Global existence and exponential decay for hyperbolic dissipative relativistic fluid theories

We consider dissipative relativistic fluid theories on a fixed flat, compact, globally hyperbolic, Lorentzian manifold. We prove that for all initial data in a small enough neighborhood of the equilibrium states (in an appropriate Sobolev norm), the solutions evolve smoothly in time forever and decay exponentially to some, in general undetermined, equilibrium state. To prove this, three conditions are imposed on these theories. The first condition requires the system of equations to be symmetric hyperbolic, a fundamental requisite to have a well posed and physically consistent initial value formulation. The second condition is a generic consequence of the entropy law, and is imposed on the non principal part of the equations. The third condition is imposed on the principal part of the equations and it implies that the dissipation affects all the fields of the theory. With these requirements we prove that all the eigenvalues of the symbol associated to the system of equations of the fluid theory have strictly negative real parts, which in fact, is an alternative characterization for the theory to be totally dissipative. Once this result has been obtained, a straight forward application of a general stability theorem due to Kreiss, Ortiz, and Reula, implies the results above mentioned.Comment: 10 pages, Late

Bulk viscous effects on flow and dilepton radiation in a hybrid approach

Starting from IP-Glasma initial conditions, we investigate the effects of bulk pressure on low mass dilepton production at the Relativistic Heavy Ion Collider (RHIC) and the Large Hadron Collider (LHC) energies. Though thermal dilepton $v_2$ is affected by the presence of both bulk and shear viscosity, whether or not these effects can be measured depends on the dilepton "cocktail" contribution to the the low mass dilepton $v_2$. Combining the thermal and "cocktail" dileptons, the effects of bulk viscosity on total dilepton $v_2$ is investigated.Comment: Proceedings for the 26th International Conference on Ultrarelativistic Nucleus-Nucleus Collisions (Quark Matter 2017), February 5-11 2017, Chicago, Illinois, US

Apoptosis in uterine epithelium and decidua in response to implantation: evidence for two different pathways

During the initial steps of implantation, the mouse uterine epithelium of the implantation chamber undergoes apoptosis in response to the interacting blastocyst. With progressing implantation, regression of the decidual cells allows a restricted and coordinated invasion of trophoblast cells into the maternal compartment. In order to investigate pathways of apoptosis in mouse uterine epithelium and decidua during early pregnancy (day 4.5–7.0 post coitum), we have investigated different proteins such as TNFalpha, TNF receptor1, Fas ligand, Fas receptor1, Bax and Bcl2 as well as caspase-9 and caspase-3 using immunohistochemistry. To detect cells undergoing apoptosis the Tunel assay was performed. Immunoreactivity for TNFalpha as well as for TNF receptor1 was observed exclusively in the epithelium of the implantation chamber and the adjacent luminal epithelium from day 4.5 post coitum onwards. In the developing decidua the Fas ligand, but not the Fas receptor, was expressed. Bax and Bcl2 revealed a complementary expression pattern with Bax in the primary and Bcl2 in the adjacent decidual zone. Strong immunolabelling for the initiator caspase-9 was restricted to the decidual compartment, whereas caspase-3 expression characterized the apoptotic uterine epithelium. Only some caspase-3 positive decidual cells were found around the embryo which correlated to the pattern of Tunel staining. Taken together, the apoptotic degeneration of the uterine epithelium seems to be mediated by TNF receptor1 followed by caspase-3, whereas the very moderate regression of the decidua did not show the investigated death receptor, but Bax and Blc2 instead and in addition caspase-9, which indicates a different regulation for epithelial versus decidual apoptosis

Understanding Taylor : Charles Taylor and the shaping of a philosophical therapy for the crisis of modernity

This thesis is a contextual examination of Charles Taylor's philosophical system applied to politics. It traces the origins of Taylor's project in Isaiah Berlin's revival of political philosophy at Oxford in the late 1950s and the critique of Stalinism. This thesis argues that Taylor's philosophy developed out of the New Left project of reconsidering the foundations of socialism. This developed into a critique of the common faults of Marxism and Liberalism as having fallen prey to a modernity characterised by a scientific and bureaucratic world-view. This thesis argues that Taylor redeveloped Hegel using linguistic and psychoanalytic theory to reconsider the foundations of Marxism and modernity, and to develop a post-modern Sittlichkeit. Finally, this thesis shows how Taylor viewed the crisis of modernity exemplified in the delayed modernisation of Quebec

Mild cognitive impairment, degenerative and vascular dementia as predictors of intra-hospital, short- and long-term mortality in the oldest old

Background and aims: The relative weight of various etiologies of dementia and mild cognitive impairment (MCI) as predictors of intra-hospital, short- and long-term mortality in very old acutely ill patients suffering from multiple comorbid conditions remains unclear. We investigated intra-hospital, 1- and 5-year mortality risk associated with dementia and its various etiologies in a very old population after discharge from acute care. Methods: Prospective cohort study of 444 patients (mean age 85 years; 74% female) discharged from the acute geriatric unit of Geneva University Hospital. On admission, each subject underwent standardized evaluation of cognitive and comorbid conditions. Patients were followed yearly by the same team. Predictive variables were age, sex, cognitive diagnosis, dementia etiology and severity. Survival during hospitalization, at 1- and 5-year follow-ups was the outcome of interest evaluated with Cox proportional hazard models. Results: Two hundred and six patients were cognitively normal, 48 had MCI, and 190 had dementia: of these, there were 75 cases of Alzheimer's disease (AD), 20 of vascular dementia (VaD), 82 of mixed dementia (MD) and 13 of other types of dementia. The groups compared were statistically similar in age, sex, education level and comorbidity score. After 5 years of follow-up, 60% of the patients had died. Regarding intra-hospital mortality, none of the predictive variables was associated with mortality. MCI, AD and MD were not predictive of short- or long-term mortality. Features significantly associated with reduced survival at 1 and 5 years were being older, male, and having vascular or severe dementia. When all the variables were added in the multiple model, the dementia effect completely disappeared. Conclusions: Dementia (all etiologies) is not predictive of mortality. The observed VaD effect is probably linked to cardiovascular risk comorbidities: hypertension, stroke and hyperlipidemi