scispace - formally typeset
Search or ask a question

Showing papers by "Stephen J. O'Brien published in 1996"


Journal ArticleDOI
27 Sep 1996-Science
TL;DR: The CKR5Δ32 deletion may act as a recessive restriction gene against HIV-1 infection and may exert a dominant phenotype of delaying progression to AIDS among infected individuals.
Abstract: The chemokine receptor 5 (CKR5) protein serves as a secondary receptor on CD4 + T lymphocytes for certain strains of human immunodeficiency virus-type 1 (HIV-1). The CKR5 structural gene was mapped to human chromosome 3p21, and a 32-base pair deletion allele ( CKR5Δ32 ) was identified that is present at a frequency of ∼0.10 in the Caucasian population of the United States. An examination of 1955 patients included among six well-characterized acquired immunodeficiency syndrome (AIDS) cohort studies revealed that 17 deletion homozygotes occurred exclusively among 612 exposed HIV-1 antibody-negative individuals (2.8 percent) and not at all in 1343 HIV-1-infected individuals. The frequency of CKR5 deletion heterozygotes was significantly elevated in groups of individuals that had survived HIV-1 infection for more than 10 years, and, in some risk groups, twice as frequent as their occurrence in rapid progressors to AIDS. Survival analysis clearly shows that disease progression is slower in CKR5 deletion heterozygotes than in individuals homozygous for the normal CKR5 gene. The CKR5Δ32 deletion may act as a recessive restriction gene against HIV-1 infection and may exert a dominant phenotype of delaying progression to AIDS among infected individuals.

2,586 citations


Journal ArticleDOI
TL;DR: An HLA profile was produced that predicted time from HIV–1 infection to the onset of AIDS and support current theory about control of antigen processing by HLA genes and have implications for immunopathogenesis of HIV-1 and other infections.
Abstract: Major histocompatibility complex (MHC) genes (HLA in humans) regulate the immune response to foreign antigens Molecular and serologic techniques were used to identify products of HLA class I, class II and transporter (TAP) genes (also part of the MHC) in homosexual seroconverters to human immunodeficiency virus type 1 (HIV-1) Comprehensive statistical analysis produced an HLA profile that predicted time from HIV-1 infection to the onset of AIDS The profile was developed in a cohort of 139 men and evaluated in a second unrelated cohort of 102 men In the evaluation cohort, the profile discriminated a sixfold difference between groups with the shortest and longest times to AIDS (P = 0001) These findings support current theory about control of antigen processing by HLA genes and have implications for immunopathogenesis of HIV-1 and other infections

990 citations


Journal ArticleDOI
01 Feb 1996-Nature
TL;DR: The identification of CDV from these lions, and the close phylogenetic relationship between CDV isolates from lions and domestic dogs are reported.
Abstract: Canine distemper virus (CDV) is thought to have caused several fatal epidemics in canids within the Serengeti-Mara ecosystem of East Africa, affecting silver-backed jackals (Canis mesomelas) and bat-eared foxes (Otocyon megalotis) in 1978 (ref. 1), and African wild dogs (Lycaon pictus) in 1991 (refs 2, 3). The large, closely monitored Serengeti lion population was not affected in these epidemics. However, an epidemic caused by a morbillivirus closely related to CDV emerged abruptly in the lion population of the Serengeti National Park, Tanzania, in early 1994, resulting in fatal neurological disease characterized by grand mal seizures and myoclonus; the lions that died had encephalitis and pneumonia. Here we report the identification of CDV from these lions, and the close phylogenetic relationship between CDV isolates from lions and domestic dogs. By August 1994, 85% of the Serengeti lion population had anti-CDV antibodies, and the epidemic spread north to lions in the Maasai Mara National reserve, Kenya, and uncounted hyaenas, bat-eared foxes, and leopards were also affected.

