Enzymatic profile of myocardial infarct

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/33419/1/0000821.pd

Study of J/ψ→ppˉJ/\psi\to p\bar{p} and J/ψ→nnˉJ/\psi\to n\bar{n}

The decays $J/\psi\to p\bar{p}$ and $J/\psi\to n\bar{n}$ have been investigated with a sample of 225.2 million $J/\psi$ events collected with the BESIII detector at the BEPCII $e^+e^-$ collider. The branching fractions are determined to be $\mathcal{B}(J/\psi\to p\bar{p})=(2.112\pm0.004\pm0.031)\times10^{-3}$ and $\mathcal{B}(J/\psi\to n\bar{n})=(2.07\pm0.01\pm0.17)\times10^{-3}$. Distributions of the angle $\theta$ between the proton or anti-neutron and the beam direction are well described by the form $1+\alpha\cos^2\theta$, and we find $\alpha=0.595\pm0.012\pm0.015$ for $J/\psi\to p\bar{p}$ and $\alpha=0.50\pm0.04\pm0.21$ for $J/\psi\to n\bar{n}$. Our branching-fraction results suggest a large phase angle between the strong and electromagnetic amplitudes describing the $J/\psi\to N\bar{N}$ decay.Comment: 16 pages, 13 figures, the 2nd version, submitted to PR

Phenotypic spectrum and transcriptomic profile associated with germline variants in TRAF7

PURPOSE: Somatic variants in tumor necrosis factor receptor-associated factor 7 (TRAF7) cause meningioma, while germline variants have recently been identified in seven patients with developmental delay and cardiac, facial, and digital anomalies. We aimed to define the clinical and mutational spectrum associated with TRAF7 germline variants in a large series of patients, and to determine the molecular effects of the variants through transcriptomic analysis of patient fibroblasts. METHODS: We performed exome, targeted capture, and Sanger sequencing of patients with undiagnosed developmental disorders, in multiple independent diagnostic or research centers. Phenotypic and mutational comparisons were facilitated through data exchange platforms. Whole-transcriptome sequencing was performed on RNA from patient- and control-derived fibroblasts. RESULTS: We identified heterozygous missense variants in TRAF7 as the cause of a developmental delay-malformation syndrome in 45 patients. Major features include a recognizable facial gestalt (characterized in particular by blepharophimosis), short neck, pectus carinatum, digital deviations, and patent ductus arteriosus. Almost all variants occur in the WD40 repeats and most are recurrent. Several differentially expressed genes were identified in patient fibroblasts. CONCLUSION: We provide the first large-scale analysis of the clinical and mutational spectrum associated with the TRAF7 developmental syndrome, and we shed light on its molecular etiology through transcriptome studies

Measurement of polarization amplitudes and CP asymmetries in B-0 -> phi K*(892)(0)

An angular analysis of the decay B (0) -> phi K (*)(892)(0) is reported based on a pp collision data sample, corresponding to an integrated luminosity of 1.0 fb(-1), collected at a centre-of-mass energy of root S = 7 TeV with the LHCb detector. The P-wave amplitudes and phases are measured with a greater precision than by previous experiments, and confirm about equal amounts of longitudinal and transverse polarization. The S-wave K+ pi(-) and K+ K- contributions are taken into account and found to be significant. A comparison of the B (0) -> phi K (*)(892)(0) and results shows no evidence for direct CP violation in the rate asymmetry, in the triple-product asymmetries or in the polarization amplitudes and phases

Assessing and treating victims of violence

San Francisco107 p.; 23 cm

Principles of trauma therapy : a guide to symptoms, evaluation and treatment/ Briere

295 hal.; 22 cm

Principles of trauma therapy : a guide to symptoms, evaluation and treatment/ Briere

295 hal.; 22 cm

Principles of trauma therapy : a guide to symptoms, evaluation and treatment/ Briere

295 hal.; 22 cm