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  • 1
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    Molecular epidemiology of HIV transmission in a dental practice (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-22
    Description: Human immunodeficiency virus type 1 (HIV-1) transmission from infected patients to health-care workers has been well documented, but transmission from an infected health-care worker to a patient has not been reported. After identification of an acquired immunodeficiency syndrome (AIDS) patient who had no known risk factors for HIV infection but who had undergone an invasive procedure performed by a dentist with AIDS, six other patients of this dentist were found to be HIV-infected. Molecular biologic studies were conducted to complement the epidemiologic investigation. Portions of the HIV proviral envelope gene from each of the seven patients, the dentist, and 35 HIV-infected persons from the local geographic area were amplified by polymerase chain reaction and sequenced. Three separate comparative genetic analyses--genetic distance measurements, phylogenetic tree analysis, and amino acid signature pattern analysis--showed that the viruses from the dentist and five dental patients were closely related. These data, together with the epidemiologic investigation, indicated that these patients became infected with HIV while receiving care from a dentist with AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ou, C Y -- Ciesielski, C A -- Myers, G -- Bandea, C I -- Luo, C C -- Korber, B T -- Mullins, J I -- Schochetman, G -- Berkelman, R L -- Economou, A N -- New York, N.Y. -- Science. 1992 May 22;256(5060):1165-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of HIV/AIDS, Centers for Disease Control, Atlanta, GA 30333.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1589796" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/blood/microbiology/*transmission ; Amino Acid Sequence ; Base Sequence ; DNA, Viral/blood/genetics/isolation & purification ; *Dentistry ; Female ; Florida ; Genetic Variation ; HIV Infections/microbiology/*transmission ; HIV-1/*genetics/isolation & purification ; Humans ; Male ; Molecular Sequence Data ; Monocytes/physiology ; Oligodeoxyribonucleotides ; *Patients ; Phylogeny ; Sequence Homology, Nucleic Acid ; Viral Envelope Proteins/*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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  • 2
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    Mutation of a mutL homolog in hereditary colon cancer (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-18
    Description: Some cases of hereditary nonpolyposis colorectal cancer (HNPCC) are due to alterations in a mutS-related mismatch repair gene. A search of a large database of expressed sequence tags derived from random complementary DNA clones revealed three additional human mismatch repair genes, all related to the bacterial mutL gene. One of these genes (hMLH1) resides on chromosome 3p21, within 1 centimorgan of markers previously linked to cancer susceptibility in HNPCC kindreds. Mutations of hMLH1 that would disrupt the gene product were identified in such kindreds, demonstrating that this gene is responsible for the disease. These results suggest that defects in any of several mismatch repair genes can cause HNPCC.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papadopoulos, N -- Nicolaides, N C -- Wei, Y F -- Ruben, S M -- Carter, K C -- Rosen, C A -- Haseltine, W A -- Fleischmann, R D -- Fraser, C M -- Adams, M D -- CA35494/CA/NCI NIH HHS/ -- CA47527/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1625-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins Oncology Center, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128251" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; *Adenosine Triphosphatases ; Amino Acid Sequence ; Bacterial Proteins/chemistry/*genetics ; Base Sequence ; Carrier Proteins ; Chromosome Mapping ; *Chromosomes, Human, Pair 3 ; Codon ; Colorectal Neoplasms, Hereditary Nonpolyposis/*genetics ; *DNA Repair ; *DNA-Binding Proteins ; *Escherichia coli Proteins ; Female ; Frameshift Mutation ; *Genes ; Genetic Markers ; Humans ; Male ; Molecular Sequence Data ; MutS Homolog 2 Protein ; Mutation ; Neoplasm Proteins/chemistry/*genetics ; Nuclear Proteins ; Open Reading Frames ; Polymerase Chain Reaction ; Proto-Oncogene Proteins/genetics ; Sequence Deletion ; Tumor Cells, Cultured
    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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    Identification of mutations in the COL4A5 collagen gene in Alport syndrome (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-08
    Description: X-linked Alport syndrome is a hereditary glomerulonephritis in which progressive loss of kidney function is often accompanied by progressive loss of hearing. Ultrastructural defects in glomerular basement membranes (GBM) of Alport syndrome patients implicate an altered structural protein as the cause of nephritis. The product of COL4A5, the alpha 5(IV) collagen chain, is a specific component of GBM within the kidney, and the gene maps to the same X chromosomal region as does Alport syndrome. Three structural aberrations were found in COL4A5, in intragenic deletion, a Pst I site variant, and an uncharacterized abnormality, which appear to cause nephritis and deafness, with allele-specific severity, in three Alport syndrome kindreds in Utah.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barker, D F -- Hostikka, S L -- Zhou, J -- Chow, L T -- Oliphant, A R -- Gerken, S C -- Gregory, M C -- Skolnick, M H -- Atkin, C L -- Tryggvason, K -- DK 36200/DK/NIDDK NIH HHS/ -- DK 39497/DK/NIDDK NIH HHS/ -- M01 RR 00064/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 8;248(4960):1224-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Informatics, University of Utah School of Medicine, Salt Lake City 84132.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2349482" target="_blank"〉PubMed〈/a〉