639 citations


Journal ArticleDOI
TL;DR: As the LAR PTPase localizes to the ends of focal adhesions, it is proposed that LAR and the Trio GEF/PSK may orchestrate cell-matrix and cytoskeletal rearrangements necessary for cell migration.
Abstract: rho-like GTP binding proteins play an essential role in regulating cell growth and actin polymerization. These molecular switches are positively regulated by guanine nucleotide exchange factors (GEFs) that promote the exchange of GDP for GTP. Using the interaction-trap assay to identify candidate proteins that bind the cytoplasmic region of the LAR transmembrane protein tyrosine phosphatase (PT-Pase), we isolated a cDNA encoding a 2861-amino acid protein termed Trio that contains three enzyme domains: two functional GEF domains and a protein serine/threonine kinase (PSK) domain. One of the Trio GEF domains (Trio GEF-D1) has rac-specific GEF activity, while the other Trio GEF domain (Trio GEF-D2) has rho-specific activity. The C-terminal PSK domain is adjacent to an Ig-like domain and is most similar to calcium/calmodulin-dependent kinases, such as smooth muscle myosin light chain kinase which similarly contains associated Ig-like domains. Near the N terminus, Trio has four spectrin-like repeats that may play a role in intracellular targeting. Northern blot analysis indicates that Trio has a broad tissue distribution. Trio appears to be phosphorylated only on serine residues, suggesting that Trio is not a LAR substrate, but rather that it forms a complex with LAR. As the LAR PTPase localizes to the ends of focal adhesions, we propose that LAR and the Trio GEF/PSK may orchestrate cell-matrix and cytoskeletal rearrangements necessary for cell migration.

486 citations


Journal ArticleDOI
15 Apr 1996-Genomics
TL;DR: Phylogenetic analysis of mitochondrial gene sequences confirms the recent transfer of the cytoplasmic mtDNA sequences to the domestic cat nucleus and recapitulates evolutionary relationships between mammal species.

258 citations


Journal ArticleDOI
TL;DR: Ten cadaveric shoulders were tested to evaluate the effect of simulated contraction of the long head of the biceps brachii on glenohumeral translation and resulted in statistically significant decreases in humeral head translation.

237 citations


Journal ArticleDOI
TL;DR: With appropriate pulse sequences, unenhanced MR imaging of the shoulder is an accurate technique for the detection and localization of labral injuries.
Abstract: PURPOSE: To prospectively assess the accuracy of unenhanced magnetic resonance (MR) imaging in the detection and localization of labral injuries. MATERIALS AND METHODS: One hundred three patients with clinically suspected shoulder injuries were prospectively examined with unenhanced MR imaging. A combination of gradient-echo and high-resolution fast-spin-echo axial pulse sequences were used. Surgical correlation was obtained in all patients. RESULTS: At surgery, 37 torn anterior, 36 torn superior, and 19 torn posterior labral were identified. The sensitivity for detection of these tears with MR imaging was 100%, 86%, and 74%, respectively; the specificity was 95%, 100%, and 95%, respectively. Overall, unenhanced MR imaging was 95% accurate in the detection of labral injuries. CONCLUSION: With appropriate pulse sequences, unenhanced MR imaging of the shoulder is an accurate technique for the detection and localization of labral injuries.

167 citations


Journal ArticleDOI
01 May 1996-Nature
TL;DR: This Letter neglected to refer to the paper by T. C. Harder et al (Vaccine 13, 521-523; 1995) which reported canine distemper virus P gene sequences from two Serengeti lions that were victims of the same epidemic as those that were the subject of the Letter.
Abstract: Nature 379, 441–445 (1996). IN this Letter, we neglected to refer to the paper by T. C. Harder et al (Vaccine 13, 521-523; 1995) which reported canine distemper virus P gene sequences from two Serengeti lions that were victims of the same epidemic as those that were the subject of our Letter. MJ.G.A. and M.

