Wolfgang Wagner

Bio: Wolfgang Wagner is an academic researcher from Vienna University of Technology. The author has contributed to research in topics: Large Hadron Collider & Top quark. The author has an hindex of 156, co-authored 2342 publications receiving 123391 citations. Previous affiliations of Wolfgang Wagner include University of Pennsylvania & University of Amsterdam.

Search for supersymmetry in pp collisions at root s=7 Te V in final states with missing transverse momentum and b-jets with the ATLAS detector

Abstract: The results of a search for supersymmetry in events with large missing transverse momentum and heavy-flavor jets using an integrated luminosity corresponding to 2.05 fb(-1) of pp collisions at root ...

Modeling of replicative senescence in hematopoietic development.

Abstract: Hematopoietic stem cells (HSC) give rise to an enormous number of blood cells throughout our life. In contrast their number of cell divisions preceding senescence is limited underin vitro culture conditions. Here we consider the question whether HSC can rejuvenate indefinitely or if the number of cell divisions is restricted. We have developed a multi-compartmental model for hematopoietic differentiation based on ordinary differential equations. The model is based on the hypothesis that in each step of maturation, the percentage of self-renewal versus differentiation is regulated by a single external feedback mechanism. We simulate the model under the assumption that hematopoietic differentiation precedes the six steps of maturation and the cells ultimately cease to proliferate after 50 divisions. Our results demonstrate that it is conceivable to maintain hematopoiesis over a life-time if HSC have a slow division rate and a high self-renewal rate. With age, the feedback signal increases and this enhances self-renewal, which results in the increase of the number of stem and progenitor cells. This study demonstrates that replicative senescence is compatible with life-long hematopoiesis and that model predictions are in line with experimental observations. Thus, HSC might not divide indefinitely with potentially important clinical implications.

Search for doubly charged Higgs bosons decaying to dileptons in p(p)over-bar collisions at root s=1.96 TeV

Abstract: We present the results of a search for doubly-charged Higgs bosons (H+/-+/-) decaying to dileptons using ~240/pb of ppbar collision data collected by the CDF II experiment at the Fermilab Tevatron. In our search region, given by same-sign dilepton mass m_ll' > 80 GeV/c^2 (100 GeV/c^2 for dielectron channel), we observe no evidence for doubly-charged Higgs production. We set limits on sigma (ppbar --> H++H-- --> l+l+l-l-) as a function of the mass of the doubly-charged Higgs boson and the chirality of its couplings. Assuming exclusive same-sign dilepton decays, we derive lower mass limits on H+/-+/-_L of 133 GeV/c^2, 136 GeV/c^2, and 115 GeV/c^2 in the ee, mu mu, and e mu channels, respectively, and a lower mass limit of 113 GeV/c^2 on H+/-+/-_R in the mu mu channel, all at the 95% confidence level.

Inclusive Search for Squark and Gluino Production in p(p)over-bar Collisions at root s = TeV

Abstract: We report on a search for inclusive production of squarks and gluinos in p{bar p} collisions at {radical}s = 1.96 TeV, in events with large missing transverse energy and multiple jets of hadrons in the final state. The study uses a CDF Run II data sample corresponding to 2 fb-1 of integrated luminosity. The data are in good agreement with the standard model predictions, giving no evidence for any squark or gluino component. In an R-parity conserving minimal supergravity scenario with A{sub 0} = 0, mu < 0 and tan beta = 5, 95% C.L. upper limits on the production cross sections in the range between 0.1 pb and 1 pb are obtained, depending on the squark and gluino masses considered. For gluino masses below 280 GeV/c2, arbitrarily large squark masses are excluded at the 95%C.L., while for mass degenerate gluinos and squarks, masses below 392 GeV/c2 are excluded at the 95% C.L.

I and i

Abstract: There is, I think, something ethereal about i —the square root of minus one. I remember first hearing about it at school. It seemed an odd beast at that time—an intruder hovering on the edge of reality. Usually familiarity dulls this sense of the bizarre, but in the case of i it was the reverse: over the years the sense of its surreal nature intensified. It seemed that it was impossible to write mathematics that described the real world in …

Fast parallel algorithms for short-range molecular dynamics

Abstract: Three parallel algorithms for classical molecular dynamics are presented. The first assigns each processor a fixed subset of atoms; the second assigns each a fixed subset of inter-atomic forces to compute; the third assigns each a fixed spatial region. The algorithms are suitable for molecular dynamics models which can be difficult to parallelize efficiently—those with short-range forces where the neighbors of each atom change rapidly. They can be implemented on any distributed-memory parallel machine which allows for message-passing of data between independently executing processors. The algorithms are tested on a standard Lennard-Jones benchmark problem for system sizes ranging from 500 to 100,000,000 atoms on several parallel supercomputers--the nCUBE 2, Intel iPSC/860 and Paragon, and Cray T3D. Comparing the results to the fastest reported vectorized Cray Y-MP and C90 algorithm shows that the current generation of parallel machines is competitive with conventional vector supercomputers even for small problems. For large problems, the spatial algorithm achieves parallel efficiencies of 90% and a 1840-node Intel Paragon performs up to 165 faster than a single Cray C9O processor. Trade-offs between the three algorithms and guidelines for adapting them to more complex molecular dynamics simulations are also discussed.

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。