51 research outputs found
New Measurement of Parity Violation in Elastic Electron-Proton Scattering and Implications for Strange Form Factors
We have measured the parity-violating electroweak asymmetry in the elastic
scattering of polarized electrons from the proton. The result is A = -15.05 +-
0.98(stat) +- 0.56(syst) ppm at the kinematic point theta_lab = 12.3 degrees
and Q^2 = 0.477 (GeV/c)^2. The measurement implies that the value for the
strange form factor (G_E^s + 0.392 G_M^s) = 0.025 +- 0.020 +- 0.014, where the
first error is experimental and the second arises from the uncertainties in
electromagnetic form factors. This measurement is the first fixed-target parity
violation experiment that used either a `strained' GaAs photocathode to produce
highly polarized electrons or a Compton polarimeter to continuously monitor the
electron beam polarization.Comment: 8 pages, 4 figures, Tex, elsart.cls; revised version as accepted for
Phys. Lett.
Display of probability densities for data from a continuous distribution
Based on cumulative distribution functions, Fourier series expansion and
Kolmogorov tests, we present a simple method to display probability densities
for data drawn from a continuous distribution. It is often more efficient than
using histograms.Comment: 5 pages, 4 figures, presented at Computer Simulation Studies XXIV,
Athens, GA, 201
Measurement of the Generalized Polarizabilities of the Proton in Virtual Scattering at Q2=0.92 and 1.76 GeV2: I. Low Energy Expansion Analysis
Virtual Compton Scattering is studied at the Thomas Jefferson National
Accelerator Facility at low Center-of-Mass energies, below pion threshold.
Following the Low Energy Theorem for the process, we obtain
values for the two structure functions Pll-Ptt/epsilon and Plt at four-momentum
transfer squared Q2=0.92 and 1.76 GeV2.Comment: 4 pages, 2 figures, to be submitted to PRL. Figs 1 and 2, lettering
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Relationship Between Cytomegalovirus Infection and Steroid Resistance in Inflammatory Bowel Disease: A Meta-Analysis
Results of Hepatitis C Birth-Cohort Testing and Linkage to Care in Selected U.S. Sites, 2012–2014
Impact of Copayment Changes on Children's Albuterol Inhaler Use and Costs after the Clean Air Act Chlorofluorocarbon Ban
Long-term outcome of patients with steroid-refractory acute severe UC treated with ciclosporin or infliximab
OBJECTIVE: Ciclosporin and infliximab have demonstrated short-term similar efficacy as second-line therapies in patients with acute severe UC (ASUC) refractory to intravenous steroids. The aim of this study was to assess long-term outcome of patients included in a randomised trial comparing ciclosporin and infliximab. DESIGN: Between 2007 and 2010, 115 patients with steroid-refractory ASUC were randomised in 29 European centres to receive ciclosporin or infliximab in association with azathioprine. Patients were followed until death or last news up to January 2015. Colectomy-free survival rates at 1 and 5 years and changes in therapy were estimated through Kaplan-Meier method and compared between initial treatment groups through log-rank test. RESULTS: After a median follow-up of 5.4 years, colectomy-free survival rates (95% CI) at 1 and 5 years were, respectively, 70.9% (59.2% to 82.6%) and 61.5% (48.7% to 74.2%) in patients who received ciclosporin and 69.1% (56.9% to 81.3%) and 65.1% (52.4% to 77.8%) in those who received infliximab (p=0.97). Cumulative incidence of first infliximab use at 1 and 5 years in patients initially treated with ciclosporin was, respectively, 45.7% (32.6% to 57.9%) and 57.1% (43.0% to 69.0%). Only four patients from the infliximab group were subsequently switched to ciclosporin. Three patients died during the follow-up, none directly related to UC or its treatment. CONCLUSIONS: In this cohort of patients with steroid-refractory ASUC initially treated by ciclosporin or infliximab, long-term colectomy-free survival was independent from initial treatment. These long-term results further confirm a similar efficacy and good safety profiles of both drugs and do not favour one drug over the other. TRIAL REGISTRATION NUMBER: EudraCT: 2006-005299-42; ClinicalTrials.gouv number: NCT00542152; post-results.status: publishe
Cost savings of anti-TNF therapy using a test-based strategy versus an empirical dose escalation in Crohn's disease patients who lose response to infliximab
Molecular modeling reveals the novel inhibition mechanism and binding mode of three natural compounds to staphylococcal α-hemolysin.
α-Hemolysin (α-HL) is a self-assembling, channel-forming toxin that is produced as a soluble monomer by Staphylococcus aureus strains. Until now, α-HL has been a significant virulence target for the treatment of S. aureus infection. In our previous report, we demonstrated that some natural compounds could bind to α-HL. Due to the binding of those compounds, the conformational transition of α-HL from the monomer to the oligomer was blocked, which resulted in inhibition of the hemolytic activity of α-HL. However, these results have not indicated how the binding of the α-HL inhibitors influence the conformational transition of the whole protein during the oligomerization process. In this study, we found that three natural compounds, Oroxylin A 7-O-glucuronide (OLG), Oroxin A (ORA), and Oroxin B (ORB), when inhibiting the hemolytic activity of α-HL, could bind to the "stem" region of α-HL. This was completed using conventional Molecular Dynamics (MD) simulations. By interacting with the novel binding sites of α-HL, the ligands could form strong interactions with both sides of the binding cavity. The results of the principal component analysis (PCA) indicated that because of the inhibitors that bind to the "stem" region of α-HL, the conformational transition of α-HL from the monomer to the oligomer was restricted. This caused the inhibition of the hemolytic activity of α-HL. This novel inhibition mechanism has been confirmed by both the steered MD simulations and the experimental data obtained from a deoxycholate-induced oligomerization assay. This study can facilitate the design of new antibacterial drugs against S. aureus
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