Measurement of the branching ratio of the decay KL -> pi e nu and extraction of the CKM parameter |Vus|

We present a new measurement of the branching ratio R of the decay KL -> pi e nu (Ke3), relative to all charged KL decays with two tracks, based on data taken with the NA48 detector at the CERN SPS. We measure R = 0.4978 +- 0.0035. From this we derive the Ke3 branching fraction and the weak coupling parameter |Vus| in the CKM matrix. We obtain |Vus|f+(0) = 0.2146 +- 0.0016, where f+(0) is the vector form factor in the Ke3 decay.Comment: 18 pages, 8 figures. accepted by Phys Lett.

Measurement of K^0_e3 form factors

The semileptonic decay of the neutral K meson, KL -> pi e nu (Ke3), was used to study the strangeness-changing weak interaction of hadrons. A sample of 5.6 million reconstructed events recorded by the NA48 experiment was used to measure the Dalitz plot density. Admitting all possible Lorentz-covariant couplings, the form factors for vector (f_+(q^2)), scalar (f_S) and tensor (f_T) interactions were measured. The linear slope of the vector form factor lambda_+ = 0.0284+-0.0007+-0.0013 and values for the ratios |f_S/f_+(0)| = 0.015^{+0.007}_{-0.010}+-0.012 and |f_T/f_+(0)| = 0.05^{+0.03}_{-0.04}+-0.03 were obtained. The values for f_S and f_T are consistent with zero. Assuming only Vector-Axial vector couplings, lambda_+ = 0.0288+-0.0004+-0.0011 and a good fit consistent with pure V-A couplings were obtained. Alternatively, a fit to a dipole form factor yields a pole mass of M = 859+-18 MeV, consistent with the K^*(892) mass.Comment: 16 pages, 7 figures. submitted to Phys. Lett.

Systematic review and meta-analysis of the diagnostic accuracy of ultrasonography for deep vein thrombosis

Background Ultrasound (US) has largely replaced contrast venography as the definitive diagnostic test for deep vein thrombosis (DVT). We aimed to derive a definitive estimate of the diagnostic accuracy of US for clinically suspected DVT and identify study-level factors that might predict accuracy. Methods We undertook a systematic review, meta-analysis and meta-regression of diagnostic cohort studies that compared US to contrast venography in patients with suspected DVT. We searched Medline, EMBASE, CINAHL, Web of Science, Cochrane Database of Systematic Reviews, Cochrane Controlled Trials Register, Database of Reviews of Effectiveness, the ACP Journal Club, and citation lists (1966 to April 2004). Random effects meta-analysis was used to derive pooled estimates of sensitivity and specificity. Random effects meta-regression was used to identify study-level covariates that predicted diagnostic performance. Results We identified 100 cohorts comparing US to venography in patients with suspected DVT. Overall sensitivity for proximal DVT (95% confidence interval) was 94.2% (93.2 to 95.0), for distal DVT was 63.5% (59.8 to 67.0), and specificity was 93.8% (93.1 to 94.4). Duplex US had pooled sensitivity of 96.5% (95.1 to 97.6) for proximal DVT, 71.2% (64.6 to 77.2) for distal DVT and specificity of 94.0% (92.8 to 95.1). Triplex US had pooled sensitivity of 96.4% (94.4 to 97.1%) for proximal DVT, 75.2% (67.7 to 81.6) for distal DVT and specificity of 94.3% (92.5 to 95.8). Compression US alone had pooled sensitivity of 93.8 % (92.0 to 95.3%) for proximal DVT, 56.8% (49.0 to 66.4) for distal DVT and specificity of 97.8% (97.0 to 98.4). Sensitivity was higher in more recently published studies and in cohorts with higher prevalence of DVT and more proximal DVT, and was lower in cohorts that reported interpretation by a radiologist. Specificity was higher in cohorts that excluded patients with previous DVT. No studies were identified that compared repeat US to venography in all patients. Repeat US appears to have a positive yield of 1.3%, with 89% of these being confirmed by venography. Conclusion Combined colour-doppler US techniques have optimal sensitivity, while compression US has optimal specificity for DVT. However, all estimates are subject to substantial unexplained heterogeneity. The role of repeat scanning is very uncertain and based upon limited data

BC-box protein domain-related mechanism for VHL protein degradation

The tumor suppressor VHL (von Hippel–Lindau) protein is a substrate receptor for Ubiquitin Cullin Ring Ligase complexes (CRLs), containing a BC-box domain that associates to the adaptor Elongin B/C. VHL targets hypoxia-inducible factor 1α to proteasome-dependent degradation. Gam1 is an adenoviral protein, which also possesses a BC-box domain that interacts with the host Elongin B/C, thereby acting as a viral substrate receptor. Gam1 associates with both Cullin2 and Cullin5 to form CRL complexes targeting the host protein SUMO enzyme SAE1 for proteasomal degradation. We show that Gam1 protein expression induces VHL protein degradation leading to hypoxia-inducible factor 1α stabilization and induction of its downstream targets. We also characterize the CRL-dependent mechanism that drives VHL protein degradation via proteasome. Interestingly, expression of Suppressor of Cytokine Signaling (SOCS) domain-containing viral proteins and cellular BC-box proteins leads to VHL protein degradation, in a SOCS domain-containing manner. Our work underscores the exquisite ability of viral domains to uncover new regulatory mechanisms by hijacking key cellular proteins