5,652 research outputs found
Systematics of heavy-ion fusion hindrance at extreme sub-barrier energies
The recent discovery of hindrance in heavy-ion induced fusion reactions at
extreme sub-barrier energies represents a challenge for theoretical models.
Previously, it has been shown that in medium-heavy systems, the onset of fusion
hindrance depends strongly on the "stiffness" of the nuclei in the entrance
channel. In this work, we explore its dependence on the total mass and the
-value of the fusing systems and find that the fusion hindrance depends in a
systematic way on the entrance channel properties over a wide range of systems.Comment: Submitted to Phys. Rev. Lett., 5 pages, 3 figure
Bid participates in genotoxic drug-induced apoptosis of HeLa cells and is essential for death receptor ligands' apoptotic and synergistic effects
Background: The BH3-only protein Bid is an important component of death receptor-mediated caspase activation. Bid is cleaved by caspase-8 or -10 into t-Bid, which translocates to mitochondria and triggers the release of caspase-activating factors. Bid has also been reported to be cleaved by other proteases. Methodology/Principal Findings: To test the hypothesis that Bid is a central mediator of stress-induced apoptosis, we investigated the effects of a small molecule Bid inhibitor on stress-induced apoptosis, and generated HeLa cells deficient for Bid. Stable knockdown of bid lead to a pronounced resistance to Fas/CD95- and TRAIL-induced caspase activation and apoptosis, and significantly increased clonogenic survival. While Bid-deficient cells were equally sensitive to ER stress-induced apoptosis, they showed moderate, but significantly reduced levels of apoptosis, as well as increased clonogenic survival in response to the genotoxic drugs Etoposide, Oxaliplatin, and Doxorubicin. Similar effects were observed using the Bid inhibitor BI6C9. Interestingly, Bid-deficient cells were dramatically protected from apoptosis when subtoxic concentrations of ER stressors, Etoposide or Oxaliplatin were combined with subtoxic TRAIL concentrations. Conclusions/Significance: Our data demonstrate that Bid is central for death receptor-induced cell death and participates in anti-cancer drug-induced apoptosis in human cervical cancer HeLa cells. They also show that the synergistic effects of TRAIL in combination with either ER stressors or genotoxic anti-cancer drugs are nearly exclusively mediated via an increased activation of Bid-induced apoptosis signalling
Upper Limit on the molecular resonance strengths in the C+C fusion reaction
Carbon burning is a crucial process for a number of important astrophysical
scenarios. The lowest measured energy is around E=2.1 MeV, only
partially overlapping with the energy range of astrophysical interest. The
currently adopted reaction rates are based on an extrapolation which is highly
uncertain because of potential resonances existing in the unmeasured energy
range and the complication of the effective nuclear potential. By comparing the
cross sections of the three carbon isotope fusion reactions,
C+C, C+C and C+C, we have
established an upper limit on the molecular resonance strengths in
C+C fusion reaction. The preliminary results are presented
and the impact on nuclear astrophysics is discussed.Comment: 4 pages, 3 figures, FUSION11 conference proceedin
Role of break-up processes in fusion enhancement of drip-line nuclei at energies below the Coulomb barrier
We carry out realistic coupled-channels calculations for
Be + Pb reaction in order to discuss the effects of break-up
of the projectile nucleus on sub-barrier fusion.
We discretize in energy the particle continuum states, which are associated
with the break-up process, and construct the coupling form factors to these
states on a microscopic basis.