165 citations


Journal ArticleDOI
TL;DR: In a recent paper as mentioned in this paper, the authors present an overview of the state-of-the-art work in animal genetics, focusing on the use of protein-protein interactions.
Abstract: L. Andersson, Department of Animal Breeding and Genetics, Swedish University of Agricultural Science, Uppsala, Sweden; A. Archibald, Roslin Institute (Edinburgh), Roslin, Midlothian, EH25 9PS, Scotland, UK; M. Ashburner, Department of Genetics, University of Cambridge, Downing Street, Cambridge, CB2 3EH, UK; S. Audun, Department of Morphology, Genetics and Aquatic Biology, Norwegian College of Veterinary Medicine, PO Box 8146 Dept, N-0033 Oslo, Norway; W. Barendse, CSIRO, Division of Tropical Animal Production, Molecular Animal Genetics Centre, University of Queensland, St Lucia, 4072, Australia; J. Bitgood, Poultry Science Department, University of Wisconsin-Madison, 260 Animal Sciences Building, 1675 Observatory Drive, Madison, Wisconsin 53706-1284, USA; C. Bottema, Department of Animal Science, Waite Agricultural Research Institute. University of Adelaide, Glen Osmond, 5064, Australia; T. Broad, AgResearch, Invermay Agricultural Centre, Mosgiel, New Zealand; S. Brown, Department of Biochemistry and Molecular Genetics, St Mary's Hospital Medical School, Norfolk Place, London W2 1PG UK; D. Burt, Division of Molecular Biology, Roslin Institute, Midlothian, UK; C. Charlier, Department of Genetics, Faculty of Medicine, Veterinary, B43, B de Colonster, 20, 4000 Liege, Belgium; N. Copeland, ABL-Basic Research Program, NCI-Frederick Cancer Research & Development Center, Frederick, MD 21702, USA; S. Davis, Department of Animal Science, Texas A&M University, College Station, Texas 77843-2471, USA; M. Davisson, The Jackson Laboratory, 600 Main Street, Bar Harbor, Maine 04609 USA; J. Edwards, Department of Biochemistry, Oxford, UK; A. Eggen, ABS Global, Inc, 6908 River Road, DeForest, Wisconsin 53532, USA; G. Elgar, Molecular Genetics, Department of Medicine, Addenbrookes Hospital, Hills Road, Cambridge CB2 2QQ, UK; J.T. Eppig, The Jackson Laboratory, 600 Main Street, Bar Harbor, Maine 04609, USA; I. Franklin, CSIRO, Division of Animal Production, Locked Bag 1, Delivery Centre, Blacktown, 2148, Australia; P. Grewe, CSIRO Fisheries, GPO Box 1538, Hobart 7001, Australia; T. Gill III, S-705 Scaife Hall, Department of Pathology/University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA; J.A.M. Graves, School of Genetics and Human Variation, LaTrobe University, Bundoora 3083, Australia; R. Hawken, Centre for Animal Biotechnology, The School of Veterinary Sciences, The University of Melbourne 3052, Australia; J. Hetzel, CSIRO, Division of Tropical Animal Production, Molecular Animal Genetics Centre, University of Queensland, St Lucia 4072, Australia; A. Hilyard, The Jackson Laboratory, 600 Main Street, Bar Harbor, Maine 04609-1500 USA; H. Jacob, Massachusetts General Hospital-East, Cardiovascular Research Center, 149 13th Street, Charlestown, Massachusetts 92129 USA; L. Jaswinska, Queensland Institute of Medical Research, Bancroft Centre, Royal Brisbane Hospital, Lutwyche Road, Herston, Queensland, Australia; N. Jenkins, ABL-Basic Research Program, NCI Frederick Cancer Research & Development Center, Frederick, Maryland 21702 USA; H. Kunz, University of Pittsburgh, School of Medicine, Department of Pathology, Pittsburgh, Pennsylvania 15261, USA; G. Levan, Department of Genetics, Medicinaregatan 9C $41390 Goteborg, Sweden; O. Lie, Norwegian College of Veterinary Medicine, Department of Morphology, Genetics and Aquatic Biology, Division of Genetics, PO Box 8176, Dep, N-0033, Norway; L. Lyons, National Cancer Institute, LVC-FCRDC, Building 560, Frederick, Maryland 21702-1201 USA; P. Maccarone, Department of Genetics & Human Variation, School of Biological Sciences, LaTrobe University, Bundoora 3083, Australia; C. Mellersh, Clinical Division M-318, Fred Hutchinson Cancer Research Center, 1124 Columbia Street, Seattle, Washington 98104, USA; G. Montgomery, AgResearch Molecular Biology Unit, Department of Biochemistry, University of Ontago, PO Box 56, Dunedin, New Zealand; S. Moore, CSIRO, Division of Tropical Animal Production, Molecular Animal Genetics Centre, University of Queensland, St Lucia 4072, Australia; C. Moran, Department of Animal Science, University of Sydney 2006, Australia; D. Morizot, University of Texas, M.D. Anderson Cancer Center, Science Park, Research Division, Smithville, Texas 78957, USA; M. Neff, Department of Molecular and Cellular Biology, University of California, Berkeley, California 94720, USA; F. Nicholas, Department of Animal Science, University of Sydney 2006, Australia; S. O'Brien, Laboratory of Viral Carcinogenesis, National Cancer Institute, Building 560, Frederick, Maryland 21702-1201, USA; Y. Parsons, School of Biological Sciences, Macquarie University 2109, Australia; J. Peters, Mammalian Genetics Unit, Medical Research Council, Harwell, Didcot, Oxon OX11 ORD, UK; J. Postlethwait, Institute of Neuroscience, 1254 University of Oregon, Eugene, Oregon 97403-1254, USA; M. Raymond, Genetics Section, Laboratory of Viral Carcinogenests, National Cancer Institute-FCRDC, Frederick, Maryland 21702-1201, USA; M. Rothschild, Department of Animal Sciences, Iowa State University, 225 Kildee Hall, Ames, Iowa 50011, USA; L. Schook, Department of Veterinary PathoBiology, University of Minnesota, 295 Animal Science/Veterinary Medical Building 1988 Fitch Avenue, St Paul, Minnesota 55108, USA; Y. Sugimoto, Shirakawa Institute of Animal Genetics, Odakura, Nishigo, Nishi-shirakawa, Fukushima 961, Japan; C. Szpirer, Department de Biologie Moleculaire, Universite Libre de Bruxelles, Rue des Chevaux 67, B-1640 Rhode-St-Genese, Belgium; M. Tate, Sheep Genomics, AgResearch Invermay Agricultural Centre, Private Bag 50034, Mosgiel, New Zealand; J. Taylor, Department of Animal Science, Texas A&M University, College Station, Texas 77843-2471, USA; J. VandeBerg, Southwest Foundation for Biomedical Research, PO Box 760549, San Antonio, Texas 78245, USA; M. Wakefield, School of Genetics & Human Variation, LaTrobe University, Bundoora 3083, Australia; J. Wienberg, Department of Pathology, Cambridge University, Tennis Court Road, Cambridge CB2 1 QP, UK; J. Womack, Department of Veterinary Pathobiology, Texas A&M University, College Station, Texas 77843, USA.

