expressing PD-L1-positive tumour-infiltrating immune cells had particularly high response rates. Moreover, owing to the favourable toxicity profile, including a lack of renal toxicity, patients with UBC, who are often older and have a higher incidence of renal impairment, may be better able to tolerate MPDL3280A versus chemotherapy. These results suggest that MPDL3280A may have an important role in treating UBC-the drug received breakthrough designation status by the US Food and Drug Administration (FDA) in June 2014.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Powles, Thomas -- Eder, Joseph Paul -- Fine, Gregg D -- Braiteh, Fadi S -- Loriot, Yohann -- Cruz, Cristina -- Bellmunt, Joaquim -- Burris, Howard A -- Petrylak, Daniel P -- Teng, Siew-leng -- Shen, Xiaodong -- Boyd, Zachary -- Hegde, Priti S -- Chen, Daniel S -- Vogelzang, Nicholas J -- England -- Nature. 2014 Nov 27;515(7528):558-62. doi: 10.1038/nature13904.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Barts Cancer Institute, Queen Mary University of London, Barts Experimental Cancer Medicine Centre, London EC1M 6BQ, UK. ; Yale Cancer Center, 333 Cedar Street, WWW211, New Haven, Connecticut 06520, USA. ; Genentech, Inc. 1 DNA Way, South San Francisco, California 94080, USA. ; Comprehensive Cancer Centers of Nevada, 3730 S. Eastern Avenue, Las Vegas, Nevada 89169, USA. ; Gustave Roussy, 114 Rue Edouard Vaillant, 94805 Villejuif, France. ; Vall d'Hebron Institute of Oncology (VHIO) and Vall d'Hebron University Hospital. Passeig Vall d'Hebron, 119-129, 08035, Barcelona, Spain. ; Bladder Cancer Center, Dana-Farber/Brigham and Women's Cancer Center, Harvard Medical School, 450 Brookline Avenue, Boston, Massachusetts 02215, USA. ; Sarah Cannon Research Institute, 3322 West End Avenue, Suite 900, Nashville, Tennessee 37203, USA. ; University of Nevada School of Medicine and US Oncology/Comprehensive Cancer Centers of Nevada, 3730 S. Eastern Avenue, Las Vegas, Nevada 89169, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25428503" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Aged ; Aged, 80 and over ; Antibodies, Monoclonal/adverse effects/*therapeutic use ; Antigens, CD274/metabolism ; Female ; Humans ; *Immunotherapy ; Male ; Middle Aged ; Treatment Outcome ; Urinary Bladder Neoplasms/*therapy
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
    Publikationsdatum: 2014-04-30
    Beschreibung: The transfer of somatic cell nuclei into oocytes can give rise to pluripotent stem cells that are consistently equivalent to embryonic stem cells, holding promise for autologous cell replacement therapy. Although methods to induce pluripotent stem cells from somatic cells by transcription factors are widely used in basic research, numerous differences between induced pluripotent stem cells and embryonic stem cells have been reported, potentially affecting their clinical use. Because of the therapeutic potential of diploid embryonic stem-cell lines derived from adult cells of diseased human subjects, we have systematically investigated the parameters affecting efficiency of blastocyst development and stem-cell derivation. Here we show that improvements to the oocyte activation protocol, including the use of both kinase and translation inhibitors, and cell culture in the presence of histone deacetylase inhibitors, promote development to the blastocyst stage. Developmental efficiency varied between oocyte donors, and was inversely related to the number of days of hormonal stimulation required for oocyte maturation, whereas the daily dose of gonadotropin or the total number of metaphase II oocytes retrieved did not affect developmental outcome. Because the use of concentrated Sendai virus for cell fusion induced an increase in intracellular calcium concentration, causing premature oocyte activation, we used diluted Sendai virus in calcium-free medium. Using this modified nuclear transfer protocol, we derived diploid pluripotent stem-cell lines from somatic cells of a newborn and, for the first time, an adult, a female with type 1 diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamada, Mitsutoshi -- Johannesson, Bjarki -- Sagi, Ido -- Burnett, Lisa Cole -- Kort, Daniel H -- Prosser, Robert W -- Paull, Daniel -- Nestor, Michael W -- Freeby, Matthew -- Greenberg, Ellen -- Goland, Robin S -- Leibel, Rudolph L -- Solomon, Susan L -- Benvenisty, Nissim -- Sauer, Mark V -- Egli, Dieter -- T32 DK007647/DK/NIDDK NIH HHS/ -- England -- Nature. 2014 Jun 26;510(7506):533-6. doi: 10.1038/nature13287. Epub 2014 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] The New York Stem Cell Foundation Research Institute, New York, New York 10032, USA [2]. ; Stem Cell Unit, Department of Genetics, Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel. ; Naomi Berrie Diabetes Center, Department of Pediatrics, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA. ; 1] Center for Women's Reproductive Care, College of Physicians and Surgeons, Columbia University, New York 10019, USA [2] Department of Obstetrics and Gynecology, College of Physicians and Surgeons, Columbia University, New York 10032, USA. ; The New York Stem Cell Foundation Research Institute, New York, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24776804" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Blastocyst/drug effects ; Cell Fusion ; Cell Nucleus/*genetics ; *Cellular Reprogramming ; Chromosomes, Mammalian/metabolism ; Diabetes Mellitus, Type 1/*genetics/*pathology ; *Diploidy ; Female ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; Infant, Newborn ; Metaphase ; Oocytes/*cytology/metabolism ; Oogenesis ; Pluripotent Stem Cells/*cytology/metabolism/pathology ; Sendai virus ; Spindle Apparatus/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
