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  • Artikel  (53)
  • Female  (53)
  • American Association for the Advancement of Science (AAAS)  (53)
  • Springer
  • Wiley
  • 2005-2009  (38)
  • 1985-1989  (15)
  • 2005  (38)
  • 1989  (15)
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  • Artikel  (53)
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  • American Association for the Advancement of Science (AAAS)  (53)
  • Springer
  • Wiley
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  • 2005-2009  (38)
  • 1985-1989  (15)
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  • 1
    Publikationsdatum: 2005-10-08
    Beschreibung: Most people hold beliefs about personality characteristics typical of members of their own and others' cultures. These perceptions of national character may be generalizations from personal experience, stereotypes with a "kernel of truth," or inaccurate stereotypes. We obtained national character ratings of 3989 people from 49 cultures and compared them with the average personality scores of culture members assessed by observer ratings and self-reports. National character ratings were reliable but did not converge with assessed traits. Perceptions of national character thus appear to be unfounded stereotypes that may serve the function of maintaining a national identity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2775052/" 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/PMC2775052/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Terracciano, A -- Abdel-Khalek, A M -- Adam, N -- Adamovova, L -- Ahn, C-k -- Ahn, H-n -- Alansari, B M -- Alcalay, L -- Allik, J -- Angleitner, A -- Avia, M D -- Ayearst, L E -- Barbaranelli, C -- Beer, A -- Borg-Cunen, M A -- Bratko, D -- Brunner-Sciarra, M -- Budzinski, L -- Camart, N -- Dahourou, D -- De Fruyt, F -- de Lima, M P -- del Pilar, G E H -- Diener, E -- Falzon, R -- Fernando, K -- Fickova, E -- Fischer, R -- Flores-Mendoza, C -- Ghayur, M A -- Gulgoz, S -- Hagberg, B -- Halberstadt, J -- Halim, M S -- Hrebickova, M -- Humrichouse, J -- Jensen, H H -- Jocic, D D -- Jonsson, F H -- Khoury, B -- Klinkosz, W -- Knezevic, G -- Lauri, M A -- Leibovich, N -- Martin, T A -- Marusic, I -- Mastor, K A -- Matsumoto, D -- McRorie, M -- Meshcheriakov, B -- Mortensen, E L -- Munyae, M -- Nagy, J -- Nakazato, K -- Nansubuga, F -- Oishi, S -- Ojedokun, A O -- Ostendorf, F -- Paulhus, D L -- Pelevin, S -- Petot, J-M -- Podobnik, N -- Porrata, J L -- Pramila, V S -- Prentice, G -- Realo, A -- Reategui, N -- Rolland, J-P -- Rossier, J -- Ruch, W -- Rus, V S -- Sanchez-Bernardos, M L -- Schmidt, V -- Sciculna-Calleja, S -- Sekowski, A -- Shakespeare-Finch, J -- Shimonaka, Y -- Simonetti, F -- Sineshaw, T -- Siuta, J -- Smith, P B -- Trapnell, P D -- Trobst, K K -- Wang, L -- Yik, M -- Zupancic, A -- McCrae, R R -- Z99 AG999999/Intramural NIH HHS/ -- ZIA AG000180-25/Intramural NIH HHS/ -- ZIA AG000180-26/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):96-100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute on Aging, NIH, DHHS, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA. terraccianoa@grc.nia.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210536" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adolescent ; Adult ; *Character ; Cross-Cultural Comparison ; *Culture ; *Ethnic Groups ; Female ; Humans ; Male ; *Personality ; Personality Assessment ; Reproducibility of Results ; Social Perception ; Stereotyping ; Surveys and Questionnaires
    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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  • 2
    Publikationsdatum: 2005-02-19
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, Carol B -- Ride, Sally M -- Fouke, Janie -- Whitney, Telle -- Denton, Denice D -- Cantor, Nancy -- Nelson, Donna J -- Plummer, Jim -- Busch-Vishniac, Ilene -- Meyers, Carolyn -- Rosser, Sue V -- Schiebinger, Londa -- Roberts, Eric -- Burgess, David -- Beeson, Craig -- Metz, Susan Staffin -- Sanders, Lucinda -- Watford, Bevlee A -- Ivey, Elizabeth S -- Frank Fox, Mary -- Wettack, Sheldon -- Klawe, Maria -- Wulf, William A -- Girgus, Joan -- Leboy, Phoebe S -- Babco, Eleanor L -- Shanahan, Betty -- Didion, Catherine -- Chubin, Daryl E -- Frize, Monique -- Ganter, Susan L -- Nalley, E Ann -- Franz, Judy -- Abruna, Hector D -- Strober, Myra H -- Zimmer Daniels, Jane -- Carter, Emily A -- Rhodes, Jean H -- Schrijver, Iris -- Zakian, Virginia A -- Simons, Barbara -- Martin, Ursula -- Boaler, Jo -- Jolluck, Katherine Rose -- Mankekar, Purnima -- Gray, Robert M -- Conkey, Margaret W -- Stansky, Peter -- Xie, Aihua -- Martin, Pino -- Katehi, Linda P B -- Miller, Jo Anne -- Tess Thornton, Amelia -- Lapaugh, Andrea -- Rhode, Deborah L -- Gelpi, Barbara C -- Harrold, Mary Jean -- Spencer, Cherrill M -- Schlatter Ellis, Carla -- Lord, Susan -- Quinn, Helen -- Murnane, Margaret -- Jones, Patricia P -- Hellman, Frances -- Wight, Gail -- O'hara, Ruth -- Pickering, Mary -- Sheppard, Sheri -- Leith, David -- Paytan, Adina -- Sommer, Matthew H -- Shafer, Audrey -- Grusky, David -- Yennello, Sherry -- Madan, Ashima -- Johnson, Denise L -- Yanagisako, Sylvia -- Chou-Green, Jennifer M -- Robinson, Sandra -- New York, N.Y. -- Science. 