2,805 research outputs found
Cross-reactivity between tumor MHC class I–restricted antigens and an enterococcal bacteriophage
No full textFluckiger, A., Daillère, R., Sassi, M., Sixt, B.S., Liu, P., Loos, F., Richard, C., Rabu, C., Alou, M.T., Goubet, A.-G., Lemaitre, F., Ferrere, G., Derosa, L., Duong, C.P.M., Messaoudene, M., Gagné, A., Joubert, P., de Sordi, L., Debarbieux, L., Simon, S., Scarlata, C.-M., Ayyoub, M., Palermo, B., Facciolo, F., Boidot, R., Wheeler, R., Boneca, I.G., Sztupinszki, Z., Papp, K., Csabai, I., Pasolli, E., Segata, N., Lopez-Otin, C., Szallasi, Z., Andre, F., Iebba, V., Quiniou, V., Klatzmann, D., Boukhalil, J., Khelaifia, S., Raoult, D., Albiges, L., Escudier, B., Eggermont, A., Mami-Chouaib, F., Nistico, P., Ghiringhelli, F., Routy, B., Labarrière, N., Cattoir, V., Kroemer, G., Zitvogel, L
Correlation energy of two electrons in a ball
No full textWe study the ground-statecorrelationenergyEc of two electrons of opposite spin confined within a D-dimensional ball (D≥2) of radius R. In the high-density regime, we report accurate results for the exact and restricted Hartree–Fock energy, using a Hylleraas-type expansion for the former and a simple polynomial basis set for the latter. By investigating the exact limiting correlationenergyEc⁽⁰⁾=limR→0Ec for various values of D, we test our recent conjecture [P.-F. Loos and P. M. W. Gill, J. Chem. Phys.131, 241101 (2009)] that in the large-D limit, Ec⁽⁰⁾∼−δ2/8 for any spherically symmetric confining external potential, where δ=1/(D−1)
Haematologia
No full text1987 / 1. szám
Niewiarowski, S.: Platelet membrane components and receptors
Fehér, I. - Gidáli, J.: Self-renewal capacity of mobilized murine haemopoietic stem cells
Couillin, Ph. - Bouvé, H. - Bétuel, H. - Hors, J. - Gebuhrer, L. - Boué, A.: Particular interest of HLS typing for genetic counselling in families with congenital adrenal hyperplasia (21-OH deficiency)
Gonzalez, M. - Cabrera, A. - San Miguel, J. F. - de Andres, M. - Gomez Morales, M. - Lopez-Borrasca, A. - Garrido, F.: Heterogeneity of chronic T-cell lymphocytosis: immunological and clinical aspects
Pagano, L. - Marra, R. - De Stefano, V. - Leone, G.: Spinal fluid procoagulant activity in leukaemic patients treated with intrathecal methotrexate
San Miguel, J. F. - Fisac, P. - Gonzalez, M. - Calmuntia, M. J. - Hernandez, J. - Bascones, C.: Immunologic phenotype of the microgranular variant of acute promyelocytic leukaemia
González, R. - Estrada, M. - Garcia, M. - Gutiérrez, a. - de la Torre, E. - Colombo, B.: Erythrocyte PK deficiency: biochemical characterization of a patient with haemolytic anemia
Zago, M. A. - Covas, D. T. - Ismael, S. J. - Bottura, C.: Splenic function in haemophilia
1987 / 2. szám
Tatsumi, N. - Tsuda, I.: Marked changes in red cell volume response to isotonic glucose solution during storage
Sipka, S. - Kávai, M. - Techmann, F. - Boldogh, I. - Szegedi, Gy.: Lymphokine effect upon the EA uptake by human monocytes
Martinez, G. - Colombo, B.: ## Thalessemia produces high levels of Hb Bart's in newborns and high HbA2 in adults
Paradoa Pérez, M. L. - Trujillo, Y. - Basanta, P.: Association of dengue hemorrhagic fever with the HLA system
Naskalski, J. W.: Proteinuria and excretion of ribonuclease in patients with chronic granulocytic leukaemia
Inyang, A. L. - Okpako, D. T. - Essien, E. M.: Platelet reactions in acute Plasmodium berghei infection in Swiss albino mice
Pálóczi, Katalin - Zeher, Margit - Lukács, Katalin, Kávai, Mária - Szegedi, Gy.: Altered monocyte functions in patients with angioimmunoblastic lymphadenopathy