141 citations


Journal ArticleDOI
TL;DR: Observations indicate that, although the pathological potential of these viral infections seemed not to be very high in free-ranging lions, relocation of seropositive animals by humans to seronegative lion populations must be considered very carefully.
Abstract: While viral infections and their impact are well studied in domestic cats, only limited information is available on their occurrence in free-ranging lions. The goals of the present study were (i) to investigate the prevalence of antibodies to feline calicivirus (FCV), herpesvirus (FHV), coronavirus (FCoV), parvovirus (FPV), and immunodeficiency virus (FIV) and of feline leukemia virus (FeLV) antigen in 311 serum samples collected between 1984 and 1991 from lions inhabiting Tanzania's national parks and (ii) to evaluate the possible biological importance and the interrelationship of these viral infections. Antibodies to FCV, never reported previously in free-ranging lions, were detected in 70% of the sera. In addition, a much higher prevalence of antibodies to FCoV (57%) was found than was previously reported in Etosha National Park and Kruger National Park. Titers ranged from 25 to 400. FeLV antigen was not detectable in any of the serum samples. FCoV, FCV, FHV, and FIV were endemic in the Serengeti, while a transient elevation of FPV titers pointed to an outbreak of FPV infection between 1985 and 1987. Antibody titers to FPV and FCV were highly prevalent in the Serengeti (FPV, 75%; FCV, 67%) but not in Ngorongoro Crater (FPV, 27%; FCV, 2%). These differences could be explained by the different habitats and biological histories of the two populations and by the well-documented absence of immigration of lions from the Serengeti plains into Ngorongoro Crater after 1965. These observations indicate that, although the pathological potential of these viral infections seemed not to be very high in free-ranging lions, relocation of seropositive animals by humans to seronegative lion populations must be considered very carefully.

