50 research outputs found
G factor of the 59/2 - isomer in Gd147
The g factor of the 10 995 keV, Je=(59/2-, and T1/2=0.8 ns level in Gd147 has been determined by the transient field method for ions recoiling through a magnetized Gd foil at a temperature of 100 K. The Ge76(76Ge,5n)147Gd reaction at E(76Ge)=310 MeV was used to provide high recoil velocity. A 100 ps flight time in vacuum between the target and the ferromagnet of 100 ps ensured that the -ray cascades fed the (59/2 level before the recoil ions traversed the Gd foil. The g factor was extracted from standard double ratios with the known parametrization of the transient field, yielding g=0.38(7). This value is in agreement with the predicted wave function and experimental single-particle moments in this mass region. Results for levels in 146,148Gd were also obtained
Nonleptonic decays to , and other final states in Factorization
We consider nonleptonic Cabibbo--allowed decays in the
factorization approximation. We calculate nonleptonic decays of the type and relative to
and where we include among the
pseudoscalar states(P) and the vector states(V) the newly discovered
resonances, and . In the ratio of decays to
and relative to the decays to these states,
the poorly known decay constants of and cancel leading
to predictions that can shed light on the nature of these new states. In
general, we predict the decays to be larger than the corresponding
decays and in particular we find the branching ratio for can be between four to five times the branching ratio
for . This enhancement of branching
ratios follows primarily from the fact that more partial waves contribute in
decays than in decays. Our predictions are largely
independent of model calculations of hadronic inputs like form factors and
decay constants.Comment: 16 pages LaTe
Hepatobiliary long-term consequences of COVID-19: dramatically increased rate of secondary sclerosing cholangitis in critically ill COVID-19 patients
BACKGROUND: Increasing evidence suggests that secondary sclerosing cholangitis (SSC), which can lead to cirrhosis or liver failure, may be a hepatobiliary long-term complication of COVID-19. The aim of this study was to estimate the frequency and outcome of this COVID-19 sequela and to identify possible risk factors. METHODS: This observational study, conducted at University Hospital Charité Berlin and Unfallkrankenhaus Berlin, Germany, involved hospitalized patients with COVID-19 pneumonia, including 1082 ventilated COVID-19 patients. We compared COVID-19 patients who developed SSC with a COVID-19 control group by univariate and multivariate analyses. RESULTS: SSC occurrence after COVID-19 was observed exclusively in critically ill patients with invasive ventilation, albeit with extreme clustering among them. One in every 43 invasively ventilated COVID-19 patients developed this complication. Risk factors preceding the development of secondary sclerosing cholangitis in critically ill COVID-19 patients (SSC-CIP) were signs of systemic reduced blood oxygen supply (e.g., low PaO(2)/FiO(2), ischemic organ infarctions), multi-organ failure (high SOFA score) at admission, high fibrinogen levels and intravenous ketamine use. Multivariate analysis confirmed fibrinogen and increased plasma lactate dehydrogenase as independent risk factors associated with cholangiopathy onset. The 1-year transplant-free survival rate of COVID-19-associated SSC-CIP was 40%. CONCLUSIONS: COVID-19 causes SSC-CIP in a substantial proportion of critically ill patients. SSC-CIP most likely develops due to severe tissue hypoxia and fibrinogen-associated circulatory disturbances. A significant increase of patients with SSC-CIP is to be expected in the post-COVID era