    Keywords: Blotting, Southern ; Cloning, Molecular ; Collagen/*genetics ; DNA/genetics/isolation & purification ; Exons ; Female ; *Genes ; Humans ; Male ; Molecular Weight ; *Mutation ; Nephritis, Hereditary/*genetics ; Pedigree ; Restriction Mapping ; X 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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  • 4
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    Atherosclerosis in transgenic mice overexpressing apolipoprotein A-II (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-23
    Description: Concentrations of plasma high density lipoprotein (HDL) are inversely correlated with atherosclerotic coronary artery disease. The two most abundant protein constituents of HDL are apolipoproteins A-I and A-II (apoA-I and apoA-II). ApoA-I is required for assembly of HDL and, when overexpressed in transgenic mice, confers resistance to early atherosclerosis. The present studies reveal that transgenic mice that overexpress mouse apoA-II had elevated HDL-cholesterol concentrations but, nevertheless, exhibited increased atherosclerotic lesion development as compared to normal mice. The HDL in the transgenic mice was larger and had an increased ratio of apoA-II to apoA-I. Thus, both the composition and amount of HDL appear to be important determinants of atherosclerosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warden, C H -- Hedrick, C C -- Qiao, J H -- Castellani, L W -- Lusis, A J -- HL-07386/HL/NHLBI NIH HHS/ -- HL-28481/HL/NHLBI NIH HHS/ -- HL-42488/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 23;261(5120):469-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8332912" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein A-I/physiology ; Apolipoprotein A-II/genetics/*physiology ; Arteriosclerosis/*blood/genetics ; Cholesterol/blood ; Crosses, Genetic ; Female ; Lipoproteins, HDL/blood/chemistry ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Transgenic
    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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    Multiple representations of pain in human cerebral cortex (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-15
    Description: The representation of pain in the cerebral cortex is less well understood than that of any other sensory system. However, with the use of magnetic resonance imaging and positron emission tomography in humans, it has now been demonstrated that painful heat causes significant activation of the contralateral anterior cingulate, secondary somatosensory, and primary somatosensory cortices. This contrasts with the predominant activation of primary somatosensory cortex caused by vibrotactile stimuli in similar experiments. Furthermore, the unilateral cingulate activation indicates that this forebrain area, thought to regulate emotions, contains an unexpectedly specific representation of pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Talbot, J D -- Marrett, S -- Evans, A C -- Meyer, E -- Bushnell, M C -- Duncan, G H -- New York, N.Y. -- Science. 1991 Mar 15;251(4999):1355-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de neurophysiologie comportementale, Faculte de medecine dentaire, Universite de Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2003220" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Anxiety/physiopathology ; Brain Mapping ; Cerebral Cortex/*physiology ; Functional Laterality ; Hot Temperature ; Humans ; Magnetic Resonance Imaging ; Male ; Pain/*physiopathology ; 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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  • 6
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    Inheritance of proliferative breast disease in breast cancer kindreds (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-21
    Description: Previous studies have emphasized that genetic susceptibility to breast cancer is rare and is expressed primarily as premenopausal breast cancer, bilateral breast cancer, or both. Proliferative breast disease (PBD) is a significant risk factor for the development of breast cancer and appears to be a precursor lesion. PBD and breast cancer were studied in 103 women from 20 kindreds that were selected for the presence of two first degree relatives with breast cancer and in 31 control women. Physical examination, screening mammography, and four-quadrant fine-needle breast aspirates were performed. Cytologic analysis of breast aspirates revealed PBD in 35% of clinically normal female first degree relatives of breast cancer cases and in 13% of controls. Genetic analysis suggests that genetic susceptibility causes both PBD and breast cancer in these kindreds. This study supports the hypothesis that this susceptibility is responsible for a considerable portion of breast cancer, including unilateral and postmenopausal breast cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skolnick, M H -- Cannon-Albright, L A -- Goldgar, D E -- Ward, J H -- Marshall, C J -- Schumann, G B -- Hogle, H -- McWhorter, W P -- Wright, E C -- Tran, T D -- CA-28854/CA/NCI NIH HHS/ -- CA-42014/CA/NCI NIH HHS/ -- CA-48711/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1715-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Utah Regional Cancer Center, University of Utah Medical Center, Salt Lake City 84132.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2270486" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Breast Diseases/*genetics/pathology ; Breast Neoplasms/*genetics/pathology ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Menopause ; Middle Aged ; Pedigree
    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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    Age-associated inclusions in normal and transgenic mouse brain (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jucker, M -- Walker, L C -- Martin, L J -- Kitt, C A -- Kleinman, H K -- Ingram, D K -- Price, D L -- New York, N.Y. -- Science. 1992 Mar 13;255(5050):1443-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1542796" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*metabolism ; Amyloid beta-Peptides/*metabolism ; Animals ; Brain/*metabolism ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic/*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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  • 8
