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  • Female  (21)
  • Life Sciences (General)  (14)
  • 2000-2004  (35)
  • 1
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    Premature aging in mice deficient in DNA repair and transcription (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-16
    Description: One of the factors postulated to drive the aging process is the accumulation of DNA damage. Here, we provide strong support for this hypothesis by describing studies of mice with a mutation in XPD, a gene encoding a DNA helicase that functions in both repair and transcription and that is mutated in the human disorder trichothiodystrophy (TTD). TTD mice were found to exhibit many symptoms of premature aging, including osteoporosis and kyphosis, osteosclerosis, early greying, cachexia, infertility, and reduced life-span. TTD mice carrying an additional mutation in XPA, which enhances the DNA repair defect, showed a greatly accelerated aging phenotype, which correlated with an increased cellular sensitivity to oxidative DNA damage. We hypothesize that aging in TTD mice is caused by unrepaired DNA damage that compromises transcription, leading to functional inactivation of critical genes and enhanced apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Boer, Jan -- Andressoo, Jaan Olle -- de Wit, Jan -- Huijmans, Jan -- Beems, Rudolph B -- van Steeg, Harry -- Weeda, Geert -- van der Horst, Gijsbertus T J -- van Leeuwen, Wibeke -- Themmen, Axel P N -- Meradji, Morteza -- Hoeijmakers, Jan H J -- AG 17242-02/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2002 May 17;296(5571):1276-9. Epub 2002 Apr 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Genetics Center, Department of Cell Biology and Genetics, Center for Biomedical Genetics, Erasmus University, 3000 DR Rotterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11950998" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Aging, Premature/*etiology ; Animals ; Apoptosis ; Bone Density ; Cachexia/etiology ; Crosses, Genetic ; *DNA Damage ; DNA Helicases/genetics/*physiology ; *DNA Repair ; DNA-Binding Proteins/genetics/physiology ; Female ; Fertility ; Gene Targeting ; Growth Disorders/etiology/genetics ; Hair Diseases/genetics ; Kyphosis/etiology/genetics/pathology ; Male ; Mice ; Mutation ; Oxidative Stress ; Phenotype ; Point Mutation ; Proteins/genetics/*physiology ; RNA-Binding Proteins/genetics/physiology ; *Transcription Factors ; Transcription, Genetic ; Xeroderma Pigmentosum Group A Protein ; Xeroderma Pigmentosum Group D Protein
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Construction and analysis of a human-chimpanzee comparative clone map (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-01-05
    Description: The recently released human genome sequences provide us with reference data to conduct comparative genomic research on primates, which will be important to understand what genetic information makes us human. Here we present a first-generation human-chimpanzee comparative genome map and its initial analysis. The map was constructed through paired alignment of 77,461 chimpanzee bacterial artificial chromosome end sequences with publicly available human genome sequences. We detected candidate positions, including two clusters on human chromosome 21 that suggest large, nonrandom regions of difference between the two genomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fujiyama, Asao -- Watanabe, Hidemi -- Toyoda, Atsushi -- Taylor, Todd D -- Itoh, Takehiko -- Tsai, Shih-Feng -- Park, Hong-Seog -- Yaspo, Marie-Laure -- Lehrach, Hans -- Chen, Zhu -- Fu, Gang -- Saitou, Naruya -- Osoegawa, Kazutoyo -- de Jong, Pieter J -- Suto, Yumiko -- Hattori, Masahira -- Sakaki, Yoshiyuki -- New York, N.Y. -- Science. 2002 Jan 4;295(5552):131-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉RIKEN Genomic Sciences Center, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. afujiyam@gsc.riken.go.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11778049" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromosomes, Artificial, Bacterial ; Chromosomes, Human, Pair 21/genetics ; Cloning, Molecular ; Contig Mapping ; Female ; Gene Library ; *Genome ; *Genome, Human ; Humans ; Male ; Pan troglodytes/*genetics ; *Physical Chromosome Mapping ; Sequence Alignment ; Sequence Analysis, DNA ; Sequence Tagged Sites ; X Chromosome/genetics ; Y Chromosome/genetics
    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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  • 3
