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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-01-05
    Description: The assumption that human mitochondrial DNA is inherited from one parent only and therefore does not recombine is questionable. Linkage disequilibrium in human and chimpanzee mitochondrial DNA declines as a function of the distance between sites. This pattern can be attributed to one mechanism only: recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Awadalla, P -- Eyre-Walker, A -- Smith, J M -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2524-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cell, Animal and Population Biology, University of Edinburgh, Edinburgh EH9 1JT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Mitochondrial/*genetics ; Evolution, Molecular ; Fathers ; Female ; Hominidae/*genetics ; Humans ; *Linkage Disequilibrium ; Male ; NADH Dehydrogenase/genetics ; Pan troglodytes/*genetics ; Polymorphism, Restriction Fragment Length ; *Recombination, 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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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-10-13
    Description: It has been suggested that sexual reproduction is maintained because it reduces the load imposed by recurrent deleterious mutations. If rates of deleterious mutation per diploid genome per generation (U) exceed 1, and mutations interact synergistically, then sexuals can overcome their inherent twofold disadvantage. We have tested this hypothesis by estimating genomic point mutation rates for protein-coding genes in a range of animal taxa. We find a positive linear relationship between U and generation time. In species with short generation times, U is predicted to be far below 1, suggesting that sex is not maintained by its capacity to purge the genome of deleterious mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keightley, P D -- Eyre-Walker, A -- New York, N.Y. -- Science. 2000 Oct 13;290(5490):331-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cell, Animal and Population Biology, University of Edinburgh, West Mains Road, Edinburgh EH9 3JT, UK. p.keightley@ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11030650" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Birds/genetics/physiology ; Cats/genetics/physiology ; Cattle/genetics/physiology ; DNA Transposable Elements ; Dogs/genetics/physiology ; Drosophila/genetics/physiology ; Female ; Haplorhini/genetics/physiology ; Humans ; Male ; Mutation ; *Point Mutation ; Proteins/genetics ; Rodentia/genetics/physiology ; *Sex ; Sheep/genetics/physiology
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-08-06
    Description: As we enter the new millennium the world is still facing the challenge of responding to the AIDS pandemic. A new report from the Joint United Nations Programme on HIV/AIDS presents the latest statistics on prevalence, spread, and impact of the disease. In their Perspective, Schwartlander and his colleagues discuss the newly released statistics and the strategies needed to combat the further spread of HIV/AIDS and to reduce prevalence in the most severely affected countries.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwartlander, B -- Garnett, G -- Walker, N -- Anderson, R -- New York, N.Y. -- Science. 2000 Jul 7;289(5476):64-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UNAIDS, 20 Avenue Appia, Geneva 27 CH-1211, Switzerland. schwartlanderb@unaids.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10928930" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/drug therapy/*epidemiology/prevention & ; control/transmission ; Anti-HIV Agents/therapeutic use ; *Disease Outbreaks ; Female ; *Global Health ; HIV Infections/drug therapy/*epidemiology/prevention & control/transmission ; Health Policy ; Humans ; Infectious Disease Transmission, Vertical ; Male ; Population Dynamics ; Prevalence ; Risk-Taking ; Sexual Behavior ; United Nations
    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
    Publication Date: 2001-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwartlander, B -- Stover, J -- Walker, N -- Bollinger, L -- Gutierrez, J P -- McGreevey, W -- Opuni, M -- Forsythe, S -- Kumaranayake, L -- Watts, C -- Bertozzi, S -- New York, N.Y. -- Science. 2001 Jun 29;292(5526):2434-6. Epub 2001 Jun 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joint United Nations Programme on HIV/AIDS (UNAIDS), Geneva, Switzerland. schwartlanderb@unaids.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11423619" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*economics/epidemiology/prevention & ; control/therapy ; Africa South of the Sahara ; Antiretroviral Therapy, Highly Active ; Developed Countries/economics ; Developing Countries/economics ; Female ; Financing, Organized ; *Global Health ; HIV Infections/*economics/epidemiology/prevention & control/therapy ; Health Care Costs ; *Health Expenditures ; *Health Resources ; Health Services/economics ; Humans ; International Cooperation ; Male ; Private Sector ; Public Sector ; United Nations