2005 Feb 18;307(5712):1043.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15718449" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Career Choice ; Female ; Humans ; Male ; *Science ; *Sex Characteristics ; Social Change
    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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  • 3
    Publikationsdatum: 2005-07-05
    Beschreibung: Group B Streptococcus (GBS) is a multiserotype bacterial pathogen representing a major cause of life-threatening infections in newborns. To develop a broadly protective vaccine, we analyzed the genome sequences of eight GBS isolates and cloned and tested 312 surface proteins as vaccines. Four proteins elicited protection in mice, and their combination proved highly protective against a large panel of strains, including all circulating serotypes. Protection also correlated with antigen accessibility on the bacterial surface and with the induction of opsonophagocytic antibodies. Multigenome analysis and screening described here represent a powerful strategy for identifying potential vaccine candidates against highly variable pathogens.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1351092/" 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/PMC1351092/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maione, Domenico -- Margarit, Immaculada -- Rinaudo, Cira D -- Masignani, Vega -- Mora, Marirosa -- Scarselli, Maria -- Tettelin, Herve -- Brettoni, Cecilia -- Iacobini, Emilia T -- Rosini, Roberto -- D'Agostino, Nunzio -- Miorin, Lisa -- Buccato, Scilla -- Mariani, Massimo -- Galli, Giuliano -- Nogarotto, Renzo -- Nardi-Dei, Vincenzo -- Vegni, Filipo -- Fraser, Claire -- Mancuso, Giuseppe -- Teti, Giuseppe -- Madoff, Lawrence C -- Paoletti, Lawrence C -- Rappuoli, Rino -- Kasper, Dennis L -- Telford, John L -- Grandi, Guido -- AI-060603/AI/NIAID NIH HHS/ -- U01 AI060603/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Jul 1;309(5731):148-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chiron srl, Via Fiorentina 1, 53100 Siena, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15994562" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Animals, Newborn ; Antibodies, Bacterial/biosynthesis ; Antigens, Bacterial/genetics/*immunology ; Antigens, Surface/genetics/immunology ; Bacterial Proteins/immunology ; Computational Biology ; Female ; *Genome, Bacterial ; Humans ; Immunity, Maternally-Acquired ; Mice ; Neutrophils/immunology ; Opsonin Proteins ; Phagocytosis ; Serotyping ; Streptococcal Infections/immunology/microbiology/*prevention & control ; Streptococcal Vaccines/*immunology ; Streptococcus agalactiae/classification/*genetics/*immunology ; Vaccination
    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: 2005-03-19
    Beschreibung: Type VII collagen defects cause recessive dystrophic epidermolysis bullosa (RDEB), a blistering skin disorder often accompanied by epidermal cancers. To study the role of collagen VII in these cancers, we examined Ras-driven tumorigenesis in RDEB keratinocytes. Cells devoid of collagen VII did not form tumors in mice, whereas those retaining a specific collagen VII fragment (the amino-terminal noncollagenous domain NC1) were tumorigenic. Forced NC1 expression restored tumorigenicity to collagen VII-null epidermis in a non-cell-autonomous fashion. Fibronectin-like sequences within NC1 (FNC1) promoted tumor cell invasion in a laminin 5-dependent manner and were required for tumorigenesis. Tumor-stroma interactions mediated by collagen VII thus promote neoplasia, and retention of NC1 sequences in a subset of RDEB patients may contribute to their increased susceptibility to squamous cell carcinoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ortiz-Urda, Susana -- Garcia, John -- Green, Cheryl L -- Chen, Lei -- Lin, Qun -- Veitch, Dallas P -- Sakai, Lynn Y -- Lee, Hyangkyu -- Marinkovich, M Peter -- Khavari, Paul A -- AR43799/AR/NIAMS NIH HHS/ -- AR44012/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 