22 research outputs found
Enhanced magnetocaloric effect in frustrated magnets
The magnetothermodynamics of strongly frustrated classical Heisenberg
antiferromagnets on kagome, garnet, and pyrochlore lattices is examined. The
field induced adiabatic temperature change (dT/dH)_S is significantly larger
for such systems compared to ordinary non-frustrated magnets and also exceeds
the cooling rate of an ideal paramagnet in a wide range of fields. An
enhancement of the magnetocaloric effect is related to presence of a
macroscopic number of soft modes in frustrated magnets below the saturation
field. Theoretical predictions are confirmed with extensive Monte Carlo
simulations.Comment: 7 page
Assessment of thrombin-activatable fibrinolysis inhibitor (TAFI) activation in acquired hemostatic dysfunction: a diagnostic challenge
Perfil de suscetibilidade antimicrobiana e presença do gene vapA em Rhodococcus equi de origem humana, ambiental e equina
Realistic mock observations of the sizes and stellar mass surface densities of massive galaxies in FIRE-2 zoom-in simulations
The galaxy sizeâstellar mass and central surface densityâstellar mass relationships are fundamental observational constraints on galaxy formation models. However, inferring the physical size of a galaxy from observed stellar emission is non-trivial due to various observational effects, such as the mass-to-light ratio variations that can be caused by non-uniform stellar ages, metallicities, and dust attenuation. Consequently, forward-modelling light-based sizes from simulations is desirable. In this work, we use the skirtâ dust radiative transfer code to generate synthetic observations of massive galaxies (â MââŒ1011Mâ at z = 2, hosted by haloes of mass MhaloâŒ1012.5Mââ ) from high-resolution cosmological zoom-in simulations that form part of the Feedback In Realistic Environments project. The simulations used in this paper include explicit stellar feedback but no active galactic nucleus (AGN) feedback. From each mock observation, we infer the effective radius (Re), as well as the stellar mass surface density within this radius and within 1kpc (ÎŁe and ÎŁ1, respectively). We first investigate how well the intrinsic half-mass radius and stellar mass surface density can be inferred from observables. The majority of predicted sizes and surface densities are within a factor of 2 of the intrinsic values. We then compare our predictions to the observed sizeâmass relationship and the ÎŁ1âMâ and ÎŁeâMâ relationships. At z âł 2, the simulated massive galaxies are in general agreement with observational scaling relations. At z âČ 2, they evolve to become too compact but still star forming, in the stellar mass and redshift regime where many of them should be quenched. Our results suggest that some additional source of feedback, such as AGN-driven outflows, is necessary in order to decrease the central densities of the simulated massive galaxies to bring them into agreement with observations at z âČ 2
PTP1B is an androgen receptor-regulated phosphatase that promotes the progression of prostate cancer
The androgen receptor (AR) signaling axis plays a key role in the pathogenesis of prostate cancer. In this study, we found that the protein tyrosine phosphatase PTP1B, a well-established regulator of metabolic signaling, was induced after androgen stimulation of AR-expressing prostate cancer cells. PTP1B induction by androgen occurred at the mRNA and protein levels to increase PTP1B activity. High-resolution chromosome mapping revealed AR recruitment to two response elements within the first intron of the PTP1B encoding gene PTPN1, correlating with an AR-mediated increase in RNA polymerase II recruitment to the PTPN1 transcriptional start site. We found that PTPN1 and AR genes were coamplified in metastatic tumors and that PTPN1 amplification was associated with a subset of high-risk primary tumors. Functionally, PTP1B depletion delayed the growth of androgen-dependent human prostate tumors and impaired androgen-induced cell migration and invasion in vitro. However, PTP1B was also required for optimal cell migration of androgen-independent cells. Collectively, our results established the AR as a transcriptional regulator of PTPN1 transcription and implicated PTP1B in a tumor-promoting role in prostate cancer. Our findings support the preclinical testing of PTP1B inhibitors for prostate cancer treatment. ©2012 AACR