1,435 research outputs found
Extramedullary plasmacytoma in a horse with ptyalism and dysphagia
No full textA Clydesdale mare was examined for weight loss, inappetence, ptyalism, and dysphagia. The main abnormality revealed by serum biochemistry was a marked hyperglobulinemia, and protein electrophoresis revealed a monoclonal gammopathy in the gamma region. The urine was positive for Bence Jones proteins. These findings suggested a plasma cell tumor. The neoplasm could not be located with extensive antemortem examination. At postmortem, neoplastic cells morphologically compatible with plasma cells and positive for equine IgG with imunoperoxidase staining infiltrated the pericardium, mediastinal stromal tissues, adrenal glands, meninges, atrioventricular valves, aorta, abdominal and thoracic fat, and nerves, including the trigeminal nerve. The neoplastic cells invading the cranial nerves were responsible for many of the presenting signs.PT: J; CR: BARLOGIE B, 1995, WILLIAMS HEMATOLOGY, P1109 BAUER JD, 1974, CLIN LAB METHODS, P15 BRAUND KG, 1978, J AM VET MED ASSOC, V172, P1407 BRAUND KG, 1979, J AM VET MED ASSOC, V174, P1321 CALNEK BW, 1991, DIS POULTRY, P342 DIMOPOULOS MA, 1994, BLOOD, V83, P1452 DREW RA, 1974, EQUINE VET J, V3, P131 DUNCAN JR, 1994, VET LAB MED CLIN PAT, P112 DUNCAN JR, 1994, VET LAB MED CLIN PAT, P63 EDWARDS DF, 1993, J VET INTERN MED, V7, P169 HENRY M, 1994, J AM VET MED ASSOC, V194, P392 JACKSON MW, 1994, J AM VET MED ASSOC, V204, P404 KENT JE, 1990, EQUINE VET J, V22, P373 MANDEL NS, 1994, J AM ANIM HOSP ASSOC, V30, P603 TRAUBDARGATZ J, 1985, EQUINE VET J, V17, P373; NR: 15; TC: 9; J9: J VET DIAGN INVEST; PG: 3; GA: 312MPSource type: Electronic(1
The Crystal Structure of Cu3(AsO4)2
No full textTitle: The Crystal Structure of Cu3(AsO4)2, Author: Sandra J. Poulsen, Location: ThodeThe crystal structure of Cu3(AsO4)2 was determined
using a direct method of crystal structure analysis. The
crystal structure is described, and its features compared
to those of several compounds which have similar molecular
formulas. The method used in the structure determination
process is described, and an assessment of its general usefulness
is attempted.ThesisMaster of Science (MS
Psychosocial needs and responses in breast cancer recovery / Sandra J. Neuling
No full textTypescript (Photocopy)Includes two papers co-authored by the author as appendix D.Bibliography: leaves 397-425xvii, 425 leaves ; 30 cm.Thesis (Ph.D.)--Dept. of Psychology, University of Adelaide, 199
The way of life of Mr. Nowhere: Review of the book Objectivity and Diversity, by Sandra Harding
No full textDr. Jill Fellows (Douglas College) reviews the book Objectivity and Diversity by Sandra Harding (2015).Final article published
Singapore, commander J. Proud from British Naval Press Relations
No full textSingapore, Malaya: [35 & 37] F29 Dennis McEvoy, Chicago Times. (son of J.P. McEvoy, the well-known American playwright & author.) [36] commander J. Proud, British Naval Press Relations contact in Singapore.GrayscaleForman Safety Negatives, Box 1
Thyroid hormone inhibition of IGF-1-mediated glucose uptake in L-6 myoblasts through intercation with alphaVbeta3 integrin
No full textThe Endocrine Society's 90th Annual MeetingFilename: 851334 Contact Author: Sandra Incerpi Dr. Department/Institution: Biology, University Roma TreAddress: Viale G. Marconi, 446City/State/Zip/Country: Rome, 00146, ItalyPhone: ++39-06-57336335 Fax: ++39-06-57336321 E-mail: [email protected]
Socioeconomic position and the transmission of psychological distress: a life course and intergenerational analysis of the panel study of income dynamics
No full textLow socioeconomic position is associated with worse mental health, yet few studies have examined how socioeconomic patterning or fluctuations over the life course can influence later psychiatric symptoms. Using the Panel Study of Income Dynamics, we examined how income patterning across the life course and across generations impacts present-day psychological distress symptoms.Ph.D.Includes bibliographical referencesby Bozena J. Kati
Homozygous mutations in the conserved ATP hinge region of the Wilson disease gene: Association with liver disease
No full textObjective: To determine whether any correlation exists between the phenotype and genotype of 2 Lebanese families with members affected with Wilson disease (WD). Background: WD is an autosomal-recessive disorder of copper transport with significant phenotypic diversity. Most patients are compound heterozygous making it difficult to establish a clear link between phenotype and genotype. Study: We investigated 14 members from 2 Lebanese families (H and Z) with 5 members affected with WD. Mutation analysis of the ATP7B gene, and clinical assessments were carried out for both families. We also performed a literature search retrieving reported phenotypes of all patients homozygous to mutations in any of the 21 exons of the ATP7B. Results: Patients of the H and Z-families were found homozygous for the respective Asn1270Ser and Pro1273Leu mutations in the adenosine triphosphate (ATP) hinge region of exon 18. Of the healthy members, 6 were heterozygous and 3 had normal sequences. Clinically, 4 patients had liver cirrhosis and 1 had asymptomatic transaminitis. One of the patients also had neurologic symptoms. Screening the literature for patients homozygous for mutations in the ATP hinge region identified 25 patients including ours. The overall prevalence of the hepatic phenotype among patients homozygous for mutation in exon 18 was 80percent and was significantly higher than those in exons 7, 14, and 21. Conclusions: We hereby report the association of liver disease with homozygous mutations in the conserved ATP hinge region of exon 18 of the ATP7B gene. 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Ecotones, herbivory, acceptance rate and electronic access
No full textEach year, we choose a paper for the Editors’ Award, normally from among those nominated by the Coordinating Editors (no money is handed out). This year,
the voting was tied, so we settled for two joint winners: Walker et al. (2003) and Bakker & Olff (2003). We had another problem this time: one of the papers
nominated had a Chief Editor as a subsidiary author and another had the daughter of a Chief Editor as the first author. According to our rules a paper with a Chief
Editor as first author can never win, and once we have a shortlist a Chief Editor cannot vote on a paper that his/her name appears on. We considered fiercer rules than this, but we thought it unfair for a young scientist to miss out on an award because s/he was associated with a Chief Editor. Anyway, as it turned out the two Chief Editors with any possible conflict of interest did not vote at all. In spite of this, the name of one Chief Editor appears on one of the joint awardees, and the daughter
of a Chief Editor on another. Sorry. We tried not to.Fil: Wilson, J. Bastow. University of Otago; Nueva ZelandaFil: White, Peter S.. University of North Carolina; Estados UnidosFil: Bakker, Jan P.. University of Groningen; Países BajosFil: Díaz, Sandra Myrna. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto Multidisciplinario de Biología Vegetal. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas Físicas y Naturales. Instituto Multidisciplinario de Biología Vegetal; Argentin
Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis
No full textMultiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis
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