Thermal compression of atomic hydrogen on helium surface

We describe experiments with spin-polarized atomic hydrogen gas adsorbed on liquid $^{4}$He surface. The surface gas density is increased locally by thermal compression up to $5.5\times10^{12}$ cm$^{-2}$ at 110 mK. This corresponds to the onset of quantum degeneracy with the thermal de-Broglie wavelength being 1.5 times larger than the mean interatomic spacing. The atoms were detected directly with a 129 GHz electron-spin resonance spectrometer probing both the surface and the bulk gas. This, and the simultaneous measurement of the recombination power, allowed us to make accurate studies of the adsorption isotherm and the heat removal from the adsorbed hydrogen gas. From the data, we estimate the thermal contact between 2D hydrogen gas and phonons of the helium film. We analyze the limitations of the thermal compression method and the possibility to reach the superfluid transition in 2D hydrogen gas.Comment: 20 pages, 11 figure

AdS Field Theory from Conformal Field Theory

We provide necessary and sufficient conditions for a Conformal Field Theory to have a description in terms of a perturbative Effective Field Theory in AdS. The first two conditions are well-known: the existence of a perturbative `1/N' expansion and an approximate Fock space of states generated by a finite number of low-dimension operators. We add a third condition, that the Mellin amplitudes of the CFT correlators must be well-approximated by functions that are bounded by a polynomial at infinity in Mellin space, or in other words, that the Mellin amplitudes have an effective theory-type expansion. We explain the relationship between our conditions and unitarity, and provide an analogy with scattering amplitudes that becomes exact in the flat space limit of AdS. The analysis also yields a simple connection between conformal blocks and AdS diagrams, providing a new calculational tool very much in the spirit of the S-Matrix program. We also begin to explore the potential pathologies associated with higher spin fields in AdS by generalizing Weinberg's soft theorems to AdS/CFT. The AdS analog of Weinberg's argument constrains the interactions of conserved currents in CFTs, but there are potential loopholes that are unavailable to theories of massless higher spin particles in flat spacetime.Comment: 31+7 pages, 5 figure

Technical Design Report for the PANDA Solenoid and Dipole Spectrometer Magnets

This document is the Technical Design Report covering the two large spectrometer magnets of the PANDA detector set-up. It shows the conceptual design of the magnets and their anticipated performance. It precedes the tender and procurement of the magnets and, hence, is subject to possible modifications arising during this process.Comment: 10 pages, 14MB, accepted by FAIR STI in May 2009, editors: Inti Lehmann (chair), Andrea Bersani, Yuri Lobanov, Jost Luehning, Jerzy Smyrski, Technical Coordiantor: Lars Schmitt, Bernd Lewandowski (deputy), Spokespersons: Ulrich Wiedner, Paola Gianotti (deputy

Feasibility studies of time-like proton electromagnetic form factors at PANDA at FAIR

Simulation results for future measurements of electromagnetic proton form factors at \PANDA (FAIR) within the PandaRoot software framework are reported. The statistical precision with which the proton form factors can be determined is estimated. The signal channel $\bar p p \to e^+ e^-$ is studied on the basis of two different but consistent procedures. The suppression of the main background channel, $\textit{i.e.}$ $\bar p p \to \pi^+ \pi^-$, is studied. Furthermore, the background versus signal efficiency, statistical and systematical uncertainties on the extracted proton form factors are evaluated using two different procedures. The results are consistent with those of a previous simulation study using an older, simplified framework. However, a slightly better precision is achieved in the PandaRoot study in a large range of momentum transfer, assuming the nominal beam conditions and detector performance

ГЕПАРИНИНДУЦИРОВАННАЯ ТРОМБОЦИТОПЕНИЯ (ОБЗОР)

Heparin-induced thrombocytopenia (HIT) is a serious and potentially life-threatening side effect of heparinotherapy. It is an antibody-mediated process that causes platelet activation, increases the procoagulant characteristics of the blood and, as a result, endangering limbs and life-threatening thrombosis. Venous thrombosis is more common than arterial thrombosis, especially deep vein thrombosis of the lower limbs and pulmonary artery thrombosis. Mortality from complications of heparinotherapy occurs with a frequency of 20–30 % of cases. Diagnosis of HIT is difficult. Such basic symptoms as thrombocytopenia and thrombosis are extremely non-specific and may be present in cancer patients and patients with cardiosurgical pathologies without the impact of heparin. Women are twice as likely to have HIT as men. This review describes pathogenesis, clinical features, modern diagnostic methods, risk factors for the emergence of this formidable complication of heparinotherapy, gives an overview of the most frequent use of drugs for the treatment of HIT, and gives modern clinical recommendations for different groups of patients.Гепарининдуцированная тромбоцитопения (ГИТ) является серьезным и потенциально опасным для жизни побочным эффектом проводимой гепаринотерапии. Это опосредованный антителами процесс, приводящий к активации тромбоцитов, повышению прокоагулянтных характеристик крови и, как результат, угрожающему конечностям и опасному для жизни тромбозу. Венозные тромбозы при этом случаются чаще, чем артериальные, особенно распространены тромбозы глубоких вен нижних конечностей и тромбоэмболии легочной артерии. Смертность от осложнений гепаринотерапии происходит с частотой 20–30% случаев. Диагностика ГИТ затруднена. Такие основные симптомы, как тромбоцитопения и тромбообразование, крайне неспецифичны и могут присутствовать у онкологических больных и больных с кардиохирургическими патологиями без воздействия гепарина. У женщин вероятность развития ГИТ в 2 раза выше, чем у мужчин. В данном обзоре описываются патогенез, клинические особенности, современные методы диагностики, факторы риска для возникновения этого грозного осложнения гепаринотерапии, приведен обзор наиболее частых в применении препаратов для лечения ГИТ, даны современные клинические рекомендации для разных групп пациентов

Analysis of eight genes modulating interferon gamma and human genetic susceptibility to tuberculosis: a case-control association study

<p>Abstract</p> <p>Background</p> <p>Interferon gamma is a major macrophage-activating cytokine during infection with <it>Mycobacterium tuberculosis</it>, the causative pathogen of tuberculosis, and its role has been well established in animal models and in humans. This cytokine is produced by activated T helper 1 cells, which can best deal with intracellular pathogens such as <it>M. tuberculosis</it>. Based on the hypothesis that genes which regulate interferon gamma may influence tuberculosis susceptibility, we investigated polymorphisms in eight candidate genes.</p> <p>Methods</p> <p>Fifty-four polymorphisms in eight candidate genes were genotyped in over 800 tuberculosis cases and healthy controls in a population-based case-control association study in a South African population. Genotyping methods used included the SNPlex Genotyping System™, capillary electrophoresis of fluorescently labelled PCR products, TaqMan^®SNP genotyping assays or the amplification mutation refraction system. Single polymorphisms as well as haplotypes of the variants were tested for association with TB using statistical analyses.</p> <p>Results</p> <p>A haplotype in interleukin 12B was nominally associated with tuberculosis (p = 0.02), but after permutation testing, done to assess the significance for the entire analysis, this was not globally significant. In addition a novel allele was found for the interleukin 12B D5S2941 microsatellite.</p> <p>Conclusions</p> <p>This study highlights the importance of using larger sample sizes when attempting validation of previously reported genetic associations. Initial studies may be false positives or may propose a stronger genetic effect than subsequently found to be the case.</p