Six New Galactic Orbits of Globular Clusters in a Milky-Way-Like Galaxy

Absolute proper motions for six new globular clusters have recently been determined. This motivated us to obtain the Galactic orbits of these six clusters both in an axisymmetric Galactic potential and in a barred potential, such as the one of our Galaxy. Orbits are also obtained for a Galactic potential that includes spiral arms. The orbital characteristics are compared and discussed for these three cases. Tidal radii and destruction rates are also computed and discussed.Comment: 29 pages, 11 figures. Accepted for publication in Ap

Relative velocities among accreting planetesimals in binary systems: the circumbinary case

We numerically investigate the possibility of planetesimal accretion in circumbinary disks, under the coupled influence of both stars' secular perturbations and friction due to the gaseous component of the protoplanetary disk. We focus on one crucial parameter: the distribution of encounter velocities between planetesimals in the 0.5 to 100km size range. An extended range of binary systems with differing orbital parameters is explored. The resulting encounter velocities are compared to the threshold velocities below which the net outcome of a collision is accumulation into a larger body instead of mass erosion. For each binary configuration, we derive the critical radial distance from the binary barycenter beyond which planetesimal accretion is possible. This critical radial distance is smallest for equal-mass binaries on almost circular orbits. It shifts to larger values for increasing eccentricities and decreasing mass ratio. The importance of the planetesimals' orbital alignments of planetesimals due to gas drag effects is discussed.Comment: accepted for publication in MNRA

Protective effects of hydrogen-rich saline on monocrotaline-induced pulmonary hypertension in a rat model

<p>Abstract</p> <p>Background</p> <p>Hydrogen-rich saline has been reported to have antioxidant and anti-inflammatory effects and effectively protect against organ damage. Oxidative stress and inflammation contribute to the pathogenesis and/or development of pulmonary hypertension. In this study, we investigated the effects of hydrogen-rich saline on the prevention of pulmonary hypertension induced by monocrotaline in a rat model.</p> <p>Methods</p> <p>In male Sprague-Dawley rats, pulmonary hypertension was induced by subcutaneous administration of monocrotaline at a concentration of 6 mg/100 g body weight. Hydrogen-rich saline (5 ml/kg) or saline was administred intraperitoneally once daily for 2 or 3 weeks. Severity of pulmonary hypertension was assessed by hemodynamic index and histologic analysis. Malondialdehyde and 8-hydroxy-desoxyguanosine level, and superoxide dismutase activity were measured in the lung tissue and serum. Levels of pro-inflammatory cytokines (tumor necrosis factor-α, interleukin-6) in serum were determined with enzyme-linked immunosorbent assay.</p> <p>Results</p> <p>Hydrogen-rich saline treatment improved hemodynamics and reversed right ventricular hypertrophy. It also decreased malondialdehyde and 8-hydroxy-desoxyguanosine levels, and increased superoxide dismutase activity in the lung tissue and serum, accompanied by a decrease in pro-inflammatory cytokines.</p> <p>Conclusions</p> <p>These results suggest that hydrogen-rich saline ameliorates the progression of pulmonary hypertension induced by monocrotaline in rats, which may be associated with its antioxidant and anti-inflammatory effects.</p

Nonlinear Effects in Models of the Galaxy: 1. Midplane Stellar Orbits in the Presence of 3D Spiral Arms

With the aim of studying the nonlinear stellar and gaseous response to the gravitational potential of a galaxy such as the Milky Way, we have modeled 3D galactic spiral arms as a superposition of inhomogeneous oblate spheroids and added their contribution to an axisymmetric model of the Galactic mass distribution. Three spiral loci are proposed here, based in different sets of observations. A comparison of our model with a tight-winding approximation shows that the self-gravitation of the whole spiral pattern is important in the middle and outer galactic regions. As a first step to full 3D calculations the model is suitable for, we have explored the stellar orbital structure in the midplane of the Galaxy. We present the standard analysis in the pattern rotating frame, and complement this analysis with orbital information from the Galactic inertial frame. Prograde and retrograde orbits are defined unambiguously in the inertial frame, then labeled as such in the Poincar\'e diagrams of the non-inertial frame. In this manner we found a sharp separatrix between the two classes of orbits. Chaos is restricted to the prograde orbits, and its onset occurs for the higher spiral perturbation considered plausible in our Galaxy.Comment: 23 pages, 22 Figures. Latex. Submitted to Ap

Impaired LXRa phosphorylation attenuates progression of fatty liver disease

Non-alcoholic fatty liver disease (NAFLD) is a very common indication for liver transplantation. How fat-rich diets promote progression from fatty liver to more damaging inflammatory and fibrotic stages is poorly understood. Here, we show that disrupting phosphorylation at Ser196 (S196A) in the liver X receptor alpha (LXRα, NR1H3) retards NAFLD progression in mice on a high-fat-high-cholesterol diet. Mechanistically, this is explained by key histone acetylation (H3K27) and transcriptional changes in pro-fibrotic and pro-inflammatory genes. Furthermore, S196A-LXRα expression reveals the regulation of novel diet-specific LXRα-responsive genes, including the induction of Ces1f, implicated in the breakdown of hepatic lipids. This involves induced H3K27 acetylation and altered LXR and TBLR1 cofactor occupancy at the Ces1f gene in S196A fatty livers. Overall, impaired Ser196-LXRα phosphorylation acts as a novel nutritional molecular sensor that profoundly alters the hepatic H3K27 acetylome and transcriptome during NAFLD progression placing LXRα phosphorylation as an alternative anti-inflammatory or anti-fibrotic therapeutic target

