Estimate of LHCb's sensitivity to the CKM angle using B0→D0K∗0B^0 \to D^0 K^{*0} Decays

In this note an updated event selection of the B0 -> D0 K*0 decay, with the D0 decaying into Kpi, KK, pipi is presented. The selection efficiencies are used to estimate the statistical error for determining the CKM phase applying a combination of the GLW and ADS methods

Instability Proof for Einstein-Yang-Mills Solitons and Black Holes with Arbitrary Gauge Groups

We prove that static, spherically symmetric, asymptotically flat soliton and black hole solutions of the Einstein-Yang-Mills equations are unstable for arbitrary gauge groups, at least for the ``generic" case. This conclusion is derived without explicit knowledge of the possible equilibrium solutions.Comment: 26 pages, LATEX, no figure

Optical vortices of slow light using tripod scheme

We consider propagation, storing and retrieval of slow light (probe beam) in a resonant atomic medium illuminated by two control laser beams of larger intensity. The probe and two control beams act on atoms in a tripod configuration of the light-matter coupling. The first control beam is allowed to have an orbital angular momentum (OAM). Application of the second vortex-free control laser ensures the adiabatic (lossles) propagation of the probe beam at the vortex core where the intensity of the first control laser goes to zero. Storing and release of the probe beam is accomplished by switching off and on the control laser beams leading to the transfer of the optical vortex from the first control beam to the regenerated probe field. A part of the stored probe beam remains frozen in the medium in the form of atomic spin excitations, the number of which increases with increasing the intensity of the second control laser. We analyse such losses in the regenerated probe beam and provide conditions for the optical vortex of the control beam to be transferred efficiently to the restored probe beam.Comment: 2 figure

Storage and Retrieval of a Squeezed Vacuum

Storage and retrieval of a squeezed vacuum was successfully demonstrated using electromagnetically induced transparency. 930ns of the squeezed vacuum pulse was incident on the laser cooled 87Rb atoms with an intense control light in a coherent state. When the squeezed vacuum pulse was slowed and spatially compressed in the cold atoms, the control light was switched off. After 3us of storage, the control light was switched on again and the squeezed vacuum was retrieved, as was confirmed using the time-domain homodyne method.Comment: 4 pages, 4 figures, to appear in Physical Review Letter

Lafutidine, a Protective H2 Receptor Antagonist, Enhances Mucosal Defense in Rat Esophagus

Luminal acid or CO2 induces a hyperemic response in the esophagus, via activation of acid sensors on capsaicin-sensitive afferent nerves (CSAN). Since disruption of the hyperemic response to luminal CO2 acidifies the interstitium of the esophageal mucosa, the hyperemic response may maintain interstitial pH (pHint). We hypothesized that acid-related hyperemia maintains pHint, preventing acid-induced injury in the esophageal mucosa. We examined the effects of capsaicin (Cap) or lafutidine (Laf), a mucosal protective H2 antagonist, on the regulation of pHint and blood flow in rat esophagus using ratiometric microimaging and laser-Doppler measurements of the lower esophageal mucosa of living rats. The esophagus was topically superfused with pH 7.0 buffer, or a pH 1.0 or pH 1.0 + pepsin (1 mg/ml) solution with or without Laf. Cap (30 or 100 µM) or Laf (0.1 or 1 mM) dose-dependently increased blood flow, accompanied by increased pHint. The pH 1.0 solution increased blood flow without pHint change, whereas Laf (1 mM) increased blood flow and pHint during acid exposure. The effects of Laf were abolished by ablation of CSAN. Perfusion of the acidified pepsin solution gradually decreased pHint, inhibited by Laf perfusion. Activation of CSAN by Laf with or without acid, accompanied by hyperemia, increased pHint, preventing acidified pepsin-induced interstitial acidification. Stimulation of the capsaicin pathway with compounds such as Laf enhances mucosal protection from acid-related injury in the upper gastrointestinal tract

The algorithm for FIR corrections of the VELO analogue links and its performance

The data from the VELO front-end is sent to the ADCs on the read-out board over a serial analogue link. Due imperfections in the link, inter-symbol cross talk occurs between adjacent time-bins in the transfer. This is corrected by an FIR filter implemented in the pre-processing FPGA locacted on the read-out board. This note reports on a method to determine the coefficients for the filter using date taken in-situ. Simulations are presented that show the performance of the methods as it is implemented in the LHCb read-out board. The effectiveness of the algorithm is demonstrated by the improvements in tracking performance on beam test data it brings

Reduced expression of Toll-like receptor 4 contributes to impaired cytokine response of monocytes in uremic patients

Toll-like receptors (TLRs) play a pivotal role in pathogen recognition and subsequent cytokine synthesis by immune cells. Uremic patients have a high infectious morbidity, but it remains unclear if this arises from the defective innate immune responses related to TLRs. We studied TLR4 expression in monocytes and their intracellular cytokine synthesis in response to lipopolysaccharide (LPS) stimulation in 35 predialysis patients with chronic kidney disease (CKD) with or without predisposition to bacterial infections and 16 age-matched controls. Expression of TLR4 in unstimulated peripheral monocytes was determined by staining with anti-TLR4 antibody and analysis with flow cytometry. Monocytes were then stimulated by LPS, labeled with anti-CD14 antibody, and subjected to intracellular cytokine staining and flow cytometry. Tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8 synthesis was examined in CD14+ monocytes. TLR4 expression was constitutively diminished in CKD patients with reduced expression being more severe in those CKD patients who were predisposed to infections. Monocytes from these infection prone CKD patients exhibited significantly reduced synthesis of TNF-α, IL-1β, IL-6, and IL-8 in response to LPS challenge compared with those from control subjects. The intensity of synthesis of each cytokine significantly correlated with TLR4 expression levels in monocytes (P<0.01). The capacity of monocytes to synthesize proinflammatory cytokines was significantly reduced in infection prone CKD patients, and this may possibly be due to the reduced monocyte expression of TLR4. Abnormal TLR4 expression by monocytes may play a role in the susceptibility of such patients to bacterial infections