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    Mutations in dynein link motor neuron degeneration to defects in retrograde transport (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: Degenerative disorders of motor neurons include a range of progressive fatal diseases such as amyotrophic lateral sclerosis (ALS), spinal-bulbar muscular atrophy (SBMA), and spinal muscular atrophy (SMA). Although the causative genetic alterations are known for some cases, the molecular basis of many SMA and SBMA-like syndromes and most ALS cases is unknown. Here we show that missense point mutations in the cytoplasmic dynein heavy chain result in progressive motor neuron degeneration in heterozygous mice, and in homozygotes this is accompanied by the formation of Lewy-like inclusion bodies, thus resembling key features of human pathology. These mutations exclusively perturb neuron-specific functions of dynein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hafezparast, Majid -- Klocke, Rainer -- Ruhrberg, Christiana -- Marquardt, Andreas -- Ahmad-Annuar, Azlina -- Bowen, Samantha -- Lalli, Giovanna -- Witherden, Abi S -- Hummerich, Holger -- Nicholson, Sharon -- Morgan, P Jeffrey -- Oozageer, Ravi -- Priestley, John V -- Averill, Sharon -- King, Von R -- Ball, Simon -- Peters, Jo -- Toda, Takashi -- Yamamoto, Ayumu -- Hiraoka, Yasushi -- Augustin, Martin -- Korthaus, Dirk -- Wattler, Sigrid -- Wabnitz, Philipp -- Dickneite, Carmen -- Lampel, Stefan -- Boehme, Florian -- Peraus, Gisela -- Popp, Andreas -- Rudelius, Martina -- Schlegel, Juergen -- Fuchs, Helmut -- Hrabe de Angelis, Martin -- Schiavo, Giampietro -- Shima, David T -- Russ, Andreas P -- Stumm, Gabriele -- Martin, Joanne E -- Fisher, Elizabeth M C -- New York, N.Y. -- Science. 2003 May 2;300(5620):808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Horn Cells/pathology ; Apoptosis ; *Axonal Transport ; Cell Differentiation ; Cell Movement ; Central Nervous System/embryology ; Chromosome Mapping ; Dimerization ; Dyneins/chemistry/*genetics/*physiology ; Female ; Ganglia, Spinal/pathology ; Golgi Apparatus/metabolism/ultrastructure ; Heterozygote ; Homozygote ; Lewy Bodies/pathology ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Motor Neuron Disease/*genetics/pathology/physiopathology ; Motor Neurons/*physiology/ultrastructure ; Mutation ; Mutation, Missense ; *Nerve Degeneration ; Peptide Fragments/metabolism ; Phenotype ; Point Mutation ; Spinal Nerves/growth & development ; Tetanus Toxin/metabolism
    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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  • 4
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    Lamin a truncation in Hutchinson-Gilford progeria (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Sandre-Giovannoli, Annachiara -- Bernard, Rafaelle -- Cau, Pierre -- Navarro, Claire -- Amiel, Jeanne -- Boccaccio, Irene -- Lyonnet, Stanislas -- Stewart, Colin L -- Munnich, Arnold -- Le Merrer, Martine -- Levy, Nicolas -- New York, N.Y. -- Science. 2003 Jun 27;300(5628):2055. Epub 2003 Apr 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Inserm U491: Genetique Medicale et Developpement, Faculte de Medecine Timone, Marseille, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12702809" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Cell Nucleus/ultrastructure ; Child ; Exons ; Female ; Humans ; Lamin Type A/analysis/*chemistry/*genetics ; Lymphocytes/chemistry/ultrastructure ; Mutation ; Polymorphism, Genetic ; Progeria/blood/*genetics ; RNA Splicing ; RNA, Messenger/genetics ; Sequence Deletion ; Transcription, Genetic
    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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  • 5
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    Regulation of cell fate decision of undifferentiated spermatogonia by GDNF (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: The molecular control of self-renewal and differentiation of stem cells has remained enigmatic. Transgenic loss-of-function and overexpression models now show that the dosage of glial cell line-derived neurotrophic factor (GDNF), produced by Sertoli cells, regulates cell fate decisions of undifferentiated spermatogonial cells that include the stem cells for spermatogenesis. Gene-targeted mice with one GDNF-null allele show depletion of stem cell reserves, whereas mice overexpressing GDNF show accumulation of undifferentiated spermatogonia. They are unable to respond properly to differentiation signals and undergo apoptosis upon retinoic acid treatment. Nonmetastatic testicular tumors are regularly formed in older GDNF-overexpressing mice. Thus, GDNF contributes to paracrine regulation of spermatogonial self-renewal and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meng, X -- Lindahl, M -- Hyvonen, M E -- Parvinen, M -- de Rooij, D G -- Hess, M W -- Raatikainen-Ahokas, A -- Sainio, K -- Rauvala, H -- Lakso, M -- Pichel, J G -- Westphal, H -- Saarma, M -- Sariola, H -- New York, N.Y. -- Science. 