Alegre, A. - Alberca, I. - Herraez, J. - Vicente, V.: Lupus anticoagulant and false positive serological tests for syphilis
Abstracts
1987 / 3. szám
Bowman, Ellen - Watts, J. - Burrows, R. - Chui, D. H. K.: Haemoglobin Barts hydrops fetalis syndrome
Heynem, M. J. - Zaman, Z. - Verwilghen, R. L.: Effect of acute lead intoxication on the ultrastructure of rat erythroblasts and reticulocytes Morphometric analysis and Röntgen micro-analysis
Phan, D. T. - Bartha, E. - Gidáli, J. - Fehér, I. - Harsányi, V. - Petrányi, G. Gy. - Hollán, S. R.: T-cell depletion of Cercopithecus Aethiops monkey bone marrow with Campath-1 monoclonal antibody and complement
Lemež, P. - Koubek, K. - Malasková, V. - Lojda, Z.: Dipeptidyl peptidase IV activity in cells of T-lymphoid origin in decreased in cultures with 12-0-tetradecanoylphorbol-13-acetate (TPA)
Berger, J.: Age-associated sensitivity to experimental, drug-induced marrow hypoplasia of laboratory rats
Capellato, M. G. - Lazzaro, A. R. - Marafioti, F. - Polato, G. - Girolami, A.: A new family with congenital Factor XIII deficiency showing a deficit of both subunit a and b. Type I Factor XIII deficiency
Boros, P. - Balázs, Gy. - Szegedi, Gy.: Natural killer activity in thyroid cancer patients
Abstracts
Book Review
Announcement
1987 / 4. szám
Phan, D. T. - Gidáli, J. - Fehér, I. - Harsányi, V. - Petrányi, G. Gy. - Hollán, S. R.: Comparison on efficiency of complements from various species for T-cell depletion from Cercopithecus aethiops bone marrow with Campath-1 MoAb in vitro
Starsia, Z. - Zitnan, D. - Loos, M. - Stefanovic, J. - Bosák, V. - Niks, M. - Tomanová, H. - Lukác, J. - Lulovicová, M.: Deficiency of C2, the second complement component, in the family of a patient with SLE-like syndrome: the first case of hereditary C2 deficiency in Czechoslovakia
Open Forum
Introduction
Finch, C. A. - Huebers, H. A.: Maintenance of normal iron balance
Worwood, M.: The diagnostic value of serum ferritin determinations for assessing iron status
Brock, J. H.: Iron and infection
Hershko, C. - Link, G. - Pinson, A. - Hasin, Y. - Moreb, J.: Iron loading and chelation as studied in a heart cell culture system
Abstracts
Contents of Volume 20
Author Index
Subject Inde
The University of Utah College of Law Introduces Its 1969 Graduating Class
No full textPhotographs and profiles of 84 graduates: Darian Bruce Andersen, Richard S. Brown, John Ashton, R. Bruce Bybee, James N. Barber, Shannon L. Bybee, Jr., George J. Berris, Herschel Bullen, Lorin Robert Blauer, Hans Q. Chamberlain, Donald S. Coleman, Richard M. Day, Christine Odell Cook, O. Wallace Earl, Michael Jeffrey Cooper, Robert S. Erickson, Paul R. Corradine, Michael D. Esplin, William F. Daines, Gregory D. Farley, Delano S. Findlay, Hays Gorey, Jr., Fred W. Finlinson, Sheldon Guttman, Philip R. Fishler, David E. Halliday, Jay W. Fitt, Ronn E. Harding, Larry M. Fallett, Robert D. Hazen, William R. Hyde, Robert D. Larsen, C. Brent Jackson, Paul H. Liapis, Leray G. Jackson, Herbert C. Livsey, Carl E. Kingston, William C. Loos, Richard Landerman, Jack Lunt, Richard E. Lyon, Jr., Wilson McCarthy, Richard P. Makoff, Robert S. McConnell, William A. Marshall, Michael T. McCoy, John McAllister, James Douglas Mitchell, Edward J. McCarthy, Jack H. Molgard, Maralee Neighbors, Larry F. Ogden, E. Miles Nelson, Rodney Smith Page, Gary Nelson, Miriam E. Parker, John T. Nielson, Lafe S. Parkin, Arthur Dennis Norton, Edwin J. Pond, Elwood P. Powell, Paul B. Saltzman, Thomas James Quinlan, Roger David Sandack, Lyle Rivera, Dell M. Saunders, David E. Roth, Jim R. Scarth, William F. Rummler, Paul W. Shields, Kevan F. Smith, Jay D. Sudweeks, Morris J. Sorenson, Marcus G. Theodore, George H. Speciale, Juliette Coleen Ward, Richard H. Stahle, Karl T. Werner, Wallace D. Stevens, Karen S. Williams, Gerald R. Williams, David S. Young, Stephen G. Wood, Michael David Zimmerman