    Publikationsdatum: 2014-06-05
    Beschreibung: Intracranial germ cell tumours (IGCTs) are a group of rare heterogeneous brain tumours that are clinically and histologically similar to the more common gonadal GCTs. IGCTs show great variation in their geographical and gender distribution, histological composition and treatment outcomes. The incidence of IGCTs is historically five- to eightfold greater in Japan and other East Asian countries than in Western countries, with peak incidence near the time of puberty. About half of the tumours are located in the pineal region. The male-to-female incidence ratio is approximately 3-4:1 overall, but is even higher for tumours located in the pineal region. Owing to the scarcity of tumour specimens available for research, little is currently known about this rare disease. Here we report the analysis of 62 cases by next-generation sequencing, single nucleotide polymorphism array and expression array. We find the KIT/RAS signalling pathway frequently mutated in more than 50% of IGCTs, including novel recurrent somatic mutations in KIT, its downstream mediators KRAS and NRAS, and its negative regulator CBL. Novel somatic alterations in the AKT/mTOR pathway included copy number gains of the AKT1 locus at 14q32.33 in 19% of patients, with corresponding upregulation of AKT1 expression. We identified loss-of-function mutations in BCORL1, a transcriptional co-repressor and tumour suppressor. We report significant enrichment of novel and rare germline variants in JMJD1C, which codes for a histone demethylase and is a coactivator of the androgen receptor, among Japanese IGCT patients. This study establishes a molecular foundation for understanding the biology of IGCTs and suggests potentially promising therapeutic strategies focusing on the inhibition of KIT/RAS activation and the AKT1/mTOR pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4532372/" 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/PMC4532372/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Linghua -- Yamaguchi, Shigeru -- Burstein, Matthew D -- Terashima, Keita -- Chang, Kyle -- Ng, Ho-Keung -- Nakamura, Hideo -- He, Zongxiao -- Doddapaneni, Harshavardhan -- Lewis, Lora -- Wang, Mark -- Suzuki, Tomonari -- Nishikawa, Ryo -- Natsume, Atsushi -- Terasaka, Shunsuke -- Dauser, Robert -- Whitehead, William -- Adekunle, Adesina -- Sun, Jiayi -- Qiao, Yi -- Marth, Gabor -- Muzny, Donna M -- Gibbs, Richard A -- Leal, Suzanne M -- Wheeler, David A -- Lau, Ching C -- 5T15 LM07093-18/LM/NLM NIH HHS/ -- 5T15 LM07093-19/LM/NLM NIH HHS/ -- 5U54HG003273/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- England -- Nature. 2014 Jul 10;511(7508):241-5. doi: 10.1038/nature13296. Epub 2014 Jun 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genome Sequencing Center, Baylor College of Medicine, Houston, Texas 77030, USA. ; Texas Children's Cancer and Hematology Centers, Baylor College of Medicine, Houston, Texas 77030, USA. ; 1] Structural and Computational Biology and Molecular Biophysics Program, Baylor College of Medicine, Houston, Texas 77030, USA [2] Medical Scientist Training Program, Baylor College of Medicine, Houston, Texas 77030, USA. ; 1] Texas Children's Cancer and Hematology Centers, Baylor College of Medicine, Houston, Texas 77030, USA [2] National Center for Child Health and Development, Tokyo, 157-8535, Japan. ; Department of Anatomical and Cellular Pathology, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong. ; Department of Neurosurgery, Kumamoto University, Kumamoto, 860-0862, Japan. ; Center for Statistical Genetics, Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Neurosurgery, Saitama Medical University, Saitama, 350-0495, Japan. ; Department of Neurosurgery, Nagoya University, Nagoya, 466-8550, Japan. ; Department of Neurosurgery, Hokkaido University, Hokkaido Prefecture, 060-0808, Japan. ; Department of Neurosurgery, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Pathology, Baylor College of Medicine, Houston, Texas 77030, USA. ; Medical Scientist Training Program, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Biology, Boston College, Chestnut Hill, Maryland 02467, USA. ; 1] Texas Children's Cancer and Hematology Centers, Baylor College of Medicine, Houston, Texas 77030, USA [2] Medical Scientist Training Program, Baylor College of Medicine, Houston, Texas 77030, USA [3] Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24896186" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Brain Neoplasms/*genetics/pathology ; Child ; Female ; Germ-Line Mutation/*genetics ; Humans ; Japan ; Male ; Mutation/*genetics ; Neoplasms, Germ Cell and Embryonal/*genetics/pathology ; Oncogene Protein v-akt/genetics ; Proto-Oncogene Proteins c-kit/genetics ; Reproducibility of Results ; Signal Transduction/genetics ; TOR Serine-Threonine Kinases/genetics ; Young Adult ; ras Proteins/genetics
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
    Publikationsdatum: 2014-03-08
