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  • 1
    Publication Date: 1988-04-29
    Description: Screening for human T-lymphotropic virus type I (HTLV-I) antibodies was performed on sera from 39,898 blood donors at eight blood centers in geographically distinct areas of the United States. Ten donors (0.025 percent) showed evidence of HTLV-I seropositivity by enzyme immunoassays; this was confirmed by protein immunoblot and radioimmunoprecipitation. Seroprevalence rates ranged from 0 to 0.10 percent at the locations sampled, with HTLV-I antibodies found predominantly in donors from the southeastern and southwestern United States. Matched case-control interviews and laboratory studies were performed on five seropositive women and two seropositive men who participated in an identity-linked collection of sera from a subset of 33,893 donors at six of the eight blood centers. Four of the women and both men are black; one woman is Caucasian. Four of the seven seropositive individuals admitted to prior intravenous drug abuse or sexual contact with an intravenous drug user. Sexual contact with native inhabitants of an HTLV-I endemic area was the only identified risk factor for one male. The distribution of HTLV-I antibodies in this U.S. blood donor sample corroborates the previously reported epidemiology of this agent and suggests that additional donor screening measures, including the testing of donated blood for HTLV-I markers, may be necessary to prevent the spread of HTLV-I to transfusion recipients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, A E -- Fang, C T -- Slamon, D J -- Poiesz, B J -- Sandler, S G -- Darr, W F 2nd -- Shulman, G -- McGowan, E I -- Douglas, D K -- Bowman, R J -- New York, N.Y. -- Science. 1988 Apr 29;240(4852):643-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉American Red Cross Jerome H. Holland Laboratory, Rockville, MD 20855.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2896386" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antibodies, Viral/*analysis ; *Blood Donors ; Deltaretrovirus/*immunology/isolation & purification ; Deltaretrovirus Infections/diagnosis/*epidemiology/transmission ; Female ; Humans ; Immunoenzyme Techniques ; Immunosorbent Techniques ; Japan ; Male ; Middle Aged ; Risk Factors ; Sexual Partners ; Substance-Related Disorders ; United States
    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: 2014-02-28
    Description: Commitment to and completion of sexual development are essential for malaria parasites (protists of the genus Plasmodium) to be transmitted through mosquitoes. The molecular mechanism(s) responsible for commitment have been hitherto unknown. Here we show that PbAP2-G, a conserved member of the apicomplexan AP2 (ApiAP2) family of DNA-binding proteins, is essential for the commitment of asexually replicating forms to sexual development in Plasmodium berghei, a malaria parasite of rodents. PbAP2-G was identified from mutations in its encoding gene, PBANKA_143750, which account for the loss of sexual development frequently observed in parasites transmitted artificially by blood passage. Systematic gene deletion of conserved ApiAP2 genes in Plasmodium confirmed the role of PbAP2-G and revealed a second ApiAP2 member (PBANKA_103430, here termed PbAP2-G2) that significantly modulates but does not abolish gametocytogenesis, indicating that a cascade of ApiAP2 proteins are involved in commitment to the production and maturation of gametocytes. The data suggest a mechanism of commitment to gametocytogenesis in Plasmodium consistent with a positive feedback loop involving PbAP2-G that could be exploited to prevent the transmission of this pernicious parasite.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4105895/" 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/PMC4105895/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sinha, Abhinav -- Hughes, Katie R -- Modrzynska, Katarzyna K -- Otto, Thomas D -- Pfander, Claudia -- Dickens, Nicholas J -- Religa, Agnieszka A -- Bushell, Ellen -- Graham, Anne L -- Cameron, Rachael -- Kafsack, Bjorn F C -- Williams, April E -- Llinas, Manuel -- Berriman, Matthew -- Billker, Oliver -- Waters, Andrew P -- 083811/Wellcome Trust/United Kingdom -- 083811/Z/07/Z/Wellcome Trust/United Kingdom -- 085349/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- 104111/Wellcome Trust/United Kingdom -- G0501670/Medical Research Council/United Kingdom -- P50 GM071508/GM/NIGMS NIH HHS/ -- P50GM071508/GM/NIGMS NIH HHS/ -- R01 AI076276/AI/NIAID NIH HHS/ -- T32 GM007388/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Mar 13;507(7491):253-7. doi: 10.1038/nature12970. Epub 2014 Feb 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Wellcome Trust Centre for Molecular Parasitology, University of Glasgow, Glasgow G12 8QQ, UK [2]. ; 1] Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK [2]. ; Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK. ; Wellcome Trust Centre for Molecular Parasitology, University of Glasgow, Glasgow G12 8QQ, UK. ; Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544-1014, USA. ; 1] Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544-1014, USA [2] Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08544, USA. ; 1] Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544-1014, USA [2] Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08544, USA [3] Department of Biochemistry and Molecular Biology and Center for Infectious Disease Dynamics, The Pennsylvania State University, State College, Pennsylvania 16802, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24572359" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Culicidae/parasitology ; DNA-Binding Proteins/deficiency/genetics/*metabolism ; Feedback, Physiological ; Female ; Gene Expression Regulation ; Germ Cells/cytology/*growth & development/metabolism ; Malaria/*parasitology ; Male ; Mutation/genetics ; Plasmodium berghei/cytology/*genetics/*physiology ; Protein Transport ; Protozoan Proteins/genetics/*metabolism ; Reproduction, Asexual ; Sexual Development/*genetics ; Transcription, Genetic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2014-02-28
