New Phase-coherent Measurements of Pulsar Braking Indices

Pulsar braking indices offer insight into the physics that underlies pulsar spin-down. Only five braking indices have been measured via phase-coherent timing; all measured values are less than 3, the value expected from magnetic dipole radiation. Here we present new measurements for three of the five pulsar braking indices, obtained with phase-coherent timing for PSRs J1846-0258 (n=2.65+/-0.01), B1509-58 (n=2.839+/-0.001) and B0540-69 (n=2.140+/-0.009). We discuss the implications of these results and possible physical explanations for them.Comment: 7 pages, 5 figures. To be published in the proceedings of the conference "Isolated Neutron Stars: from the Interior to the Surface" (April 24-28, 2006, London, UK), eds. D. Page, R. Turolla, & S. Zan

Recent glitches detected in the Crab pulsar

From 2000 to 2010, monitoring of radio emission from the Crab pulsar at Xinjiang Observatory detected a total of nine glitches. The occurrence of glitches appears to be a random process as described by previous researches. A persistent change in pulse frequency and pulse frequency derivative after each glitch was found. There is no obvious correlation between glitch sizes and the time since last glitch. For these glitches $\Delta\nu_{p}$ and $\Delta\dot{\nu}_{p}$ span two orders of magnitude. The pulsar suffered the largest frequency jump ever seen on MJD 53067.1. The size of the glitch is $\sim$ 6.8 $\times 10^{-6}$ Hz, $\sim$ 3.5 times that of the glitch occured in 1989 glitch, with a very large permanent changes in frequency and pulse frequency derivative and followed by a decay with time constant $\sim$ 21 days. The braking index presents significant changes. We attribute this variation to a varying particle wind strength which may be caused by glitch activities. We discuss the properties of detected glitches in Crab pulsar and compare them with glitches in the Vela pulsar.Comment: Accepted for publication in Astrophysics & Space Scienc

Cerebrospinal fluid biomarkers for Alzheimer's disease in Down syndrome

Down syndrome (DS), present in nearly six million people, is associated with an extremely high risk to develop Alzheimer's disease (AD). Amyloid-β and tau pathology are omnipresent from age 40 years onward, but clinical symptoms do not appear in all DS individuals. Dementia diagnostics is complex in this population, illustrating the great need for predictive biomarkers. Although blood biomarkers have not yet proven useful, cerebrospinal fluid (CSF) biomarkers (low amyloid-β42, high t-tau, and high p-tau) effectively contribute to AD diagnoses in the general population and are increasingly used in clinical practice. Surprisingly, CSF biomarkers have been barely evaluated in DS. Breaking the taboo on CSF analyses would finally allow for the elucidation of its utility in (differential) diagnoses and staging of disease severity. A sensitive and specific biomarker profile for AD in DS would be of paramount importance to daily care, adaptive caregiving, and specific therapeutic interventions

FTO genotype and weight loss: systematic review and meta-analysis of 9563 individual participant data from eight randomised controlled trials

Objective To assess the effect of the FTO genotype on weight loss after dietary, physical activity, or drug based interventions in randomised controlled trials. Design Systematic review and random effects meta-analysis of individual participant data from randomised controlled trials. Data sources Ovid Medline, Scopus, Embase, and Cochrane from inception to November 2015. Eligibility criteria for study selection Randomised controlled trials in overweight or obese adults reporting reduction in body mass index, body weight, or waist circumference by FTO genotype (rs9939609 or a proxy) after dietary, physical activity, or drug based interventions. Gene by treatment interaction models were fitted to individual participant data from all studies included in this review, using allele dose coding for genetic effects and a common set of covariates. Study level interactions were combined using random effect models. Metaregression and subgroup analysis were used to assess sources of study heterogeneity. Results We identified eight eligible randomised controlled trials for the systematic review and meta-analysis (n=9563). Overall, differential changes in body mass index, body weight, and waist circumference in response to weight loss intervention were not significantly different between FTO genotypes. Sensitivity analyses indicated that differential changes in body mass index, body weight, and waist circumference by FTO genotype did not differ by intervention type, intervention length, ethnicity, sample size, sex, and baseline body mass index and age category. Conclusions We have observed that carriage of the FTO minor allele was not associated with differential change in adiposity after weight loss interventions. These findings show that individuals carrying the minor allele respond equally well to dietary, physical activity, or drug based weight loss interventions and thus genetic predisposition to obesity associated with the FTO minor allele can be at least partly counteracted through such interventions. Systematic review registration PROSPERO CRD42015015969

Effects of dexamethasone on fibre subtypes in rat muscle

The extent to which dexamethasone treatment produced atrophy of fast-twitch (EDL) and slow-twitch (SOL) muscles in the rat was investigated. The mean weight of steroid-treated EDL muscles was decreased as compared to normal, whereas SOL muscles from normal and dexamethasone-treated animals showed no significant difference. Muscle fibre diameters also showed comparatively minor changes in SOL, which consists of Type 1 (slow oxidative) and Type 2A (fast oxidative/glycolytic) fibres. Rat EDL contains, in addition to Type 1 and Type 2A fibres, two sub-populations of fast glycolytic fibres (Types 2B and 2B'). These fibre types showed the most severe degree of atrophy both after dexamethasone treatment and after denervation. The mean ratio of the weights of denervated to innervated EDL muscles was lower in steroid-treated rats than in normal animals suggesting that the atrophy produced by steroid treatment in conjunction with denervation was more than simply additive. Analysis of the proportions of histochemical fibre types in SOL and EDL showed that dexamethasone treatment produced no major alterations in the fibre type constitution of these muscles. However, further histochemical studies showed that there was relatively severe impairment of myophosphorylase activity in Type 2B' (fast glycolytic) fibres as compared to other fibre types; conversely Type 1 fibres frequently contained increased myophosphorylase. Levels of β-hydroxybutyrate dehydrogenase were low in both normal and steroid-treated EDL but high in SOL which also showed higher general oxidative activity. It is suggested that the particular susceptibility of fast glycolytic fibres to atrophy as a result of steroid treatment may be linked to: 1 the relatively severe reduction of myophosphorylase activity in these fibres and 2 their comparative inability to utilize alternative energy sources, especially substrates derived from free fatty acids