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  • 1
    Publication Date: 1990-03-16
    Description: Major epidemic outbreaks of viral hepatitis in underdeveloped countries result from a type of non-A, non-B hepatitis distinct from the parenterally transmitted form. The viral agent responsible for this form of epidemic, or enterically transmitted non-A, non-B hepatitis (ET-NANBH), has been serially transmitted in cynomolgus macaques (cynos) and has resulted in typical elevation in liver enzymes and the detection of characteristic virus-like particles (VLPs) in both feces and bile. Infectious bile was used for the construction of recombinant complementary DNA libraries. One clone, ET1.1, was exogenous to uninfected human and cyno genomic liver DNA, as well as to genomic DNA from infected cyno liver. ET1.1 did however, hybridize to an approximately 7.6-kilobase RNA species present only in infected cyno liver. The translated nucleic acid sequence of a portion of ET1.1 had a consensus amino acid motif consistent with an RNA-directed RNA polymerase; this enzyme is present in all positive strand RNA viruses. Furthermore, ET1.1 specifically identified similar sequences in complementary DNA prepared from infected human fecal samples collected from five geographically distinct ET-NANBH outbreaks. Therefore, ET1.1 represents a portion of the genome of the principal viral agent, to be named hepatitis E virus, which is responsible for epidemic outbreaks of ET-NANBH.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reyes, G R -- Purdy, M A -- Kim, J P -- Luk, K C -- Young, L M -- Fry, K E -- Bradley, D W -- New York, N.Y. -- Science. 1990 Mar 16;247(4948):1335-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Virology Department, Genelabs Incorporated, Redwood City, CA 94063.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2107574" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Hepatitis E/*microbiology ; Hepatitis Viruses/*genetics ; Hepatitis, Viral, Human/*microbiology ; Humans ; Macaca fascicularis ; Molecular Sequence Data ; Polymerase Chain Reaction ; RNA Viruses/genetics ; RNA, Viral/genetics ; Restriction Mapping
    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
    Publication Date: 2011-06-02
    Description: Members of the gammaretroviruses--such as murine leukemia viruses (MLVs), most notably XMRV [xenotropic murine leukemia virus (X-MLV)-related virus--have been reported to be present in the blood of patients with chronic fatigue syndrome (CFS). We evaluated blood samples from 61 patients with CFS from a single clinical practice, 43 of whom had previously been identified as XMRV-positive. Our analysis included polymerase chain reaction and reverse transcription polymerase chain reaction procedures for detection of viral nucleic acids and assays for detection of infectious virus and virus-specific antibodies. We found no evidence of XMRV or other MLVs in these blood samples. In addition, we found that these gammaretroviruses were strongly (X-MLV) or partially (XMRV) susceptible to inactivation by sera from CFS patients and healthy controls, which suggested that establishment of a successful MLV infection in humans would be unlikely. Consistent with previous reports, we detected MLV sequences in commercial laboratory reagents. Our results indicate that previous evidence linking XMRV and MLVs to CFS is likely attributable to laboratory contamination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knox, Konstance -- Carrigan, Donald -- Simmons, Graham -- Teque, Fernando -- Zhou, Yanchen -- Hackett, John Jr -- Qiu, Xiaoxing -- Luk, Ka-Cheung -- Schochetman, Gerald -- Knox, Allyn -- Kogelnik, Andreas M -- Levy, Jay A -- New York, N.Y. -- Science. 2011 Jul 1;333(6038):94-7. doi: 10.1126/science.1204963. Epub 2011 May 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wisconsin Viral Research Group, Milwaukee, WI 53226, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21628393" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Antibodies, Viral/blood ; Base Sequence ; Blood/*virology ; Child ; Child, Preschool ; Complement System Proteins/immunology ; DNA Contamination ; DNA, Viral/blood ; Drug Contamination ; Fatigue Syndrome, Chronic/blood/immunology/*virology ; Female ; Humans ; Indicators and Reagents ; Leukemia Virus, Murine/genetics/isolation & purification ; Leukocytes, Mononuclear/*virology ; Male ; Middle Aged ; Molecular Sequence Data ; Polymerase Chain Reaction ; Retroviridae Infections/diagnosis/*virology ; Xenotropic murine leukemia virus-related virus/genetics/immunology/*isolation & ; purification ; Young Adult