    Description: The life cycles of many parasites involve transitions between disparate host species, requiring these parasites to go through multiple developmental stages adapted to each of these specialized niches. Transmission of malaria parasites (Plasmodium spp.) from humans to the mosquito vector requires differentiation from asexual stages replicating within red blood cells into non-dividing male and female gametocytes. Although gametocytes were first described in 1880, our understanding of the molecular mechanisms involved in commitment to gametocyte formation is extremely limited, and disrupting this critical developmental transition remains a long-standing goal. Here we show that expression levels of the DNA-binding protein PfAP2-G correlate strongly with levels of gametocyte formation. Using independent forward and reverse genetics approaches, we demonstrate that PfAP2-G function is essential for parasite sexual differentiation. By combining genome-wide PfAP2-G cognate motif occurrence with global transcriptional changes resulting from PfAP2-G ablation, we identify early gametocyte genes as probable targets of PfAP2-G and show that their regulation by PfAP2-G is critical for their wild-type level expression. In the asexual blood-stage parasites pfap2-g appears to be among a set of epigenetically silenced loci prone to spontaneous activation. Stochastic activation presents a simple mechanism for a low baseline of gametocyte production. Overall, these findings identify PfAP2-G as a master regulator of sexual-stage development in malaria parasites and mark the first discovery of a transcriptional switch controlling a differentiation decision in protozoan parasites.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4040541/" 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/PMC4040541/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kafsack, Bjorn F C -- Rovira-Graells, Nuria -- Clark, Taane G -- Bancells, Cristina -- Crowley, Valerie M -- Campino, Susana G -- Williams, April E -- Drought, Laura G -- Kwiatkowski, Dominic P -- Baker, David A -- Cortes, Alfred -- Llinas, Manuel -- 090532/Wellcome Trust/United Kingdom -- 090532/Z/09/Z/Wellcome Trust/United Kingdom -- 090770/Wellcome Trust/United Kingdom -- 094752/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- G0600230/Medical Research Council/United Kingdom -- G0600718/Medical Research Council/United Kingdom -- J005398/Medical Research Council/United Kingdom -- P50GM071508/GM/NIGMS NIH HHS/ -- R01 AI076276/AI/NIAID NIH HHS/ -- T32 GM007388/GM/NIGMS NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Mar 13;507(7491):248-52. doi: 10.1038/nature12920. Epub 2014 Feb 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08544, USA [2] Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA (B.F.C.K.); Department of Molecular Biology and Center for Infectious Disease Dynamics, The Pennsylvania State University, State College, Pennsylvania 16802, USA (V.M.C., M.L.). ; 1] Barcelona Centre for International Health Research (CRESIB, Hospital Clinic-Universitat de Barcelona), Barcelona, 08036 Catalonia, Spain [2] Institute for Research in Biomedicine (IRB), Barcelona, 08028 Catalonia, Spain. ; 1] Faculty of Infectious and Tropical Diseases, London School of Hygiene & Tropical Medicine, London WC1E 7HT, UK [2] Faculty of Epidemiology and Population Health, London School of Hygiene & Tropical Medicine, London WC1E 7HT, UK. ; Barcelona Centre for International Health Research (CRESIB, Hospital Clinic-Universitat de Barcelona), Barcelona, 08036 Catalonia, Spain. ; 1] Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08544, USA [2] Institute for Research in Biomedicine (IRB), Barcelona, 08028 Catalonia, Spain [3] Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA (B.F.C.K.); Department of Molecular Biology and Center for Infectious Disease Dynamics, The Pennsylvania State University, State College, Pennsylvania 16802, USA (V.M.C., M.L.). ; Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK. ; Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA. ; Faculty of Infectious and Tropical Diseases, London School of Hygiene & Tropical Medicine, London WC1E 7HT, UK. ; 1] Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK [2] Wellcome Trust Sanger Centre for Human Genetics, Oxford OX3 7BN, UK. ; 1] Barcelona Centre for International Health Research (CRESIB, Hospital Clinic-Universitat de Barcelona), Barcelona, 08036 Catalonia, Spain [2] Institute for Research in Biomedicine (IRB), Barcelona, 08028 Catalonia, Spain [3] Catalan Institution for Research and Advanced Studies (ICREA), Barcelona, 08010 Catalonia, Spain. ; 1] Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08544, USA [2] Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA [3] Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA (B.F.C.K.); Department of Molecular Biology and Center for Infectious Disease Dynamics, The Pennsylvania State University, State College, Pennsylvania 16802, USA (V.M.C., M.L.).〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24572369" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA-Binding Proteins/deficiency/genetics/metabolism ; Female ; Gene Expression Regulation/*genetics ; Gene Silencing ; Genes, Protozoan/genetics ; Genome, Protozoan/genetics ; Germ Cells/cytology/*growth & development/metabolism ; Malaria/*parasitology ; Male ; Parasites/cytology/genetics/*physiology ; Plasmodium falciparum/cytology/*genetics/physiology ; Protozoan Proteins/genetics/metabolism ; Reproduction, Asexual ; Sex Differentiation/genetics ; Sexual Development/*genetics ; Transcription, Genetic/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2013-06-04