18;307(5716):1773-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉VA Palo Alto Healthcare System, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15774758" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adolescent ; Adult ; Animals ; Antibodies/immunology ; Apoptosis ; Carcinoma, Squamous Cell/etiology/*physiopathology ; Cell Adhesion Molecules/immunology/metabolism ; Cell Proliferation ; Cell Transformation, Neoplastic ; Child ; Collagen Type VII/chemistry/*genetics/immunology/*physiology ; Disease Susceptibility ; Epidermolysis Bullosa Dystrophica/complications/*genetics/metabolism/pathology ; Female ; *Genes, ras ; Humans ; I-kappa B Proteins/genetics/metabolism ; Keratinocytes/*metabolism/pathology ; Male ; Mice ; Mice, SCID ; Middle Aged ; Mutation ; Neoplasm Invasiveness ; Protein Structure, Tertiary ; Skin Neoplasms/etiology/pathology/*physiopathology
    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: 2005-11-08
    Beschreibung: Local catabolism of the amino acid tryptophan (Trp) by indoleamine 2,3-dioxygenase (IDO) is considered an important mechanism of regulating T cell immunity. We show that IDO transcription was increased when myelin-specific T cells were stimulated with tolerogenic altered self-peptides. Catabolites of Trp suppressed proliferation of myelin-specific T cells and inhibited production of proinflammatory T helper-1 (T(H)1) cytokines. N-(3,4,-Dimethoxycinnamoyl) anthranilic acid (3,4-DAA), an orally active synthetic derivative of the Trp metabolite anthranilic acid, reversed paralysis in mice with experimental autoimmune encephalomyelitis, a model of multiple sclerosis (MS). Trp catabolites and their derivatives offer a new strategy for treating T(H)1-mediated autoimmune diseases such as MS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Platten, Michael -- Ho, Peggy P -- Youssef, Sawsan -- Fontoura, Paulo -- Garren, Hideki -- Hur, Eun Mi -- Gupta, Rohit -- Lee, Lowen Y -- Kidd, Brian A -- Robinson, William H -- Sobel, Raymond A -- Selley, Michael L -- Steinman, Lawrence -- New York, N.Y. -- Science. 2005 Nov 4;310(5749):850-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, Stanford University, Stanford, CA 94305, USA. michael.platten@uni-tuebingen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16272121" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adoptive Transfer ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/administration & ; dosage/pharmacology/*therapeutic use ; Antigen-Presenting Cells/drug effects/immunology ; Brain/pathology ; Cell Line ; Cytokines/biosynthesis ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/*drug therapy/immunology ; Female ; Histocompatibility Antigens Class II/immunology/metabolism ; Immune Tolerance ; Immunosuppressive Agents/pharmacology/therapeutic use ; Indoleamine-Pyrrole 2,3,-Dioxygenase/genetics/metabolism ; Interferon-gamma/immunology ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Microglia/drug effects/immunology ; Multiple Sclerosis/drug therapy/immunology/pathology ; Myelin Proteins/immunology ; Signal Transduction ; Spinal Cord/pathology ; T-Lymphocytes/immunology ; Th1 Cells/immunology ; Th2 Cells/immunology ; Tryptophan/*metabolism ; ortho-Aminobenzoates/administration & dosage/pharmacology/*therapeutic use
    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: 2005-02-26
    Beschreibung: We identified axonal defects in mouse models of Alzheimer's disease that preceded known disease-related pathology by more than a year; we observed similar axonal defects in the early stages of Alzheimer's disease in humans. Axonal defects consisted of swellings that accumulated abnormal amounts of microtubule-associated and molecular motor proteins, organelles, and vesicles. Impairing axonal transport by reducing the dosage of a kinesin molecular motor protein enhanced the frequency of axonal defects and increased amyloid-beta peptide levels and amyloid deposition. Reductions in microtubule-dependent transport may stimulate proteolytic processing of beta-amyloid precursor protein, resulting in the development of senile plaques and Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokin, Gorazd B -- Lillo, Concepcion -- Falzone, Tomas L -- Brusch, Richard G -- Rockenstein, Edward -- Mount, Stephanie L -- Raman, Rema -- Davies, Peter -- Masliah, Eliezer -- Williams, David S -- Goldstein, Lawrence S B -- EY12598/EY/NEI NIH HHS/ -- EY13408/EY/NEI NIH HHS/ -- P50 AG05131/AG/NIA NIH HHS/ -- R01 EY007042/EY/NEI NIH HHS/ -- R01 EY007042-19/EY/NEI NIH HHS/ -- R01 EY013408/EY/NEI NIH HHS/ -- R01 EY013408-02/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1282-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cellular