2000 Feb 25;287(5457):1489-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Programs of Developmental Biology, Molecular Neurobiology, Electron Microscopy Unit, Institute of Biotechnology, Viikki Biocenter, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10688798" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/drug effects ; Cell Cycle ; Cell Differentiation/drug effects ; Cobalt/metabolism ; *Drosophila Proteins ; Female ; Gene Expression ; Gene Targeting ; Glial Cell Line-Derived Neurotrophic Factor ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Male ; Mice ; Mice, Transgenic ; Mitosis ; *Nerve Growth Factors ; Nerve Tissue Proteins/genetics/*physiology ; Proto-Oncogene Proteins/genetics/metabolism ; Proto-Oncogene Proteins c-ret ; Receptor Protein-Tyrosine Kinases/genetics/metabolism ; Sertoli Cells/cytology/physiology ; *Spermatogenesis ; Spermatogonia/*cytology/drug effects ; Stem Cells/*cytology ; Testicular Neoplasms/pathology ; Testis/anatomy & histology ; Vitamin A/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Expectation and dopamine release: mechanism of the placebo effect in Parkinson's disease (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-08-11
    Description: The power of placebos has long been recognized for improving numerous medical conditions such as Parkinson's disease (PD). Little is known, however, about the mechanism underlying the placebo effect. Using the ability of endogenous dopamine to compete for [11C]raclopride binding as measured by positron emission tomography, we provide in vivo evidence for substantial release of endogenous dopamine in the striatum of PD patients in response to placebo. Our findings indicate that the placebo effect in PD is powerful and is mediated through activation of the damaged nigrostriatal dopamine system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de la Fuente-Fernandez, R -- Ruth, T J -- Sossi, V -- Schulzer, M -- Calne, D B -- Stoessl, A J -- New York, N.Y. -- Science. 2001 Aug 10;293(5532):1164-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurodegenerative Disorders Centre, TRIUMF, University of British Columbia, Vancouver, BC, Canada V6T 2B5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11498597" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Antiparkinson Agents/administration & dosage/*therapeutic use ; Apomorphine/administration & dosage/*therapeutic use ; Corpus Striatum/*metabolism/radionuclide imaging ; Dopamine/*metabolism ; Female ; Humans ; Male ; Middle Aged ; Parkinson Disease/*drug therapy/metabolism ; *Placebo Effect ; Placebos/administration & dosage ; Raclopride/metabolism ; Synapses/metabolism ; Tomography, Emission-Computed
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Is face processing species-specific during the first year of life? (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-23
    Description: Between 6 and 10 months of age, the infant's ability to discriminate among native speech sounds improves, whereas the same ability to discriminate among foreign speech sounds decreases. Our study aimed to determine whether this perceptual narrowing is unique to language or might also apply to face processing. We tested discrimination of human and monkey faces by 6-month-olds, 9-month-olds, and adults, using the visual paired-comparison procedure. Only the youngest group showed discrimination between individuals of both species; older infants and adults only showed evidence of discrimination of their own species. These results suggest that the "perceptual narrowing" phenomenon may represent a more general change in neural networks involved in early cognition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pascalis, Olivier -- de Haan, Michelle -- Nelson, Charles A -- New York, N.Y. -- Science. 2002 May 17;296(5571):1321-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, The University of Sheffield, Sheffield S10 2TP, UK. o.pascalis@sheffield.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12016317" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Aging ; Animals ; Evoked Potentials ; *Face ; Female ; Humans ; Infant ; Macaca fascicularis ; Male ; *Pattern Recognition, Visual ; *Recognition (Psychology) ; Species Specificity ; Speech Perception
    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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  • 8
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    The genetic legacy of Paleolithic Homo sapiens sapiens in extant Europeans: a Y chromosome perspective (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-10