Hundreds of variants clustered in genomic loci and biological pathways affect human height
No full textMost common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits(1), but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait(2,3). The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P<0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways
Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index
No full textObesity is globally prevalent and highly heritable, but its underlying genetic factors remain largely elusive. To identify genetic loci for obesity susceptibility, we examined associations between body mass index and similar to 2.8 million SNPs in up to 123,865 individuals with targeted follow up of 42 SNPs in up to 125,931 additional individuals. We confirmed 14 known obesity susceptibility loci and identified 18 new loci associated with body mass index (P < 5 x 10(-8)), one of which includes a copy number variant near GPRC5B. Some loci (at MC4R, POMC, SH2B1 and BDNF) map near key hypothalamic regulators of energy balance, and one of these loci is near GIPR, an incretin receptor. Furthermore, genes in other newly associated loci may provide new insights into human body weight regulation
Glycogen synthase kinase-3β phosphorylates protein tau and rescues the axonopathy in the central nervous system of human four-repeat tau transgenic mice
No full textProtein tau filaments in brain of patients suffering from Alzheimer's disease, frontotemporal dementia, and other tauopathies consist of protein tau that is hyperphosphorylated.,The responsible kinases operating in vivo in neurons still need to be identified. Here we demonstrate that glycogen synthase kinase-3 beta (GSK-3 beta) is an effective kinase for protein tau in cerebral neurons in vivo in adult GSK-3 beta and GSK-3 beta x human tau40 transgenic mice; Phosphorylated protein tau migrates slower during electrophoretic separation and is revealed by phosphorylation-dependent anti-tau antibodies in Western blot analysis. In addition, its capacity to bind to re-assembled paclitaxel (Taxol(R))-stabilized microtubules is reduced, compared with protein tau isolated from mice not overexpressing GSK-3 beta. Co-expression of GSK-3 beta reduces the number of axonal dilations and alleviates the motoric impairment that was typical for single htau40 transgenic animals (Spittaels, K., Van den Haute, C., Van Dorpe, J., Bruynseels, K., Vandezande, K., Laenen, I., Geerts, H., Mercken, M., Sciot, R., Van Lommel, A., Loos, R., and Van Leuven, F. (1999) Am. J. Pathol. 155, 2153-2165). Although more hyperphosphorylated protein tau is available, neither an increase in insoluble protein tau aggregates nor the presence of paired helical filaments or tangles was observed. These findings could have therapeutic implications in the field of neurodegeneration, as discussed
New Mexico vs Utah, September 4, 1984
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Evaluating the role of LPIN1 variation in insulin resistance, body weight, and human lipodystrophy in UK populations
