Keele University

About: Keele University is a education organization based out in Newcastle-under-Lyme, United Kingdom. It is known for research contribution in the topics: Population & Stars. The organization has 11318 authors who have published 26323 publications receiving 894671 citations. The organization is also known as: Keele University.

Predictions for mass-loss rates and terminal wind velocities of massive O-type stars

Abstract: Context. Mass loss from massive stars forms an important aspect of the evolution of massive stars, as well as for the enrichment of the surrounding interstellar medium. Aims. Our goal is to predict accurate mass-loss rates and terminal wind velocities. These quantities can be compared to empirical values, thereby testing radiation-driven wind models. One specific topical issue is that of the so-called “weak-wind problem”, where empirically derived mass-loss rates and (modified) wind momenta fall orders of magnitude short of predicted values. Methods. We employ an established Monte Carlo model and a recently suggested new line acceleration formalism to solve the wind dynamics more consistently. Results. We provide a new grid of mass-loss rates and terminal wind velocities of O-type stars, and compare the values to empirical results. Our models fail to provide mass-loss rates for main-sequence stars below a luminosity of log(L/L� ) = 5.2, where we appear to run into a fundamental limit. At luminosities below this critical value there is insufficient momentum transferred to the wind in the region below the sonic point in order to kick-start the acceleration of the flow. This problem occurs at almost the exact location of the onset of the weak-wind problem. For O dwarfs, the boundary between being able to start a wind, and failing to do so, is at spectral type O6/O6.5. The direct cause of this failure for O6.5 stars is a combination of the lower luminosity and a lack of Fev lines at the base of the wind. This might indicate that – in addition to radiation pressure – another mechanism is required to provide the necessary driving to initiate the wind acceleration. Conclusions. For stars more luminous than 10 5.2 L� , our new mass-loss rates are in excellent agreement with the mass-loss prescription by Vink et al. (2000, A&A, 362, 295) using our terminal wind velocities as input to this recipe. This implies that the main assumption entering the method of the Vink et al. prescriptions – i.e. that the momentum equation is not explicitly solved for – does not compromise the reliability of the Vink et al. results for this part of parameter space. Finally, our new models predict terminal velocities that are typically 35 and 45 percent larger than observed values. Such over-predictions are similar to those from (modified) CAK-theory.

Populism for political theorists

Abstract: Political theorists do not in general pay much attention to populism; are there any good reasons why they should do so? This paper will consider a number of positive answers to this question Most attention has so far been paid to issues of methodology—can we define ‘populism’? Recently there has also been some interest in the relation between populism and democracy, but there are two further topics that may be worth investigating, first the possibility of a distinctive political ideology that might be called ‘populist’, and second the meanings and significance of populism's core concept, the elusive ‘people’

Tsc1 (hamartin) confers neuroprotection against ischemia by inducing autophagy.

Abstract: Previous attempts to identify neuroprotective targets by studying the ischemic cascade and devising ways to suppress it have failed to translate to efficacious therapies for acute ischemic stroke. We hypothesized that studying the molecular determinants of endogenous neuroprotection in two well-established paradigms, the resistance of CA3 hippocampal neurons to global ischemia and the tolerance conferred by ischemic preconditioning (IPC), would reveal new neuroprotective targets. We found that the product of the tuberous sclerosis complex 1 gene (TSC1), hamartin, is selectively induced by ischemia in hippocampal CA3 neurons. In CA1 neurons, hamartin was unaffected by ischemia but was upregulated by IPC preceding ischemia, which protects the otherwise vulnerable CA1 cells. Suppression of hamartin expression with TSC1 shRNA viral vectors both in vitro and in vivo increased the vulnerability of neurons to cell death following oxygen glucose deprivation (OGD) and ischemia. In vivo, suppression of TSC1 expression increased locomotor activity and decreased habituation in a hippocampal-dependent task. Overexpression of hamartin increased resistance to OGD by inducing productive autophagy through an mTORC1-dependent mechanism.

Subordinating hegemonic masculinity

Abstract: This article starts with a paradox, namely, the widespread talk of a ‘crisis of masculinity’ alongside the strong endorsement of Bob Connell’s concept of ‘hegemonic masculinity’, a term which impli...