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    Trypsin-sensitive, rapid inactivation of a calcium-activated potassium channel (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-18
    Description: Most calcium-activated potassium channels couple changes in intracellular calcium to membrane excitability by conducting a current with a probability that depends directly on submembrane calcium concentration. In rat adrenal chromaffin cells, however, a large conductance, voltage- and calcium-activated potassium channel (BK) undergoes rapid inactivation, suggesting that this channel has a physiological role different than that of other BK channels. The inactivation of the BK channel, like that of the voltage-gated Shaker B potassium channel, is removed by trypsin digestion and channels are blocked by the Shaker B amino-terminal inactivating domain. Thus, this BK channel shares functional and possibly structural homologies with other inactivating voltage-gated potassium channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Solaro, C R -- Lingle, C J -- New York, N.Y. -- Science. 1992 Sep 18;257(5077):1694-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1529355" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/physiology ; Animals ; Calcium/*pharmacology ; Cattle ; Cell Line ; Cell Membrane/physiology ; Chromaffin System/physiology ; Electric Conductivity ; Ion Channel Gating/drug effects/physiology ; Male ; Membrane Potentials/physiology ; Potassium Channels/*physiology ; Rats ; Rats, Inbred Strains ; Trypsin/*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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  • 9
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    The skeletal muscle chloride channel in dominant and recessive human myotonia (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-07
    Description: Autosomal recessive generalized myotonia (Becker's disease) (GM) and autosomal dominant myotonia congenita (Thomsen's disease) (MC) are characterized by skeletal muscle stiffness that is a result of muscle membrane hyperexcitability. For both diseases, alterations in muscle chloride or sodium currents or both have been observed. A complementary DNA for a human skeletal muscle chloride channel (CLC-1) was cloned, physically localized on chromosome 7, and linked to the T cell receptor beta (TCRB) locus. Tight linkage of these two loci to GM and MC was found in German families. An unusual restriction site in the CLC-1 locus in two GM families identified a mutation associated with that disease, a phenylalanine-to-cysteine substitution in putative transmembrane domain D8. This suggests that different mutations in CLC-1 may cause dominant or recessive myotonia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koch, M C -- Steinmeyer, K -- Lorenz, C -- Ricker, K -- Wolf, F -- Otto, M -- Zoll, B -- Lehmann-Horn, F -- Grzeschik, K H -- Jentsch, T J -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):797-800.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Center for Human Genetics, Marburg University, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1379744" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Southern ; Chloride Channels ; *Chromosomes, Human, Pair 7 ; Cloning, Molecular ; DNA/genetics ; Female ; *Genes, Dominant ; *Genes, Recessive ; Genetic Linkage ; Humans ; Ion Channels/*genetics ; Lod Score ; Male ; Membrane Proteins/*genetics ; Molecular Sequence Data ; Muscular Dystrophies/*genetics ; Myotonia Congenita/*genetics ; Pedigree ; Polymorphism, Restriction Fragment Length ; Receptors, Antigen, T-Cell/genetics ; Recombination, Genetic ; Sequence Homology, Nucleic Acid
    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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    Thalamic abnormalities in schizophrenia visualized through magnetic resonance image averaging (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: Schizophrenia is a complex illness characterized by multiple types of symptoms involving many aspects of cognition and emotion. Most efforts to identify its underlying neural substrates have focused on a strategy that relates a single symptom to a single brain region. An alternative hypothesis, that the variety of symptoms could be explained by a lesion in midline neural circuits mediating attention and information processing, is explored. Magnetic resonance images from patients and controls were transformed with a "bounding box" to produce an "average schizophrenic brain" and an "average normal brain." After image subtraction of the two averages, the areas of difference were displayed as an effect size map. Specific regional abnormalities were observed in the thalamus and adjacent white matter. An abnormality in the thalamus and related circuitry explains the diverse symptoms of schizophrenia parsimoniously because they could all result from a defect in filtering or gating sensory input, which is one of the primary functions of the thalamus in the human brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andreasen, N C -- Arndt, S -- Swayze, V 2nd -- Cizadlo, T -- Flaum, M -- O'Leary, D -- Ehrhardt, J C -- Yuh, W T -- MH31593/MH/NIMH NIH HHS/ -- MH40856/MH/NIMH NIH HHS/ -- MHCRC 43271/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):294-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mental Health Clinical Research Center, College of Medicine.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939669" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/pathology ; Female ; Humans ; Image Processing, Computer-Assisted ; Magnetic Resonance Imaging/*methods ; Male ; Schizophrenia/*pathology ; Software ; Subtraction Technique ; Thalamus/*pathology
    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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