    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
    Publication Date: 1999-12-22
    Description: Mice lacking estrogen receptors alpha and beta were generated to clarify the roles of each receptor in the physiology of estrogen target tissues. Both sexes of alphabeta estrogen receptor knockout (alphabetaERKO) mutants exhibit normal reproductive tract development but are infertile. Ovaries of adult alphabetaERKO females exhibit follicle transdifferentiation to structures resembling seminiferous tubules of the testis, including Sertoli-like cells and expression of Mullerian inhibiting substance, sulfated glycoprotein-2, and Sox9. Therefore, loss of both receptors leads to an ovarian phenotype that is distinct from that of the individual ERKO mutants, which indicates that both receptors are required for the maintenance of germ and somatic cells in the postnatal ovary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couse, J F -- Hewitt, S C -- Bunch, D O -- Sar, M -- Walker, V R -- Davis, B J -- Korach, K S -- New York, N.Y. -- Science. 1999 Dec 17;286(5448):2328-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Receptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10600740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Mullerian Hormone ; Cell Differentiation ; Clusterin ; *Disorders of Sex Development ; Estradiol/physiology ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Female ; Gene Targeting ; Glycoproteins/analysis ; Growth Inhibitors/analysis ; High Mobility Group Proteins/analysis ; Luteinizing Hormone/blood ; Male ; Mice ; Mice, Knockout ; *Molecular Chaperones ; Ovary/*anatomy & histology/cytology/growth & development/*physiology ; Receptors, Estrogen/genetics/*physiology ; SOX9 Transcription Factor ; Seminiferous Tubules/anatomy & histology/cytology ; Sertoli Cells/cytology ; Signal Transduction ; Testicular Hormones/analysis ; Testis/anatomy & histology/cytology/growth & development/physiology ; Transcription Factors/analysis
    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
    Publication Date: 2004-07-27
    Description: The extent to which large duplications and deletions contribute to human genetic variation and diversity is unknown. Here, we show that large-scale copy number polymorphisms (CNPs) (about 100 kilobases and greater) contribute substantially to genomic variation between normal humans. Representational oligonucleotide microarray analysis of 20 individuals revealed a total of 221 copy number differences representing 76 unique CNPs. On average, individuals differed by 11 CNPs, and the average length of a CNP interval was 465 kilobases. We observed copy number variation of 70 different genes within CNP intervals, including genes involved in neurological function, regulation of cell growth, regulation of metabolism, and several genes known to be associated with disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sebat, Jonathan -- Lakshmi, B -- Troge, Jennifer -- Alexander, Joan -- Young, Janet -- Lundin, Par -- Maner, Susanne -- Massa, Hillary -- Walker, Megan -- Chi, Maoyen -- Navin, Nicholas -- Lucito, Robert -- Healy, John -- Hicks, James -- Ye, Kenny -- Reiner, Andrew -- Gilliam, T Conrad -- Trask, Barbara -- Patterson, Nick -- Zetterberg, Anders -- Wigler, Michael -- 5T32 CA069311/CA/NCI NIH HHS/ -- CA078544/CA/NCI NIH HHS/ -- CA81674/CA/NCI NIH HHS/ -- DC004209/DC/NIDCD NIH HHS/ -- GM057070/GM/NIGMS NIH HHS/ -- HG02606/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2004 Jul 23;305(5683):525-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15273396" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Bacterial Proteins/metabolism ; Cell Line, Transformed ; Chromosome Aberrations ; Chromosome Mapping ; Chromosomes, Human/genetics ; Deoxyribonuclease HindIII/metabolism ; Deoxyribonucleases, Type II Site-Specific/metabolism ; Female ; Gene Deletion ; *Gene Dosage ; Gene Duplication ; Gene Frequency ; *Genetic Variation ; *Genome, Human ; Humans ; Male ; Markov Chains ; Oligonucleotide Array Sequence Analysis ; *Polymorphism, 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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  • 7
    Publication Date: 1996-11-22