    Description: Opinion is divided over whether the fluid responsible for the formation of high sulfidation epithermal deposits is a vapor or a liquid, and whether it is entirely volcanic or of mixed volcanic-meteoric origin. Observations made at Kawah Ijen, an active stratovolcano (mainly andesitic in composition) located in the Ijen Caldera Complex in Java, Indonesia, are used to address these issues. The Kawah Ijen crater is approximately 1 km in diameter, and hosts one of the world’s largest hyperacidic lakes (pH ~0). On the lake edge is a small and actively degassing solfatara field, which is surrounded by a much larger area of acid-sulfate alteration. This area was exposed during a phreatomagmatic eruption in 1817, which excavated the crater to a depth of 250 m, and comprises zones of residual silica, alunite-pyrite, and dickite/kaolinite. Based on the fractionation of 34 S and 32 S between alunite and pyrite, the acid-sulfate alteration occurred at a temperature between 200° and 300°C. High sulfidation epithermal mineralization accompanied the alteration in the form of massive and vein-hosted pyrite that contains up to 192 ppb Au, 9.2 ppm Ag, 6,800 ppm Cu, and 3,430 ppm As; these elements are invisible at the highest resolution of scanning electron microscopy, and thus either occur in the form of nanoparticles or are in solid solution in the pyrite. Condensed fumarolic gases released from the solfatara field and sampled at temperatures between 330° and 495°C contain up to 3 ppm Cu and 3.8 ppm As; the concentrations of Au and Ag are below detection. The pH of the condensed gas (water vapor) is ~–0.5. The above observations support a model in which highly acidic gases condensed ~250 m beneath the floor of the crater. Depending on the fluid/rock ratio, the condensed liquids altered the andesitic host rocks by leaching them to leave behind a residue of "vuggy silica" (high fluid/rock ratio), by replacing the primary minerals with alunite and pyrite (intermediate fluid/rock ratio), or by converting them to dickite/kaolinite (lower fluid/rock ratio). Gold-, silver-, and copper-bearing phases were undersaturated in the condensed liquids. However, they were able to concentrate by adsorbing on the surfaces of the growing pyrite crystals, which developed p-type conductive properties as a result of the uptake of arsenic. The metals were incorporated in the pyrite either by their electrochemical reduction to form native metal nanoparticles or through coupled substitutions with arsenic for iron and sulfur. The results of this study provide compelling evidence that high sulfidation epithermal precious metal mineralization can form directly from condensed magmatic gases.
    Print ISSN: 0361-0128
    Topics: Geosciences
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  • 5
    Publication Date: 2018-03-06
    Description: Immune memory evolved to protect hosts from reinfection, but incomplete responses that allow future reinfection may inadvertently select for more-harmful pathogens. We present empirical and modeling evidence that incomplete immunity promotes the evolution of higher virulence in a natural host-pathogen system. We performed sequential infections of house finches with Mycoplasma gallisepticum strains of various levels of virulence. Virulent bacterial strains generated stronger host protection against reinfection than less virulent strains and thus excluded less virulent strains from infecting previously exposed hosts. In a two-strain model, the resulting fitness advantage selected for an almost twofold increase in pathogen virulence. Thus, the same immune systems that protect hosts from infection can concomitantly drive the evolution of more-harmful pathogens in nature.
    Keywords: Epidemiology, Evolution
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 33 (1961), S. 221-225 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
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  • 7
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 82 (1960), S. 288-289 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
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  • 8
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] IN brucellosis of pregnant cows, the predilection of Brucella abortus for foetal rather than adult tissue is well known1. General pathological findings have indicated an especially heavy infection in the foetal cotyledons (placental tissue), the chorion and the purulent foetal fluids2'3, and we ...
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 222 (1969), S. 893-895 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] We have chosen to study the attachment of tumour cells to the diaphragms of hooded rats. Diaphragms were removed from normal rats and from rats carrying ascites tumour cells (WBPl) (ref. 1). Pieces were mounted on clamp stubs, peritoneum side upward, and either left unwashed or gently washed with ...
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Plant pathology 19 (1970), S. 0 
    ISSN: 1365-3059
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Notes: A measurement of the effect of mildew and leaf blotch on both yield and quality of Lolium multiflorum (cv. Lior) was undertaken in two trials sown in 1966 and 1967.Plots were sprayed with a fungicide at 10-day intervals, and four cuts were taken during the season. Disease assessments were made at the time of cutting. Considerable differences in yield and quality were recorded which could be broadly related to the levels of disease infection in the treatments.
    Type of Medium: Electronic Resource
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