    Description: A genetic perspective of human history in Europe was derived from 22 binary markers of the nonrecombining Y chromosome (NRY). Ten lineages account for 〉95% of the 1007 European Y chromosomes studied. Geographic distribution and age estimates of alleles are compatible with two Paleolithic and one Neolithic migratory episode that have contributed to the modern European gene pool. A significant correlation between the NRY haplotype data and principal components based on 95 protein markers was observed, indicating the effectiveness of NRY binary polymorphisms in the characterization of human population composition and history.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Semino, O -- Passarino, G -- Oefner, P J -- Lin, A A -- Arbuzova, S -- Beckman, L E -- De Benedictis, G -- Francalacci, P -- Kouvatsi, A -- Limborska, S -- Marcikiae, M -- Mika, A -- Mika, B -- Primorac, D -- Santachiara-Benerecetti, A S -- Cavalli-Sforza, L L -- Underhill, P A -- GM 28428/GM/NIGMS NIH HHS/ -- GM 55273/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 10;290(5494):1155-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dipartimento di Genetica e Microbiologia, Universita di Pavia, Via Ferrata 1, 27100 Pavia, Italy. semino@ipvgen.univp.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11073453" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Anthropology, Physical ; Climate ; DNA, Mitochondrial/genetics ; Emigration and Immigration ; Europe ; Female ; *Gene Pool ; Genetic Markers ; *Genetics, Population ; History, Ancient ; Humans ; Male ; Middle East ; *Y Chromosome
    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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  • 9
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    Transcriptional regulation of cortical neuron migration by POU domain factors (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-02-23
    Description: The identification of pathways mediated by the kinase Cdk5 and the ligand reelin has provided a conceptual framework for exploring the molecular mechanisms underlying proper lamination of the developing mammalian cerebral cortex. In this report, we identify a component of the regulation of Cdk5-mediated cortical lamination by genetic analysis of the roles of the class III POU domain transcription factors, Brn-1 and Brn-2, expressed during the development of the forebrain and coexpressed in most layer II-V cortical neurons. Brn-1 and Brn-2 appear to critically control the initiation of radial migration, redundantly regulating the cell-autonomous expression of the p35 and p39 regulatory subunits of Cdk5 in migrating cortical neurons, with Brn-1(-/-)/Brn-2(-/-) mice exhibiting cortical inversion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McEvilly, Robert J -- de Diaz, Marcela Ortiz -- Schonemann, Marcus D -- Hooshmand, Farideh -- Rosenfeld, Michael G -- New York, N.Y. -- Science. 2002 Feb 22;295(5559):1528-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department and School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92037-0648, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11859196" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/embryology/metabolism ; Cell Adhesion Molecules, Neuronal/genetics/metabolism ; Cell Line ; Cell Movement ; Cerebral Cortex/cytology/embryology/*metabolism ; Cyclin-Dependent Kinase 5 ; Cyclin-Dependent Kinases/metabolism ; Extracellular Matrix Proteins/genetics/metabolism ; Female ; Gene Targeting ; Hippocampus/cytology/embryology/metabolism ; Homeodomain Proteins ; In Situ Hybridization ; Male ; Mice ; Mutation ; Nerve Tissue Proteins/genetics/metabolism ; Neurons/*physiology ; Neuropeptides/genetics/*physiology ; POU Domain Factors ; Serine Endopeptidases ; Trans-Activators/genetics/*physiology ; Transcription Factors/genetics/*physiology ; *Transcription, Genetic
    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
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    Mother-to-child HIV transmission and ARVs (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Vlas, Sake J -- Nagelkerke, Nico J D -- Jha, Prabhat -- Plummer, Frank A -- New York, N.Y. -- Science. 2002 Dec 13;298(5601):2129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12481779" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-HIV Agents/economics/*therapeutic use ; Child ; Developing Countries ; Drug Costs ; Drug Resistance, Viral ; Female ; HIV/drug effects/physiology ; HIV Infections/drug therapy/prevention & control/*transmission/virology ; Humans ; Infant ; Infant, Newborn ; Infectious Disease Transmission, Vertical/*prevention & control ; Pregnancy ; Pregnancy Complications, Infectious/drug therapy ; Viral Load
    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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