University of Würzburg

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.

Performance of pile-up mitigation techniques for jets in pp collisions at √s = 8 TeV using the ATLAS detector

Abstract: The large rate of multiple simultaneous protonproton interactions, or pile-up, generated by the Large Hadron Collider in Run 1 required the development of many new techniques to mitigate the advers ...

Wender Utah Rating Scale (WURS-k). Die deutsche Kurzform zur retrospektiven Erfassung des hyperkinetischen Syndroms bei Erwachsenen

Abstract: Die diagnostische Abklarung einer Aufmerksamkeitsdefizit/Hyperaktivitatsstorung beim Erwachsenen macht die retrospektive Erfassung von Krankheitssymptomen, die bereits im Kindesalter bestanden, notwendig. Die Wender Utah Rating Scale (WURS) ist ein hierfur entwickelter Fragebogen. In der vorliegenden Arbeit wurde die deutsche Ubersetzung der WURS einer statistischen Analyse unterzogen. Grundlage fur diese Analyse bildete die Untersuchung von insgesamt 703 Probanden. Anhand der korrigierten Trennscharfeindizes wurde unter Berucksichtigung der mittleren Antwortauspragung sowie inhaltlicher Aspekte der Items eine Itemselektion durchgefuhrt. Nach der Itemselektion verblieben 21 Items mit einer korrigierten Trennscharfe ri(t–i) zwischen 0,19 und 0,61 in der Fragebogenendform. Die Retestreliabilitat der gekurzten Version betrug r=0,9.

The Genetic Basis of Resistance to Anticoagulants in Rodents

Abstract: Anticoagulant compounds, i.e., derivatives of either 4-hydroxycoumarin (e.g., warfarin, bromadiolone) or indane-1,3-dione (e.g., diphacinone, chlorophacinone), have been in worldwide use as rodenticides for >50 years. These compounds inhibit blood coagulation by repression of the vitamin K reductase reaction (VKOR). Anticoagulant-resistant rodent populations have been reported from many countries and pose a considerable problem for pest control. Resistance is transmitted as an autosomal dominant trait although, until recently, the basic genetic mutation was unknown. Here, we report on the identification of eight different mutations in the VKORC1 gene in resistant laboratory strains of brown rats and house mice and in wild-caught brown rats from various locations in Europe with five of these mutations affecting only two amino acids (Tyr139Cys, Tyr139Ser, Tyr139Phe and Leu128Gln, Leu128Ser). By recombinant expression of VKORC1 constructs in HEK293 cells we demonstrate that mutations at Tyr139 confer resistance to warfarin at variable degrees while the other mutations, in addition, dramatically reduce VKOR activity. Our data strongly argue for at least seven independent mutation events in brown rats and two in mice. They suggest that mutations in VKORC1 are the genetic basis of anticoagulant resistance in wild populations of rodents, although the mutations alone do not explain all aspects of resistance that have been reported. We hypothesize that these mutations, apart from generating structural changes in the VKORC1 protein, may induce compensatory mechanisms to maintain blood clotting. Our findings provide the basis for a DNA-based field monitoring of anticoagulant resistance in rodents.

Serum levels of autoantibodies to BP180 correlate with disease activity in patients with bullous pemphigoid.

Abstract: Objective To investigate the possible correlation of levels of circulating anti-BP180 autoantibodies with disease activity in bullous pemphigoid (BP). Design Diagnostic study. Setting Regional referral center at a university dermatology department. Patients Fifteen patients with typical clinical, histologic, and immunofluorescence findings of BP who had not received prior systemic treatment. Interventions Initially, 6 consecutive patients with BP were treated with oral doxycycline and niacinamide. Subsequently, 9 consecutive patients with BP received a combination of oral dapsone and prednisolone. Main Outcome Measures Disease activity, serum levels of autoantibodies to BP180, and titers of anti–basement membrane zone autoantibodies were assayed before initiation of treatment and 4 and 8 weeks later. Reactivity to BP180 was analyzed by enzyme-linked immunosorbent assay using a recombinant form of BP180 NC16A. Titers of anti–basement membrane zone autoantibodies were assayed by indirect immunofluorescence on 1-mol/L sodium chloride–split human skin. Results In both treatment groups, disease activity correlated with serum levels of autoantibodies to BP180 NC16A ( P = .004 [dapsone-prednisolone] and .007 [doxycycline-niacinamide]). No correlation was seen between disease activity and indirect immunofluorescence reactivity ( P = .18 and .16, respectively). In patients receiving dapsone plus prednisolone, the dose of corticosteroids necessary to suppress new blister formation correlated with anti-BP180 reactivity ( P = .002). Conclusions In contrast to indirect immunofluorescence reactivity that reflects reactivity to both BP180 and BP230, serum levels of autoantibodies to BP180 correlate with disease activity in BP. Assaying reactivity to BP180 should be a helpful guide for the therapeutic management of patients with this disease. Our results underline the pathogenic relevance of autoantibodies to human BP180.

Genome-wide association study reveals two new risk loci for bipolar disorder

Abstract: Bipolar disorder (BD) is a common and highly heritable mental illness and genome-wide association studies (GWAS) have robustly identified the first common genetic variants involved in disease aetiology. The data also provide strong evidence for the presence of multiple additional risk loci, each contributing a relatively small effect to BD susceptibility. Large samples are necessary to detect these risk loci. Here we present results from the largest BD GWAS to date by investigating 2.3 million single-nucleotide polymorphisms (SNPs) in a sample of 24,025 patients and controls. We detect 56 genome-wide significant SNPs in five chromosomal regions including previously reported risk loci ANK3, ODZ4 and TRANK1, as well as the risk locus ADCY2 (5p15.31) and a region between MIR2113 and POU3F2 (6q16.1). ADCY2 is a key enzyme in cAMP signalling and our finding provides new insights into the biological mechanisms involved in the development of BD.