Hard gluon damping in hot QCD

The gluon collisional width in hot QCD plasmas is discussed with emphasis on temperatures near $T_c$, where the coupling is large. Considering its effect on the entropy, which is known from lattice calculations, it is argued that the width, which in the perturbative limit is given by $\gamma \sim g^2 \ln(1/g) T$, should be sizeable at intermediate temperatures but has to be small close to $T_c$. Implications of these results for several phenomenologically relevant quantities, such as the energy loss of hard jets, are pointed out.Comment: uses RevTex and graphic

Migration strategies of skuas in the southwest Atlantic Ocean revealed by stable isotopes

Stable isotope ratios of carbon (δ13C) and nitrogen (δ15N) were measured in feathers to compare the non-breeding distributions and habitat use of adult brown skuas Stercorarius antarcticus lönnbergi from high-latitude colonies at Esperanza/Hope Bay (Antarctic Peninsula, 63°S) and Signy Island (South Orkneys, 60°S), with those from Bird Island (South Georgia, 54°S), which have also been tracked previously using geolocators. Breeding colony, but not sex, had a significant effect on feather δ13C and δ15N values. Feather stable isotope data from South Georgia birds mostly corresponded to oceanic, mixed subtropical–subantarctic to subantarctic waters, which agrees with the tracking data, as did a subset of the birds from the two higher latitude populations. However, other individuals displayed feather stable isotope ratios that were consistent with continental shelf or shelf-slope waters, suggesting that unlike the vast majority of brown skuas from South Georgia, many birds from higher latitude colonies spend the non-breeding season on, or near, the Patagonian Shelf. These population-level differences may have implications for exposure to anthropogenic threats or have carryover effects on subsequent breeding behaviour or performance

Altered glucose homeostasis and hepatic function in obese mice deficient for both kinin receptor genes

The Kallikrein-Kinin System (KKS) has been implicated in several aspects of metabolism, including the regulation of glucose homeostasis and adiposity. Kinins and des-Arg-kinins are the major effectors of this system and promote their effects by binding to two different receptors, the kinin B2 and B1 receptors, respectively. To understand the influence of the KKS on the pathophysiology of obesity and type 2 diabetes (T2DM), we generated an animal model deficient for both kinin receptor genes and leptin (obB1B2KO). Six-month-old obB1B2KO mice showed increased blood glucose levels. Isolated islets of the transgenic animals were more responsive to glucose stimulation releasing greater amounts of insulin, mainly in 3-month-old mice, which was corroborated by elevated serum C-peptide concentrations. Furthermore, they presented hepatomegaly, pronounced steatosis, and increased levels of circulating transaminases. This mouse also demonstrated exacerbated gluconeogenesis during the pyruvate challenge test. The hepatic abnormalities were accompanied by changes in the gene expression of factors linked to glucose and lipid metabolisms in the liver. Thus, we conclude that kinin receptors are important for modulation of insulin secretion and for the preservation of normal glucose levels and hepatic functions in obese mice, suggesting a protective role of the KKS regarding complications associated with obesity and T2DM