133 citations



Journal ArticleDOI
TL;DR: The incorporation of precise definitions for taxonomic units into wildlife legislation has necessitated the reevaluation of the taxonomy of endangered and threatened species, and it is recommended that subspecific leopard taxonomy be revised to comprise eight subspecies.
Abstract: The incorporation of precise definitions for taxonomic units into wildlife legislation has necessitated the reevaluation of the taxonomy of endangered and threatened species. We used the subspecies recognition criteria proposed by Avise and Ball (1990) and O’Brien and Mayr (1991) to examine the infraspecific taxonomy of the leopard, Panthera pardus, a geographically widespread species with 27 currently recognized trinomial designations. Samples from named subspecies revealed appreciable genetic diversity using three molecular methods: allozymes, mitochondrial DNA restriction sites, and feline-specific minisatellites. Continental populations and subspecies from Africa and Asia possessed the highest amount of molecular genetic variation, whereas relatively lower amounts of diversity were present in island populations. Molecular data were analyzed using three phylogenetic methods (distance-matrix, maximum parsimony, and maximum likelihood) to resolve genetic differentiation below the species level The combined results revealed phylogenetic distinction of six geographically isolated groups of leopards: (1) African, (2) central Asian, (3) Indian, (4) Sri Lankan, (5) Javan, and (6) east Asian. Based on the combined molecular analyses and supporting morphological data (Miththapala 1992), u,e recommend that subspecific leopard taxonomy be revised to comprise eight subspecies: (1) P. p. pardus, Africa; (2) P. p. saxicolor, central Asia; (3) P. p. fusca, Indian subcontinent; (4) P. p. kotiya, Sri Lanka; (5) P. p. melas, Java; (6) P. p. orientalis, Amur; (7) P. p. japonensis, northern China; and (8) P. p. delacouri, southern China. In most cases, designated subspecies conform to historic geological barriers that would have facilitated allopatric genetic divergence. La incorporacion de definiciones precisas para unidades taxonomicas en legislacion de la vida silvestre ha necesitado de la re-evaluacion de la taxonomia de especies amenazadas y en peligo de extincion. Utilizamos los criterios de reconocimiento de subespecies propuestos por Avise y Ball (1990) y O’Brien y Mayr (1991) para examinar la taxonomia intraespecifica del leopardo Panthera pardus, una especie ampliamente dispersa con 27 designaciones trinomiales reconocidas. Muestras de supuestas subespecies revelaron una diversidad genetica apreciable, usando tres metodos moleculares: Alozimas, sitios de restriccion en ADN mitocondrial y minisatelites felino-especificos: Poblaciones continentales y subespecies de Africa y Asia poseen la mas alta cantidad de variacion genetica molecular, mientras que en poblaciones insulares estuvieron presentes cantidades relativamente bajas de diversidad. Los datos moleculares fueron analizados utilizando tres metodos filogeneticos (Matriz de distancia, maxima parsimonia y maxima proximidad) para resolver diferenciaciones geneticas por debajo del nivel de especie. Los resultados combinados revelaron la distincion filo-genetica de seis grupos de leopardos geograficamente aislados: 1) Africano, 2) Centro asiatico, 3) Hindu, 4) Sri Lankano, 5) Javano y, 6) Este asiatico. Basados en el analisis molecular combinado y soportados en datos morfologicos (Miththapala, 1992), recomendamos la revision taxonomica a nivel de subespecie que comprende ocho subespecies: 1) P. p. pardus, Africa; 2) P. p. saxicolor, Asia central; 3) P. p. fusca, subcontinente Hindu; 4) P. p. kotiya, Sri Lanka; 5) P. p. melas, Java; 6) P. p. orientalis, Amur; 7) P. p. japonensis, norte Chino; 8) P. p. delacouri, sur Chino. En la mayoria de los casos las subespecies designadas estan conformadas por barreras geologicas historicas que pudieron haber facilitado divergencia genetica alopatrica.

Journal ArticleDOI
TL;DR: Target cell-induced NK cell degranulation results in translocation of GMP-17 from granules to the plasma membrane, suggesting a possible role for GMP -17 in regulating the effector function of lymphocytes and neutrophils.
Abstract: Cytotoxic lymphocytes are characterized by their inclusion of cytoplasmic granules that fuse with the plasma membrane following target cell recognition. We previously identified a cytotoxic granule membrane protein designated p15-TIA-1 that is immunochemically related to an RNA-recognition motif (RRM)-type RNA-binding protein designated p40-TIA-1. Although it was suggested that p15-TIA-1 might be derived from p40-T1A-1 by proteolysis, N-terminal amino acid sequencing of p15-TIA-1 immunoaffinity purified from a natural killer (NK) cell line by using monoclonal antibody (mAb) 2G9 revealed that p15-T1A-1 is identical to the deduced amino acid sequence of NKG7 and GIG-1, cDNAs isolated from NK cells and granulocyte-colony-stimulating factor-treated mononuclear cells, respectively. Epitope mapping revealed that mAb 2G9 recognizes the C terminus of p15-T1A-1 and p40-T1A-1. The deduced amino acid sequence of p15-T1A-1/NKG7/GIG-1 predicts that the protein possesses four transmembrane domains, and immuno-electron microscopy localizes the endogenous protein to the membranes of cytotoxic granules in NK cells. Given its subcellular localization, we propose to rename-this protein GMP-17, for granule membrane protein of 17 kDa. Immunofluorescence microscopy of freshly isolated NK cells confirms this granular localization. Target cell-induced NK cell degranulation results in translocation of GMP-17 from granules to the plasma membrane, suggesting a possible role for GMP-17 in regulating the effector function of lymphocytes and neutrophils.

