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Institution

University of Würzburg

EducationWurzburg, 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.


Papers
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Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
01 Apr 2006-Genetics
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

Journal ArticleDOI
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

NameH-indexPapersCitations
Peer Bork206697245427
Cyrus Cooper2041869206782
D. M. Strom1763167194314
George P. Chrousos1691612120752
David A. Bennett1671142109844
Marc W. Kirschner162457102145
Josef M. Penninger154700107295
William A. Catterall15453683561
Rui Zhang1512625107917
Niels Birbaumer14283577853
Kim Nasmyth14229459231
James J. Gross139529100206
Michael Schmitt1342007114667
Jean-Luc Brédas134102685803
Alexander Schmidt134118583879
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023111
2022398
20212,960
20202,899
20192,714
20182,447