Changes In LXRα Phosphorylation Promote A Novel Diet-Induced Transcriptome That Alters The Transition From Fatty Liver To Steatohepatitis

Understanding the transition from fatty liver or steatosis to more advanced inflammatory and fibrotic stages of non-alcoholic fatty liver disease (steatohepatitis), is key to define strategies that alter or even reverse the progression of this pathology. The Liver X Receptor alpha (LXRα) controls hepatic lipid homeostasis and inflammation. Here we show that mice carrying a mutation that abolishes phosphorylation at Ser196 (S196A) in LXRα exhibit reduced hepatic inflammation and fibrosis when challenged with a high fat-high cholesterol diet, despite displaying enhanced hepatic lipid accumulation. This protective effect is associated with reduced cholesterol accumulation, a key promoter of lipid-mediated hepatic damage. Reduced steatohepatitis in S196A mice involves the reprogramming of the liver transcriptome by promoting diet-induced changes in the expression of genes involved in endoplasmic reticulum stress, extracellular matrix remodelling, inflammation and lipid metabolism. Unexpectedly, changes in LXRα phosphorylation uncover novel diet-specific target genes, whose regulation does not simply mirror ligand-induced LXR activation. These unique LXRα phosphorylation-sensitive, diet-responsive target genes are revealed by promoting LXR occupancy and cofactor recruitment in the context of a cholesterol-rich diet. Therefore, LXRα phosphorylation at Ser196 critically acts as a novel nutritional sensor that promotes a unique diet-induced transcriptome thereby modulating metabolic, inflammatory and fibrotic responses important in the transition to steatohepatitis

"The contribution of chronic diseases to the prevalence of dependence among older people in Latin America, China and India: a 10/66 Dementia Research Group population-based survey"

<p>Abstract</p> <p>Background</p> <p>The number of older people is set to increase dramatically worldwide. Demographic changes are likely to result in the rise of age-related chronic diseases which largely contribute to years lived with a disability and future dependence. However dependence is much less studied although intrinsically linked to disability. We investigated the prevalence and correlates of dependence among older people from middle income countries.</p> <p>Methods</p> <p>A one-phase cross-sectional survey was carried out at 11 sites in seven countries (urban sites in Cuba, Venezuela, and Dominican Republic, urban and rural sites in Peru, Mexico, China and India). All those aged 65 years and over living in geographically defined catchment areas were eligible. In all, 15,022 interviews were completed with an informant interview for each participant. The full 10/66 Dementia Research Group survey protocol was applied, including ascertainment of depression, dementia, physical impairments and self-reported diagnoses. Dependence was interviewer-rated based on a key informant's responses to a set of open-ended questions on the participant's needs for care. We estimated the prevalence of dependence and the independent contribution of underlying health conditions. Site-specific prevalence ratios were meta-analysed, and population attributable prevalence fractions (PAPF) calculated.</p> <p>Results</p> <p>The prevalence of dependence increased with age at all sites, with a tendency for the prevalence to be lower in men than in women. Age-standardised prevalence was lower in all sites than in the USA. Other than in rural China, dementia made the largest independent contribution to dependence, with a median PAPF of 34% (range 23%-59%). Other substantial contributors were limb impairment (9%, 1%-46%), stroke (8%, 2%-17%), and depression (8%, 1%-27%).</p> <p>Conclusion</p> <p>The demographic and health transitions will lead to large and rapid increases in the numbers of dependent older people particularly in middle income countries (MIC). The prevention and control of chronic neurological and neuropsychiatric diseases and the development of long-term care policies and plans should be urgent priorities.</p

Impaired LXRα Phosphorylation Attenuates Progression of Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is a very common indication for liver transplantation. How fat-rich diets promote progression from fatty liver to more damaging inflammatory and fibrotic stages is poorly understood. Here, we show that disrupting phosphorylation at Ser196 (S196A) in the liver X receptor alpha (LXRα, NR1H3) retards NAFLD progression in mice on a high-fat-high-cholesterol diet. Mechanistically, this is explained by key histone acetylation (H3K27) and transcriptional changes in pro-fibrotic and pro-inflammatory genes. Furthermore, S196A-LXRα expression reveals the regulation of novel diet-specific LXRα-responsive genes, including the induction of Ces1f, implicated in the breakdown of hepatic lipids. This involves induced H3K27 acetylation and altered LXR and TBLR1 cofactor occupancy at the Ces1f gene in S196A fatty livers. Overall, impaired Ser196-LXRα phosphorylation acts as a novel nutritional molecular sensor that profoundly alters the hepatic H3K27 acetylome and transcriptome during NAFLD progression placing LXRα phosphorylation as an alternative anti-inflammatory or anti-fibrotic therapeutic target