No full textOBJECTIVE-Loss of lipin 1 activity causes lipodystrophy and insulin resistance in the fld mouse, and LPIN1 expression and common genetic variation were recently suggested to influence adiposity and insulin sensitivity in humans. We aimed to conduct a comprehensive association study to clarify the influence of common LPIN1 variation on adiposity and insulin sensitivity in U.K. populations and to examine the role of LPIN1 mutations in insulin resistance syndromes. RESEARCH DESIGN AND METHOD-Twenty-two single nucleotide polymorphisms tagging common LPIN1 variation were genotyped in Medical Research Council (MRC) Ely (n = 1,709) and Hertfordshire (n = 2,901) population-based cohorts. LPIN1 exons, exon/intron boundaries, and 3' untranslated region were sequenced in 158 patients with idiopathic severe insulin resistance (including 23 lipodystrophic patients) and 48 control subjects. RESULTS-We found no association between LPIN1 single nucleotide polymorphisms and fasting insulin but report a nominal association between rs13412852 and BMI (P = 0.042) in a meta-analysis of 8,504 samples from in-house and publicly available studies. Three rare nonsynonymous variants (A353T, R552K, and G582R) were detected in severely insulin-resistant patients. However, these did not cosegregate with disease in affected families, and Lipin1 protein expression and phosphorylation in patients with variants were indistinguishable from those in control subjects. CONCLUSIONS-Our data do not support a major effect of common LPIN1 variation on metabolic traits and suggest that mutations in LPIN1 are not a common cause of lipodystrophy in humans. The nominal associations with BMI and other metabolic traits in U.K. cohorts require replication in larger cohort
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RBP4 variants are significantly associated with plasma RBP4 levels and hypertriglyceridemia risk in Chinese Hans
No full textWe previously found that plasma RBP4 levels were strongly associated with metabolic syndrome components. This study aimed to determine whether RBP4 variants are associated with the metabolic syndrome components and plasma RBP4 levels, and to investigate whether the associations between plasma RBP4 and the metabolic syndrome components are causal. Five tagSNPs were tested for their associations with plasma RBP4 levels and metabolic syndrome components in a population-based sample of 3,210 Chinese Hans. A possible causal relationship between plasma RBP4 levels and hypertriglyceridemia was explored by Mendelian randomization. Plasma RBP4 levels were significantly associated with rs10882273 (beta z -0.10SD[-0.17, -0.03], P = 0.0050), rs3758538 (beta z -0.13SD[-0.24, -0.02], P = 0.0249) in all participants, and with rs17108993 in Shanghai participants (beta z -0.19SD[-0.32, -0.05], P = 0.0061). The single nucleotide polymorphism (SNP) rs3758538 was significantly associated with hypertriglyceridemia (OR 0.62 [0.45-0.85], P = 0.0026) and triglycerides (beta z -0.19SD [20.30, 20.07], P = 0.001) in all participants. In Mendelian randomization analysis, the observed effect size of association between rs3758538 and hypertriglyceridemia was different from the expected effect size (P = 0.0213). This is the first study to show that the RBP4 variants are significantly associated with plasma RBP4 levels and hypertriglyceridemia risk in Chinese Hans. However, results of Mendelian randomization do not support the hypothesis thatRBP4 levels are causally related to hypertriglyceridemia risk.-Wu, Y., H. Li, R. J. F. Loos, Q. Qi, F. B. Hu, Y. Liu, and X. Lin. RBP4 variants are significantly associated with plasma RBP4 levels and hypertriglyceridemia risk in ChineseHans. J. Lipid Res. 2009. 50: 1479-1486.Version of Recor
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