Journal ArticleDOI
TL;DR: The results are consistent with the view that the genetic differentiation between Sumatran and Bornean orang-utans has reached the level of distinct species, and indicate that there is not a genetic imperative for the separate management of geographically isolated Borneo populations.

Journal ArticleDOI
TL;DR: Molecular characterization of murine TIA-1 and TIAR RNA binding proteins provides the basis for a genetic analysis of the functional roles of these proteins during mammalian development.
Abstract: TIA-1 and TIAR are RNA binding proteins of the RNA recognition motif (RRM)/ribonucleoprotein (RNP) family that have been implicated as effectors of apoptotic cell death. We report the structures of murine TIA-1 and TIAR (mTIA-1 and mTIAR) deduced from cDNA cloning, the mRNA and protein tissue distribution of mTIA-1 and mTIAR, and the exon-intron structures of the mTIA-1 and mTIAR genes. Both mTIA-1 and mTIAR are comprised of three approximately 100 amino acid N-terminal RRM domains and a approximately 90 amino acid C-terminal auxiliary domain. This subfamily of RRM proteins is evolutionarily well conserved; mTIA-1 and mTIAR are 80% similar to each other, and 96 and 99% similar to hTIA-1 and hTIAR, respectively. The overall exon-intron structures of the mTIA-1 and mTIAR genes are also similar to each other, as well as to the human TIA-1 gene structure. While Northern blot analysis reveals that mTIA-1 and mTIAR mRNAs have a broad tissue distribution, mTIA-1 and mTIAR proteins are predominantly expressed in brain, testis and spleen. At least two isoforms of both mTIA-1 and mTIAR are generated by alternative splicing. Murine TIA-1 isoforms including or lacking the exon 5 encoded sequences are expressed at a ratio of approximately 1:1, whereas mTIAR isoforms including or lacking the 5'-end of exon 3 sequences are expressed in a approximately 1:6 ratio. Molecular characterization of murine TIA-1 and TIAR RNA binding proteins provides the basis for a genetic analysis of the functional roles of these proteins during mammalian development.

Journal ArticleDOI
TL;DR: Large sequence divergence among isolates, nearly complete species monophyly, and widespread geographic distribution suggest that FIV-Pco has evolved within the puma species for a long period.
Abstract: Feline immunodeficiency virus (FIV) is a lentivirus which causes an AIDS-like disease in domestic cats (Felis catus). A number of other felid species, including the puma (Puma concolor), carry a virus closely related to domestic cat FIV. Serological testing revealed the presence of antibodies to FIV in 22% of 434 samples from throughout the geographic range of the puma. FIV-Pco pol gene sequences isolated from pumas revealed extensive sequence diversity, greater than has been documented in the domestic cat. The puma sequences formed two highly divergent groups, analogous to the clades which have been defined for domestic cat and lion (Panthera leo) FIV. The puma clade A was made up of samples from Florida and California, whereas clade B consisted of samples from other parts of North America, Central America, and Brazil. The difference between these two groups was as great as that reported among three lion FIV clades. Within puma clades, sequence variation is large, comparable to between-clade differences seen for domestic cat clades, allowing recognition of 15 phylogenetic lineages (subclades) among puma FIV-Pco. Large sequence divergence among isolates, nearly complete species monophyly, and widespread geographic distribution suggest that FIV-Pco has evolved within the puma species for a long period. The sequence data provided evidence for vertical transmission of FIV-Pco from mothers to their kittens, for coinfection of individuals by two different viral strains, and for cross-species transmission of FIV from a domestic cat to a puma. These factors may all be important for understanding the epidemiology and natural history of FIV in the puma.