    Description: Despite its high prevalence, very little is known regarding genetic predisposition to prostate cancer. A genome-wide scan performed in 66 high-risk prostate cancer families has provided evidence of linkage to the long arm of chromosome 1 (1q24-25). Analysis of an additional set of 25 North American and Swedish families with markers in this region resulted in significant evidence of linkage in the combined set of 91 families. The data provide strong evidence of a major prostate cancer susceptibility locus on chromosome 1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, J R -- Freije, D -- Carpten, J D -- Gronberg, H -- Xu, J -- Isaacs, S D -- Brownstein, M J -- Bova, G S -- Guo, H -- Bujnovszky, P -- Nusskern, D R -- Damber, J E -- Bergh, A -- Emanuelsson, M -- Kallioniemi, O P -- Walker-Daniels, J -- Bailey-Wilson, J E -- Beaty, T H -- Meyers, D A -- Walsh, P C -- Collins, F S -- Trent, J M -- Isaacs, W B -- CA58236/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1371-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Center for Human Genome Research, National Institutes of Health, Bethesda, MD, USA. jtrent@nchgr.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8910276" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; *Chromosome Mapping ; *Chromosomes, Human, Pair 1 ; Dinucleotide Repeats ; *Genes ; Genetic Linkage ; Genetic Markers ; Genetic Predisposition to Disease ; Humans ; Likelihood Functions ; Male ; Middle Aged ; North America ; Oncogenes ; Pedigree ; Prostatic Neoplasms/*genetics ; Risk Factors ; Statistics, Nonparametric ; Sweden
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1982-12-10
    Description: Intracerebroventricular administration of dynorphin produced potent and long-lasting effects on motor function and the electroencephalogram in rats. In addition, local iontophoretic or pressure ejection of dynorphin consistently inhibited hippocampal unit activity. None of these effects were significantly affected by naloxone even at high doses. Moreover, a fragment of dynorphin that failed to displace any of a number of tritiated narcotics from rat brain homogenates produced similar effects on these physiological measures in vivo. On the basis of a variety of criteria for "opiate action," the results suggest that a second biologically active site within the dynorphin sequence is capable of quite potent but nonopiate effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walker, J M -- Moises, H C -- Coy, D H -- Baldrighi, G -- Akil, H -- 1F32DA04183/DA/NIDA NIH HHS/ -- DA02265/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1982 Dec 10;218(4577):1136-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6128791" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Amino Acid Sequence ; Animals ; Dynorphins ; Endorphins/*physiology ; Hippocampus/*physiology ; Male ; Pain/*physiopathology ; Rats ; Structure-Activity Relationship
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1980-12-12
    Description: alpha-Melanocyte-stimulating hormone (alpha-MSH), a modified fragment of adrenocorticotropic hormone, derives from the same biosynthetic route as beta-endorphin and is stored by the same arcuate neurons. Microinjection of alpha-melanocyte-stimulating hormone and several related peptides into the periaqueductal gray matter significantly reduced responsiveness to pain and had a behavioral profile similar to that produced by beta-endorphin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walker, J M -- Akil, H -- Watson, S J -- 1F32DAO5183/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1980 Dec 12;210(4475):1247-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6254152" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/*pharmacology ; Analgesia ; Animals ; Brain/*drug effects ; Cerebral Aqueduct ; Endorphins/*pharmacology ; Male ; Melanocyte-Stimulating Hormones/*pharmacology ; Pain/*physiopathology ; Pituitary Hormones, Anterior/*metabolism ; Pro-Opiomelanocortin ; Protein Precursors/*pharmacology ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 1980-08-08
    Description: Quantitative neurohistological techniques were used to examine the hippocampal complex of laboratory rats maintained on ethanol-containing or control diets for 5 months followed by a 2-month alcohol-free period. Chronic ethanol consumption resulted in a significant loss of hippocampal pyramidal and dentate gyrus granule cells. This study provides direct evidence that long-term ethanol consumption, in the absence of malnutrition, produces neuronal loss in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walker, D W -- Barnes, D E -- Zornetzer, S F -- Hunter, B E -- Kubanis, P -- New York, N.Y. -- Science. 1980 Aug 8;209(4457):711-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7394532" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ethanol/*pharmacology ; Hippocampus/drug effects/*physiology ; Male ; Neurons/drug effects/*physiology ; Pyramidal Tracts/drug effects/physiology ; Rats ; Time Factors
    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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