and Molecular Medicine, School of Medicine, University of California San Diego (UCSD), 9500 Gilman Drive, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15731448" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aged ; Aged, 80 and over ; Alzheimer Disease/genetics/*metabolism/*pathology ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Animals ; *Axonal Transport ; Axons/*pathology/physiology ; Basal Nucleus of Meynert/pathology ; Brain/*metabolism/*pathology ; Cells, Cultured ; Cytoplasmic Vesicles/ultrastructure ; Female ; Hippocampus ; Humans ; Kinesin/metabolism ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/genetics/metabolism ; Neurons/metabolism ; Organelles/ultrastructure ; Plaque, Amyloid/pathology ; Time Factors
    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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  • 7
    Publikationsdatum: 2005-09-24
    Beschreibung: Aneuploidies are common chromosomal defects that result in growth and developmental deficits and high levels of lethality in humans. To gain insight into the biology of aneuploidies, we manipulated mouse embryonic stem cells and generated a trans-species aneuploid mouse line that stably transmits a freely segregating, almost complete human chromosome 21 (Hsa21). This "transchromosomic" mouse line, Tc1, is a model of trisomy 21, which manifests as Down syndrome (DS) in humans, and has phenotypic alterations in behavior, synaptic plasticity, cerebellar neuronal number, heart development, and mandible size that relate to human DS. Transchromosomic mouse lines such as Tc1 may represent useful genetic tools for dissecting other human aneuploidies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1378183/" 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/PMC1378183/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Doherty, Aideen -- Ruf, Sandra -- Mulligan, Claire -- Hildreth, Victoria -- Errington, Mick L -- Cooke, Sam -- Sesay, Abdul -- Modino, Sonie -- Vanes, Lesley -- Hernandez, Diana -- Linehan, Jacqueline M -- Sharpe, Paul T -- Brandner, Sebastian -- Bliss, Timothy V P -- Henderson, Deborah J -- Nizetic, Dean -- Tybulewicz, Victor L J -- Fisher, Elizabeth M C -- 076700/Wellcome Trust/United Kingdom -- MC_U117512674/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2005 Sep 23;309(5743):2033-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16179473" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Aneuploidy ; Animals ; Behavior, Animal ; Brain/pathology ; Cell Count ; Cell Line ; Chimera ; *Chromosomes, Human, Pair 21 ; *Disease Models, Animal ; *Down Syndrome/genetics/physiopathology ; Embryo, Mammalian/cytology ; Facial Bones/pathology ; Female ; Gene Expression ; *Genetic Engineering ; Genetic Markers ; Heart Defects, Congenital/embryology ; Hippocampus/physiopathology ; Humans ; Long-Term Potentiation ; Lymphocyte Activation ; Male ; Maze Learning ; Memory ; Mice ; Mice, Inbred Strains ; *Mice, Transgenic ; Neurons/cytology ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Skull/pathology ; Stem Cells ; Synaptic Transmission ; T-Lymphocytes/immunology
    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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  • 8
    Publikationsdatum: 2005-10-15
    Beschreibung: Tourette's syndrome (TS) is a genetically influenced developmental neuropsychiatric disorder characterized by chronic vocal and motor tics. We studied Slit and Trk-like 1 (SLITRK1) as a candidate gene on chromosome 13q31.1 because of its proximity to a de novo chromosomal inversion in a child with TS. Among 174 unrelated probands, we identified a frameshift mutation and two independent occurrences of the identical variant in the binding site for microRNA hsa-miR-189. These variants were absent from 3600 control chromosomes. SLITRK1 mRNA and hsa-miR-189 showed an overlapping expression pattern in brain regions previously implicated in TS. Wild-type SLITRK1, but not the frameshift mutant, enhanced dendritic growth in primary neuronal cultures. Collectively, these findings support the association of rare SLITRK1 sequence variants with TS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abelson, Jesse F -- Kwan, Kenneth Y -- O'Roak, Brian J -- Baek, Danielle Y -- Stillman, Althea A -- Morgan, Thomas M -- Mathews, Carol A -- Pauls, David L -- Rasin, Mladen-Roko -- Gunel, Murat -- Davis, Nicole R -- Ercan-Sencicek, A Gulhan -- Guez, Danielle H -- Spertus, John A -- Leckman, James F -- Dure, Leon S 4th -- Kurlan, Roger -- Singer, Harvey S -- Gilbert, Donald L -- Farhi, Anita -- Louvi, Angeliki -- Lifton, Richard P -- Sestan, Nenad -- State, Matthew W -- K23 RR16118/RR/NCRR NIH HHS/ -- R01 NS054273/NS/NINDS NIH HHS/ -- R01 NS43520/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):317-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Child Study Center, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16224024" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3' Untranslated Regions ; Adolescent ; Animals ; Attention Deficit Disorder with Hyperactivity/complications/genetics ; Brain/metabolism ; Child ; Child, Preschool ; Chromosome Inversion ; Chromosome Mapping ; *Chromosomes, Human, Pair 13 ; Dna ; DNA Mutational Analysis ; Female ; Frameshift Mutation ; Humans ; In Situ Hybridization, Fluorescence ; Male ; Membrane Proteins/*genetics ; Mice ; *Mutation ; Nerve Tissue Proteins/*genetics ; Pedigree ; Sequence Analysis, DNA ; Tourette Syndrome/complications/*genetics
    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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  • 9
    Publikationsdatum: 1989-10-27
    Beschreibung: Immunization with chemically detoxified pertussis toxin can prevent severe whooping cough with an efficacy similar to that of the cellular pertussis vaccine, which normally gives unwanted side effects. To avoid the reversion to toxicity and the loss of immunogenicity that may follow chemical treatment of pertussis toxin, inactive toxins were constructed by genetic manipulation. A number of genetically engineered alleles of the pertussis toxin genes, constructed by replacing either one or two key amino acids within the enzymatically active S1 subunit, were introduced into the chromosome of strains of Bordetella pertussis, B. parapertussis, and B. bronchiseptica. These strains produce mutant pertussis toxin molecules that are nontoxic and immunogenic and that protect mice from the intracerebral challenge with virulent Bordetella pertussis. Such molecules are ideal for the development of new and safer vaccines against whooping cough.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pizza, M -- Covacci, A -- Bartoloni, A -- Perugini, M -- Nencioni, L -- De Magistris, M T -- Villa, L -- Nucci, D -- Manetti, R -- Bugnoli, M -- New York, N.Y. -- Science. 1989 Oct 27;246(4929):497-500.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sclavo Research Center, Siena, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2683073" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Female ; Genetic Techniques ; Mice ; Mice, Inbred BALB C ; Mutation ; *Pertussis Toxin ; Pertussis Vaccine/*toxicity ; Rabbits ; Vaccines, Synthetic/toxicity ; Virulence Factors, Bordetella/genetics/immunology/*toxicity
    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: 2005-02-01
    Beschreibung: Obesity occurs when energy intake exceeds energy expenditure. Humans expend energy through purposeful exercise and through changes in posture and movement that are associated with the routines of daily life [called nonexercise activity thermogenesis (NEAT)]. To examine NEAT's role in obesity, we recruited 10 lean and 10 mildly obese sedentary volunteers and measured their body postures and movements every half-second for 10 days. Obese individuals were seated, on average, 2 hours longer per day than lean individuals. Posture allocation did not change when the obese individuals lost weight or when lean individuals gained weight, suggesting that it is biologically determined. If obese individuals adopted the NEAT-enhanced behaviors of their lean counterparts, they might expend an additional 350 calories (kcal) per day.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levine, James A -- Lanningham-Foster, Lorraine M -- McCrady, Shelly K -- Krizan, Alisa C -- Olson, Leslie R -- Kane, Paul H -- Jensen, Michael D -- Clark, Matthew M -- DK56650/DK/NIDDK NIH HHS/ -- DK63226/DK/NIDDK NIH HHS/ -- DK66270/DK/NIDDK NIH HHS/ -- M01 RR00585/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2005 Jan 28;307(5709):584-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Endocrine Research Unit, Mayo Clinic, Rochester, MN 55905, USA. Jim@Mayo.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15681386" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Activities of Daily Living ; Adult ; *Body Weight ; Energy Intake ; *Energy Metabolism ; Female ; Humans ; Locomotion ; Male ; Middle Aged ; *Motor Activity ; *Movement ; Obesity/*physiopathology ; Overnutrition ; Pilot Projects ; *Posture ; *Thermogenesis ; Weight Gain ; Weight Loss
    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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