Journal Article
TL;DR: Nurses who have cared for patients with cancer are more knowledgeable and have more liberal attitudes toward pain management from nurses who have not cared for Patients with cancer.
Abstract: PURPOSE/OBJECTIVES: To describe the knowledge and attitudes of North Carolina nurses toward the management of cancer-related pain. The analysis focused on knowledge, attitude, and perception of barriers to pain management. DESIGN: Exploratory, descriptive. SETTING: North Carolina. SAMPLE: A survey of 1,400 RNs were stratified by educational background and Area Health Education Center regions of the state; the response rate was 24%. METHODS: An adapted version of The Wisconsin Pain Initiative Survey mailed to participants. MAIN RESEARCH VARIABLES: Nurses' knowledge, attitudes, and perception of perceived barriers to managing cancer-related pain. FINDINGS: Nurses who have cared for patients with cancer are more knowledgeable and have more liberal attitudes toward pain management from nurses who have not cared for patients with cancer. North Carolina nurses report knowledge and perception of barriers to pain management similar to those of Wisconsin nurses. CONCLUSIONS: The experience of caring for patients who have cancer and pain influences nurses to report more liberal attitudes toward pain management. IMPLICATIONS FOR NURSING PRACTICE: Although nurses report increased knowledge of pain management in general, deficits continue to exist. Further research is needed to more fully understand the effect of educational and experience on practice.

Journal ArticleDOI
TL;DR: Phylogenetic reconstruction supports more recent, intralineage associations but fails to completely resolve interlineage relationships, and implications of the relative recency of felid evolution, presence of ancestral polymorphisms, and influence of outgroups in placement of the topological root are discussed.


Journal ArticleDOI
01 May 1996-Nature
TL;DR: In this Letter, the received and accepted dates for the manuscript were incorrectly listed as being in 1994, instead of 1995.
Abstract: Nature 379, 441–445 (1996) In this Letter, the received and accepted dates for the manuscript were incorrectly listed as being in 1994, instead of 1995. The correct dates are: received 2 October; accepted 24 November 1995.

Journal ArticleDOI
TL;DR: Patterns of mitochondrial restriction fragment length polymorphism (RFLP) variation were used to resolve more recent relationships among the species of the Felidae ocelot lineage, domestic cat lineage, and pantherine lineage.
Abstract: Patterns of mitochondrial restriction fragment length polymorphism (RFLP) variation were used to resolve more recent relationships among the species of the Felidae ocelot lineage, domestic cat lineage, and pantherine lineage. Twenty-five of 28 restriction enzymes revealed site variation in at least 1 of 21 cat species. The ocelot lineage was resolved into three separate sistertaxa groups: Geoffroy's cat (Oncifelis geoffroyi) and kodkod (O. guigna), ocelot (Leopardus pardalis) and margay (L. wiedii), and pampas cat (Lynchailurus colocolo) and most of the tigrina samples (Leopardus tigrina). Within the domestic cat lineage, domestic cat (Felis catus), European wild cat (F. silvestris), and African wild cat (F. libyca) formed a monophyletic trichotomy, which was joined with sand cat (F. margarita) to a common ancestor. Jungle cat (F. chaus) and black-footed cat (F. nigripes) mtDNAs diverged earlier than those of the other domestic cat lineage species and are less closely related. Within the pantherine lineage, phylogenetic analysis identified two distinct groups, uniting lion (P. leo) with leopard (P. pardus) and tiger (P. tigris) with snow leopard (P. uncia).

Book ChapterDOI
01 Jan 1996

Journal ArticleDOI
TL;DR: The spread of AIDS through sexual contact, blood transfusion and contaminated syringes has led to a recent estimate of nearly four million AIDS cases worldwide and some 21 million people infected with HIV-1 or HIV-2.

Journal Article
TL;DR: A method for the preparation of bi Daryl compounds is disclosed which comprises contacting an aromatic halide in the presence of a catalyst comprising zerovalent nickel, a bidentate phosphorus-containing coordinating ligand and a reducing metal in a polar, aprotic solvent system for a time and under conditions suitable for the formation of biaryl compound.
Abstract: A method for the preparation of biaryl compounds is disclosed which comprises contacting an aromatic halide in the presence of a catalyst comprising zerovalent nickel, a bidentate phosphorus-containing coordinating ligand and a reducing metal in a polar, aprotic solvent system for a time and under conditions suitable for the formation of biaryl compound.