    Beschreibung: Little is known about how human genetic variation affects the responses to environmental stimuli in the context of complex diseases. Experimental and computational approaches were applied to determine the effects of genetic variation on the induction of pathogen-responsive genes in human dendritic cells. We identified 121 common genetic variants associated in cis with variation in expression responses to Escherichia coli lipopolysaccharide, influenza, or interferon-beta (IFN-beta). We localized and validated causal variants to binding sites of pathogen-activated STAT (signal transducer and activator of transcription) and IRF (IFN-regulatory factor) transcription factors. We also identified a common variant in IRF7 that is associated in trans with type I IFN induction in response to influenza infection. Our results reveal common alleles that explain interindividual variation in pathogen sensing and provide functional annotation for genetic variants that alter susceptibility to inflammatory diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4124741/" 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/PMC4124741/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Mark N -- Ye, Chun -- Villani, Alexandra-Chloe -- Raj, Towfique -- Li, Weibo -- Eisenhaure, Thomas M -- Imboywa, Selina H -- Chipendo, Portia I -- Ran, F Ann -- Slowikowski, Kamil -- Ward, Lucas D -- Raddassi, Khadir -- McCabe, Cristin -- Lee, Michelle H -- Frohlich, Irene Y -- Hafler, David A -- Kellis, Manolis -- Raychaudhuri, Soumya -- Zhang, Feng -- Stranger, Barbara E -- Benoist, Christophe O -- De Jager, Philip L -- Regev, Aviv -- Hacohen, Nir -- DP1 CA174427/CA/NCI NIH HHS/ -- DP1 MH100706/DP/NCCDPHP CDC HHS/ -- DP1 MH100706/MH/NIMH NIH HHS/ -- DP2 OD002230/OD/NIH HHS/ -- F32 AG043267/AG/NIA NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- P50 HG006193/HG/NHGRI NIH HHS/ -- R01 AI091568/AI/NIAID NIH HHS/ -- R01 AR063759/AR/NIAMS NIH HHS/ -- R01 DK097768/DK/NIDDK NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- RC2 GM093080/GM/NIGMS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- T32 HG002295/HG/NHGRI NIH HHS/ -- U19 AI082630/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Mar 7;343(6175):1246980. doi: 10.1126/science.1246980.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Massachusetts Institute of Technology (MIT) and Harvard, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24604203" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Autoimmune Diseases/genetics ; Communicable Diseases/genetics ; Dendritic Cells/drug effects/*immunology ; Escherichia coli ; Female ; *Gene-Environment Interaction ; Genetic Loci ; Genome-Wide Association Study ; HEK293 Cells ; Host-Pathogen Interactions/*genetics ; Humans ; Influenza A virus ; Interferon Regulatory Factor-7/*genetics ; Interferon-beta/pharmacology ; Lipopolysaccharides/immunology ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Quantitative Trait Loci ; STAT Transcription Factors/*genetics ; Transcriptome ; Young Adult
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
    Publikationsdatum: 2014-07-12
    Beschreibung: This paper presents a new data infrastructure for measuring economic activity. The infrastructure records transactions and account balances, yielding measurements with scope and accuracy that have little precedent in economics. The data are drawn from a diverse population that overrepresents males and younger adults but contains large numbers of underrepresented groups. The data infrastructure permits evaluation of a benchmark theory in economics that predicts that individuals should use a combination of cash management, saving, and borrowing to make the timing of income irrelevant for the timing of spending. As in previous studies and in contrast to the predictions of the theory, there is a response of spending to the arrival of anticipated income. The data also show, however, that this apparent excess sensitivity of spending results largely from the coincident timing of regular income and regular spending. The remaining excess sensitivity is concentrated among individuals with less liquidity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gelman, Michael -- Kariv, Shachar -- Shapiro, Matthew D -- Silverman, Dan -- Tadelis, Steven -- P30 AG012839/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2014 Jul 11;345(6193):212-5. doi: 10.1126/science.1247727.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Economics, University of Michigan, Ann Arbor, MI 48109, USA. ; Department of Economics, University of California, Berkeley, Berkeley, CA 94720, USA. ; Department of Economics, University of Michigan, Ann Arbor, MI 48109, USA. National Bureau of Economic Research (NBER), Cambridge, MA 02138, USA. shapiro@umich.edu. ; National Bureau of Economic Research (NBER), Cambridge, MA 02138, USA. Department of Economics, Arizona State University, Tempe, AZ 85287, USA. ; National Bureau of Economic Research (NBER), Cambridge, MA 02138, USA. Haas School of Business, University of California, Berkeley, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25013075" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Administrative Personnel ; Adolescent ; Adult ; Aged ; Female ; *Human Activities ; Humans ; *Income ; Male ; Middle Aged ; Policy Making ; Young Adult
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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