Institution
University of Würzburg
Education•Wurzburg, Bayern, Germany•
About: University of Würzburg is a education organization based out in Wurzburg, Bayern, Germany. It is known for research contribution in the topics: Population & Gene. The organization has 31437 authors who have published 62203 publications receiving 2337033 citations. The organization is also known as: Julius-Maximilians-Universität Würzburg & Würzburg University.
Topics: Population, Gene, Immune system, Receptor, CAS Registry Number
Papers published on a yearly basis
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TL;DR: In this article, a renormalization scheme for the electroweak standard model is presented in which the electric charge and the masses of the gauge bosons, Higgs particle and fermions are used as physical parameters.
Abstract: A renormalization scheme for the electroweak standard model is presented in which the electric charge and the masses of the gauge bosons, Higgs particle and fermions are used as physical parameters. The photon is treated such that quantum electrodynamics is contained as a simple substructure. Field renormalization respecting the gauge symmetry gives finite propagators and vertex functions. The Ward identities between the Green functions of the unphysical sector allow a renormalization that maintains the simple pole structure of the propagators in the t'Hooft-Feynman gauge. We give a complete list of self energies and all renormalization constants also in the unphysical Higgs and ghost sector. Explicit results are given for the renormalized self energies, vertex functions and boxes that enter the evaluation of 1-loop radiative corrections to fermionic processes. We calculate the 1-loop radiative corrections to purely leptonic reactions like $\mu$ decay, $
u \mu \mu e$ scattering and $\mu$ pair production in $e^+ e^−$ annihilation. A test of the standard model is performed by comparing these low energy data with the results of the $p \bar{p}$ collider experiments for the W and Z boson masses.
352 citations
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352 citations
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University of Barcelona1, University of Würzburg2, Netherlands Cancer Institute3, Pompeu Fabra University4, University of Nebraska Medical Center5, University of Oslo6, National Institutes of Health7, Autonomous University of Barcelona8, Duke University9, University of Arizona10, Oregon Health & Science University11, University of British Columbia12, Bosch13
TL;DR: The clinico-pathological features and outcomes of the patients with cyclin D1-negative mantle cell lymphoma identified by SOX11 expression were similar to those of patients with conventional mantlecell lymphoma.
Abstract: Background Cyclin D1-negative mantle cell lymphoma is difficult to distinguish from other small B-cell lymphomas. The clinical and pathological characteristics of patients with this form of lymphoma have not been well defined. Overexpression of the transcription factor SOX11 has been observed in conventional mantle cell lymphoma. The aim of this study was to determine whether this gene is expressed in cyclin D1-negative mantle cell lymphoma and whether its detection may be useful to identify these tumors.Design and Methods The microarray database of 238 mature B-cell neoplasms was re-examined. SOX11 protein expression was investigated immunohistochemically in 12 cases of cyclin D1-negative mantle cell lymphoma, 54 cases of conventional mantle cell lymphoma, and 209 additional lymphoid neoplasms.Results SOX11 mRNA was highly expressed in conventional and cyclin D1-negative mantle cell lymphoma and in 33% of the cases of Burkitt’s lymphoma but not in any other mature lymphoid neoplasm. SOX11 nuclear protein was detected in 50 cases (93%) of conventional mantle cell lymphoma and also in the 12 cyclin D1-negative cases of mantle cell lymphoma, the six cases of lymphoblastic lymphomas, in two of eight cases of Burkitt’s lymphoma, and in two of three T-prolymphocytic leukemias but was negative in the remaining lymphoid neoplasms. Cyclin D2 and D3 mRNA levels were significantly higher in cyclin D1-negative mantle cell lymphoma than in conventional mantle cell lymphoma but the protein expression was not discriminative. The clinico-pathological features and outcomes of the patients with cyclin D1-negative mantle cell lymphoma identified by SOX11 expression were similar to those of patients with conventional mantle cell lymphoma.Conclusions SOX11 mRNA and nuclear protein expression is a highly specific marker for both cyclin D1-positive and negative mantle cell lymphoma.