Journal ArticleDOI
TL;DR: The results of an extensive RVF serological survey among a diversity of African carnivore species show that cattle, sheep, goats, dogs, cats, mice, hamsters, rats, camels, water buffaloes, horses, monkeys, and humans are known to be susceptible to RVFV.
Abstract: Rift Valley fever (RVF) was first described in 1931 by Daubney et al.' as a highly fatal epizootic disease of sheep in Kenya. The causative agent, RVF virus (RVFV), is a Bunyavims in the genus Phlebovirus* and is spread mainly by mosquitoes, particularly species of Aedes and Culex. While RVFV is known to be endemic in the Rift Valley, it has caused outbreaks in Egypt,) South Africa: Mauritania: and Madagascar.6 Cattle, sheep, goats, dogs, cats, mice, hamsters, rats, camels, water buffaloes, horses, monkeys, and humans are known to be susceptible to RVFV, as recently reviewed by House? This paper reports the results of an extensive RVF serological survey among a diversity of African carnivore species.

Journal ArticleDOI
15 Nov 1996-Science
TL;DR: In the footnotes for table 1, the report “Genetic restriction of HIV-1 infection and progression to AIDS by a deletion allele of the CKR5 structural gene” was neglected to identify 63 patients who were intravenous drug users enrolled in a New Zealand hospital.
Abstract: In the footnotes for table 1 ([p. 1857][1]) in our report “Genetic restriction of HIV-1 infection and progression to AIDS by a deletion allele of the CKR5 structural gene” ([27 Sept., p. 1856][1]) ([1][2]), we neglected to identify 63 patients who were intravenous drug users enrolled in a New

Journal Article
01 Jan 1996-Leukemia
TL;DR: Severe gastrointestinal and renal side-effects were the dose-limiting toxicities occurring in four of five patients treated with CI-973 1200 to 1350 mg/m2 per course.
Abstract: The purpose of the study was to define the maximally tolerated dose (MTD), major toxicities, and possible antitumor activity of CI-973 a new platinum analogue, in patients with refractory or relapsed acute leukemia. CI-973 was given as a 5-day continuous infusion every 3 to 4 weeks to patients with refractory or relapsed acute leukemia, at doses ranging from 150 mg/m2 to 1350 mg/m2 per course. Thirty-six patients were treated including 18 patients with acute myelogenous leukemia (AML), four with acute lymphocytic leukemia (ALL) and 14 with chronic myelogenous leukemia in blastic phase (CML-BP). Severe gastrointestinal and renal side-effects were the dose-limiting toxicities occurring in four of five patients treated with CI-973 1200 to 1350 mg/m2 per course. At the MTD of 1000 mg/m2 per course, three of 13 patients treated (23%) had moderate to severe nausea and vomiting, three (23%) had moderate diarrhea and one had moderate mucositis. Among 21 patients treated at > or = 1000 mg/m2 (15 AML, 6 CML-BP) no objective complete or partial responses were observed. Twelve of 18 patients (66%) with evaluable marrows on day 14 showed significant suppression of marrow blasts percentage and marrow leukemic infiltrate percentage. Tests for measurement of DNA adduct formation in leukemic cells in vivo after CI-973 therapy, and in vitro following exposure of leukemic cells to CI-973 were developed. This study defined the MTD of CI-973 to be 1000 mg/m2 by continuous infusion over 5 days every 3 to 4 weeks in patients with refractory or relapsed acute leukemia. Gastrointestinal and renal side-effects were dose-limiting. No objective responses were noted in this heavily resistant population. Correlations between CI-973-induced DNA adduct formation and individual patient response to CI-973 will help to define its role in leukemia subsets.



Book ChapterDOI
01 Jan 1996
TL;DR: The establishment of universal Type I (coding gene) genetic markers, which can be mapped in all species, will allow true comparisons of genome organization across species and will provide the framework for comparative genetic research (O’Brien, 1991).
Abstract: The discovery of hypervariable microsatellite markers and the technical advances of marker typing has facilitated efforts towards the construction of genetic linkage maps in several diverse vertebrate species. These mapping projects have advanced the exploration of each organism’s genome and its biology. But less effort has been focused on the mapping of coding genes, genetic markers which allow comparisons of genome organization across species. The establishment of universal Type I (coding gene) genetic markers, which can be mapped in all species, will allow true comparisons of genome organization across species and will provide the framework for comparative genetic research (O’Brien, 1991). Comparative genetics allows the gene poor species to consider the information of gene rich species, exponentially increasing the perspective available for disease and genetic trait analyses. In developing the genetic map of the cat (O’Brien and Nash; Nash and O’Brien; Gilbert et al., 1988; O’Brien et al., 1988), we have focused on the mapping of Type I markers in order to capture the information locked in the genome of other species and to assist the use of the feline genome in evolutionary and inherited disease research (O’Brien et al., 1993).