Testing Gluino Spin with Three-Body Decays

We examine the possibility of distinguishing a supersymmetric gluino from a Kaluza-Klein gluon of universal extra dimensions (UED) at the Large Hadron Collider (LHC). We focus on the case when all kinematically allowed tree-level decays of this particle are 3-body decays into two jets and a massive daughter (typically weak gaugino or Kaluza-Klein weak gauge boson). We show that the shapes of the dijet invariant mass distributions differ significantly in the two models, as long as the mass of the decaying particle mA is substantially larger than the mass of the massive daughter mB. We present a simple analysis estimating the number of events needed to distinguish between the two models under idealized conditions. For example, for mA/mB=10, we find the required number of events to be of order several thousand, which should be available at the LHC within a few years. This conclusion is confirmed by a parton level Monte Carlo study which includes the effects of experimental cuts and the combinatoric background.Comment: 19 pages, 10 figure

Modeling electrolytically top gated graphene

We investigate doping of a single-layer graphene in the presence of electrolytic top gating. The interfacial phenomena is modeled using a modified Poisson-Boltzmann equation for an aqueous solution of simple salt. We demonstrate both the sensitivity of graphene's doping levels to the salt concentration and the importance of quantum capacitance that arises due to the smallness of the Debye screening length in the electrolyte.Comment: 7 pages, including 4 figures, submitted to Nanoscale Research Letters for a special issue related to the NGC 2009 conference (http://asdn.net/ngc2009/index.shtml

The ARID1B spectrum in 143 patients: from nonsyndromic intellectual disability to Coffin–Siris syndrome

Purpose: Pathogenic variants in ARID1B are one of the most frequent causes of intellectual disability (ID) as determined by large-scale exome sequencing studies. Most studies published thus far describe clinically diagnosed Coffin–Siris patients (ARID1B-CSS) and it is unclear whether these data are representative for patients identified through sequencing of unbiased ID cohorts (ARID1B-ID). We therefore sought to determine genotypic and phenotypic differences between ARID1B-ID and ARID1B-CSS. In parallel, we investigated the effect of different methods of phenotype reporting. Methods: Clinicians entered clinical data in an extensive web-based survey. Results: 79 ARID1B-CSS and 64 ARID1B-ID patients were included. CSS-associated dysmorphic features, such as thick eyebrows, long eyelashes, thick alae nasi, long and/or broad philtrum, small nails and small or absent fifth distal phalanx and hypertrichosis, were observed significantly more often (p < 0.001) in ARID1B-CSS patients. No other significant differences were identified. Conclusion: There are only minor differences between ARID1B-ID and ARID1B-CSS patients. ARID1B-related disorders seem to consist of a spectrum, and patients should be managed similarly. We demonstrated that data collection methods without an explicit option to report the absence of a feature (such as most Human Phenotype Ontology-based methods) tended to underestimate gene-related features

Catalase activity expression in patients with Plasmodium vivax malaria

Plasmodium vivax (P. vivax) causes the most geographically widespread human malaria. It infects mainly the reticulocytes. Free radicals and related species have attracted a great deal of attention in recent years. They are mainly derived from oxygen and is generated in our body by various endogenous systems, exposure to different pathophysiological states. Catalase seems to be the main regulator of hydrogen peroxide metabolism. Hydrogen peroxide at high concentrations is a toxic agent, while at low concentrations it appears to modulate some physiological processes. We have analyzed the catalase levels to investigate the role of antioxidant enzymes against toxic reactive oxygen species in Plasmodium vivax infected patients and compared with healthy controls. The difference between catalase levels of patients was lower than control group and was statistically significant (p < 0.05). In neither the patient nor control group was correlation found between age and catalase levels

Role of vitamin D in children with hepatosteatosis

Background: The increasing incidence of obesity in children is a significant risk factor for nonalcoholic fatty liver disease and obesity-associated morbidity. Vitamin D has a major role in bone mineral metabolism and has antimicrobial, antioxidant properties. In this study we aimed to investigate the role of vitamin D in children with obesity with hepatosteatosis. Methods: A total of 101 children with obesity were included in this study. Hepatosteatosis was diagnosed and graded using ultrasonography. Serum levels of 25-hydroxyvitamin D (25-(OH) vitamin D), calcium, phosphate, alkaline phosphatase, and parathormone were tested. Two-sided t test and Pearson x2 tests were used for the relation between vitamin D and hepatosteatosis. Results: In our study group, 45.5% were girls (n=46) and the mean age was 11.5?2.8 years (range 3-17 years). Hepatosteatosis was identified in 58 children (57.4%). The diagnosis of grade 1 and grade 2 hepatosteatosis was made in 41 (40.6%) and 17 (16.8%) children, respectively. Median serum 25-(OH) vitamin D levels in children without hepatosteatosis was 16.4 ng/ mL (interquartile range 12.4-24.8 ng/mL), whereas children with grade 1 and grade 2 hepatosteatosis had 25-(OH) vitamin D levels of 14.2 ng/mL (interquartile range 9.5-21.2 ng/mL) and 11.5 ng/mL (interquartile range 7.5-16.7 ng/mL), respectively (P=0.005). There was a positive correlation between insulin resistance and the grade of hepatosteatosis (P=0.03). Conclusions: Serum vitamin D levels in children with obesity with hepatosteatosis are significantly lower than vitamin D levels in children with obesity without hepatosteatosis. In this observational study we only refer to the association of vitamin D deficiency/insufficiency with hepatosteatosis. Copyright © 2014 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition

HMG-CoA reductase inhibitor rosuvastatin improves abnormal brain electrical activity via mechanisms involving eNOS

Apart from its repressing effect on plasma lipid levels, 3-hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase inhibitors exert neuroprotective functions in animal models of neurodegenerative disorders. In view of these promising observations, we were interested in whether HMG-CoA reductase inhibition would affect epileptiform activity in the brain. To elucidate this issue, atorvastatin, simvastatin and rosuvastatin were administered orally at a dose of 20. mg/kg each for 3. days and their anti-epileptic activities were tested and compared in rats. Epileptiform activity in the brain was induced by an intracortical penicillin G injection. Among HMG-CoA reductase inhibitors, simvastatin-treatment was less effective in terms of spike frequency as compared with atorvastatin- and rosuvastatin-treated animals. Atorvastatin treatment reduced spike frequencies and amplitudes significantly throughout the experiment. However, the most pronounced anti-epileptic effect was observed in rosuvastatin-treated animals, which was associated with improved blood-brain barrier (BBB) integrity, increased expression of endothelial nitric oxide synthase (eNOS) mRNA and decreased expressions of pro-apoptotic p53, Bax and caspase-3 mRNAs. Inhibition of eNOS activity with l-NG-Nitroarginine Methyl Ester (. l-NAME) reversed the anti-epileptic effect of rosuvastatin significantly. However, l-NAME did not alter the effect of rosuvastatin on the levels of p53, Bax and caspase-3 mRNA expression. Here, we provide evidence that among HMG-CoA reductase inhibitors, rosuvastatin was the most effective statin on the reduction of epileptiform activity, which was associated with improved BBB permeability, increased expression of eNOS and decreased expressions of pro-apoptotic p53, Bax and caspase-3. Our observation also revealed that the anti-epileptic effect of rosuvastatin was dependent on the increased expression level of eNOS. The robust anti-epileptic effect encourages proof-of-concept studies with rosuvastatin in human epilepsy patients with hypercholesterolemia