    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
    Publication Date: 2012-11-20
    Description: Parkinson's disease is characterized by abundant alpha-synuclein (alpha-Syn) neuronal inclusions, known as Lewy bodies and Lewy neurites, and the massive loss of midbrain dopamine neurons. However, a cause-and-effect relationship between Lewy inclusion formation and neurodegeneration remains unclear. Here, we found that in wild-type nontransgenic mice, a single intrastriatal inoculation of synthetic alpha-Syn fibrils led to the cell-to-cell transmission of pathologic alpha-Syn and Parkinson's-like Lewy pathology in anatomically interconnected regions. Lewy pathology accumulation resulted in progressive loss of dopamine neurons in the substantia nigra pars compacta, but not in the adjacent ventral tegmental area, and was accompanied by reduced dopamine levels culminating in motor deficits. This recapitulation of a neurodegenerative cascade thus establishes a mechanistic link between transmission of pathologic alpha-Syn and the cardinal features of Parkinson's disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552321/" 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/PMC3552321/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luk, Kelvin C -- Kehm, Victoria -- Carroll, Jenna -- Zhang, Bin -- O'Brien, Patrick -- Trojanowski, John Q -- Lee, Virginia M-Y -- NS053488/NS/NINDS NIH HHS/ -- P50 NS053488/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 16;338(6109):949-53. doi: 10.1126/science.1227157.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, Institute on Aging and Center for Neurodegenerative Disease Research, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104-4283, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23161999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Corpus Striatum/drug effects/*metabolism/pathology ; Dopamine ; Dopaminergic Neurons/drug effects/metabolism/pathology ; Injections ; Lewy Bodies/drug effects/*metabolism/pathology ; Mice ; Parkinsonian Disorders/*metabolism/pathology ; Protein Folding ; Protein Transport ; Recombinant Proteins/administration & dosage/chemistry/metabolism ; Substantia Nigra/drug effects/metabolism/pathology ; alpha-Synuclein/administration & dosage/chemistry/*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
    Publication Date: 1982-04-02
    Description: The ornithine decarboxylase inhibitor DL-alpha-difluoromethyl ornithine inhibited a proliferation-associated increase in ornithine decarboxylase activity in cultured human promyelocytic leukemia cells, resulting in a marked suppression of cell proliferation and subsequent cell loss. It also inhibited increases in ornithine decarboxylase activity associated with the phorbol ester-induced conversion of promyelocytic HL-60 cells to monocyte-like cells and the retinoic acid-induced conversion to granulocyte-like cells. However, the inhibition of ornithine decarboxylase activity did not prevent cellular differentiation. These results suggest that polyamine biosynthesis has a specific role in cell proliferation rather than in inducing differentiation that is not accompanied by proliferation. The data also demonstrate that cessation of proliferation in HL-60 cells is not necessarily associated with differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luk, G D -- Civin, C I -- Weissman, R M -- Baylin, S B -- AM-27447/AM/NIADDK NIH HHS/ -- CA-18404/CA/NCI NIH HHS/ -- HL-19157/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1982 Apr 2;216(4541):75-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6950518" target="_blank"〉PubMed〈/a〉
    Keywords: Carboxy-Lyases/*physiology ; Cell Adhesion ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Female ; Granulocytes/pathology ; Humans ; Leukemia, Myeloid, Acute/*enzymology/pathology ; Macrophages/pathology ; Ornithine Decarboxylase/*physiology ; Polyamines/biosynthesis ; Tetradecanoylphorbol Acetate/pharmacology ; Tretinoin/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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