352 citations
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TL;DR: The mechanisms by which hyperactive alleles become homozygous was addressed by comparative genome hybridization and single nucleotide polymorphism arrays and indicated that loss of TAC1 heterozygosity can occur by recombination between portions of chromosome 5 or by chromosome 5 duplication.
Abstract: TAC1, a Candida albicans transcription factor situated near the mating-type locus on chromosome 5, is necessary for the upregulation of the ABC-transporter genes CDR1 and CDR2, which mediate azole resistance. We showed previously the existence of both wild-type and hyperactive TAC1 alleles. Wild-type alleles mediate upregulation of CDR1 and CDR2 upon exposure to inducers such as fluphenazine, while hyperactive alleles result in constitutive high expression of CDR1 and CDR2. Here we recovered TAC1 alleles from two pairs of matched azole-susceptible (DSY294; FH1: heterozygous at mating-type locus) and azole-resistant isolates (DSY296; FH3: homozygous at mating-type locus). Two different TAC1 wild-type alleles were recovered from DSY294 (TAC1-3 and TAC1-4) while a single hyperactive allele (TAC1-5) was isolated from DSY296. A single amino acid (aa) difference between TAC1-4 and TAC1-5 (Asn977 to Asp or N977D) was observed in a region corresponding to the predicted activation domain of Tac1p. Two TAC1 alleles were recovered from FH1 (TAC1-6 and TAC1-7) and a single hyperactive allele (TAC1-7) was recovered from FH3. The N977D change was seen in TAC1-7 in addition to several other aa differences. The importance of N977D in conferring hyperactivity to TAC1 was confirmed by site-directed mutagenesis. Both hyperactive alleles TAC1-5 and TAC1-7 were codominant with wild-type alleles and conferred hyperactive phenotypes only when homozygous. The mechanisms by which hyperactive alleles become homozygous was addressed by comparative genome hybridization and single nucleotide polymorphism arrays and indicated that loss of TAC1 heterozygosity can occur by recombination between portions of chromosome 5 or by chromosome 5 duplication.
352 citations
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TL;DR: This review summarizes the present knowledge on GC action, the mechanisms employed to induce apoptosis and the currently discussed models of how they may participate in thymocyte development.
Abstract: Glucocorticoids (GCs) are a class of steroid hormones which regulate a variety of essential biological functions The profound anti-inflammatory and immunosuppressive activity of synthetic GCs, combined with their power to induce lymphocyte apoptosis place them among the most commonly prescribed drugs worldwide Endogenous GCs also exert a wide range of immunomodulatory activities, including the control of T cell homeostasis Most, if not all of these effects are mediated through the glucocorticoid receptor, a member of the nuclear receptor superfamily However, the signaling pathways and their cell type specificity remain poorly defined In this review, we summarize our present knowledge on GC action, the mechanisms employed to induce apoptosis and the currently discussed models of how they may participate in thymocyte development Although our knowledge in this field has substantially increased during recent years, we are still far from a comprehensive picture of the role that GCs play in T lymphocytes
352 citations
Authors
Showing all 31653 results
Name | H-index | Papers | Citations |
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Peer Bork | 206 | 697 | 245427 |
Cyrus Cooper | 204 | 1869 | 206782 |
D. M. Strom | 176 | 3167 | 194314 |
George P. Chrousos | 169 | 1612 | 120752 |
David A. Bennett | 167 | 1142 | 109844 |
Marc W. Kirschner | 162 | 457 | 102145 |
Josef M. Penninger | 154 | 700 | 107295 |
William A. Catterall | 154 | 536 | 83561 |
Rui Zhang | 151 | 2625 | 107917 |
Niels Birbaumer | 142 | 835 | 77853 |
Kim Nasmyth | 142 | 294 | 59231 |
James J. Gross | 139 | 529 | 100206 |
Michael Schmitt | 134 | 2007 | 114667 |
Jean-Luc Brédas | 134 | 1026 | 85803 |
Alexander Schmidt | 134 | 1185 | 83879 |