The incoming boundary condition is employed in solving coupled-channels
equations, which enables us to define the flux for complete fusion inside the
Coulomb barrier. It is shown that complete fusion cross sections are
significantly enhanced due to the couplings to the continuum states compared
with the no coupling case at energies below the Coulomb barrier, while they are
hindered at above barrier energies.Comment: RevTex, 3 pages, 5 figure
Determination of Omega_b From Big Bang Nucleosynthesis in the Presence of Regions of Antimatter
Production of regions of antimatter in the early universe is predicted in
many baryogenesis models. Small scale antimatter regions would annihilate
during or soon after nucleosynthesis, affecting the abundances of the light
elements. In this paper we study how the acceptable range in Omega_b changes in
the presence of antimatter regions, as compared to the standard big bang
nucleosynthesis. It turns out that it is possible to produce at the same time
both a low 4He value (Y_p < 0.240) and a low D/H value (D/H < 4e-5), but
overproduction of 7Li is unavoidable at large Omega_b.Comment: 9 pages, PRD version, ref. 6 correcte
Mortality risk and mental disorders: longitudinal results from the Upper Bavarian Study
The object of the study was the assessment of the mortality risk for persons with a mental disorder in an unselected representative community sample assessed longitudinally. Subjects from a rural area in Upper Bavaria (Germany) participated in semi-structured interviews conducted by research physicians in the 1970s (first assessment) and death-certificate diagnoses were obtained after an interval up to 13 years later. The sample consisted of 1668 community residents aged 15 years and over. Cox regression estimates resulted in an odds ratio of 1·35 (confidence interval 1·01 to 1·81) for persons with a mental disorder classified as marked to very severe. The odds ratio increased with increasing severity of mental illness from 1·04 for mild disorders, 1·30 for marked disorders, to 1·64 for severe or very severe disorders. The relative risk (odds ratio) for persons with a mental disorder only and no somatic disorder was 1·22, for persons with only a somatic disorder 2·00, and for those with both a mental and a somatic disorder 2·13. The presence of somatic illness was responsible for most of the excess mortality. Somatic disorders associated with excess mortality in mental disorders were diseases of the nervous system or sensory organs, diseases of the circulatory system, diseases of the gastrointestinal tract, and diseases of the skeleton, muscles and connective tissue (ICD-8). Thus, while mental illness alone had a limited effect on excess mortality, comorbidity with certain somatic disorders had a significant effec
The endothelial glycocalyx prefers albumin for evoking shear stress-induced, nitric oxide-mediated coronary dilatation
Background: Shear stress induces coronary dilatation via production of nitric oxide ( NO). This should involve the endothelial glycocalyx ( EG). A greater effect was expected of albumin versus hydroxyethyl starch ( HES) perfusion, because albumin seals coronary leaks more effectively than HES in an EG-dependent way. Methods: Isolated hearts ( guinea pigs) were perfused at constant pressure with Krebs-Henseleit buffer augmented with 1/3 volume 5% human albumin or 6% HES ( 200/0.5 or 450/0.7). Coronary flow was also determined after EG digestion ( heparinase) and with nitro-L-arginine ( NO-L-Ag). Results: Coronary flow ( 9.50 +/- 1.09, 5.10 +/- 0.49, 4.87 +/- 1.19 and 4.15 +/- 0.09 ml/ min/ g for `albumin', `HES 200', `HES 450' and `control', respectively, n = 5-6) did not correlate with perfusate viscosity ( 0.83, 1.02, 1.24 and 0.77 cP, respectively). NO-L-Ag and heparinase diminished dilatation by albumin, but not additively. Alone NO-L-Ag suppressed coronary flow during infusion of HES 450. Electron microscopy revealed a coronary EG of 300 nm, reduced to 20 nm after heparinase. Cultured endothelial cells possessed an EG of 20 nm to begin with. Conclusions: Albumin induces greater endothelial shear stress than HES, despite lower viscosity, provided the EG contains negative groups. HES 450 causes some NO-mediated dilatation via even a rudimentary EG. Cultured endothelial cells express only a rudimentary glycocalyx, limiting their usefulness as a model system. Copyright (c) 2007 S. Karger AG, Basel
Alcohol-attributable mortality in Switzerland in 2011--age-specific causes of death and impact of heavy versus non-heavy drinking.
BACKGROUND: Alcohol use causes high burden of disease and injury globally. Switzerland has a high consumption of alcohol, almost twice the global average. Alcohol-attributable deaths and years of life lost in Switzerland were estimated by age and sex for the year 2011. Additionally, the impact of heavy drinking (40+grams/day for women and 60+g/day for men) was estimated.
METHODS: Alcohol consumption estimates were based on the Addiction Monitoring in Switzerland study and were adjusted to per capita consumption based on sales data. Mortality data were taken from the Swiss mortality register. Methodology of the Comparative Risk Assessment for alcohol was used to estimate alcohol-attributable fractions.
RESULTS: Alcohol use caused 1,600 (95% CI: 1,472 - 1,728) net deaths (1,768 deaths caused, 168 deaths prevented) among 15 to 74 year olds, corresponding to 8.7% of all deaths (men: 1,181 deaths; women: 419 deaths). Overall, 42,627 years of life (9.7%, 95% CI: 40,245 - 45,008) were lost due to alcohol. Main causes of alcohol-attributable mortality were injuries at younger ages (15-34 years), with increasing age digestive diseases (mainly liver cirrhosis) and cancers (particularly breast cancers among women). The majority (62%) of all alcohol-attributable deaths was caused by chronic heavy drinking (men: 67%; women: 48 %).
CONCLUSION: Alcohol is a major cause of premature mortality in Switzerland. Its impact, among young people mainly via injuries, among men mainly through heavy drinking, calls for a mix of preventive actions targeting chronic heavy drinking, binge drinking and mean consumption
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