Probing the Goldstone equivalence theorem in Heavy Weak Doublet Decays

This paper investigates the decays from heavy higgsino-like weak-doublets into Z, h bosons and missing particles. When pair-produced at the LHC, the subsequent Z, h to 2l, 2b decays in the doublet decay cascade can yield 4l, 2l 2b, and 4b + MET + jets final states. Mutual observation of any two of these channels would provide information on the the associated doublets' decay branching fractions into a Z or h, thereby probing the Goldstone equivalence relation, shedding additional light on the Higgs sector of beyond the Standard Model theories, and facilitating the discrimination of various contending models, in turn. We compare the Z/h decay ratio expected in the Minimal Supersymmetric model, the Next-to Minimal Supersymmetric model and a minimal singlet-doublet dark matter model. Additionally, we conduct a full Monte Carlo analysis of the prospects for detecting the targeted final states during 14 TeV running of the LHC in the context of a representative NMSSM benchmark model.Comment: As accepted to PRD; 15 pages, 12 figures, 5 table

Changes in neuronal CycD/Cdk4 activity affect aging, neurodegeneration, and oxidative stress.

Mitochondrial dysfunction has been implicated in human diseases, including cancer, and proposed to accelerate aging. The Drosophila Cyclin-dependent protein kinase complex cyclin D/cyclin-dependent kinase 4 (CycD/Cdk4) promotes cellular growth by stimulating mitochondrial biogenesis. Here, we examine the neurodegenerative and aging consequences of altering CycD/Cdk4 function in Drosophila. We show that pan-neuronal loss or gain of CycD/Cdk4 increases mitochondrial superoxide, oxidative stress markers, and neurodegeneration and decreases lifespan. We find that RNAi-mediated depletion of the mitochondrial transcription factor, Tfam, can abrogate CycD/Cdk4's detrimental effects on both lifespan and neurodegeneration. This indicates that CycD/Cdk4's pathological consequences are mediated through altered mitochondrial function and a concomitant increase in reactive oxygen species. In support of this, we demonstrate that CycD/Cdk4 activity levels in the brain affect the expression of a set of 'oxidative stress' genes. Our results indicate that the precise regulation of neuronal CycD/Cdk4 activity is important to limit mitochondrial reactive oxygen species production and prevent neurodegeneration

Autophagy as a promoter of longevity: insights from model organisms.

Autophagy is a conserved process that catabolizes intracellular components to maintain energy homeostasis and to protect cells against stress. Autophagy has crucial roles during development and disease, and evidence accumulated over the past decade indicates that autophagy also has a direct role in modulating ageing. In particular, elegant studies using yeasts, worms, flies and mice have demonstrated a broad requirement for autophagy-related genes in the lifespan extension observed in a number of conserved longevity paradigms. Moreover, several new and interesting concepts relevant to autophagy and its role in modulating longevity have emerged. First, select tissues may require or benefit from autophagy activation in longevity paradigms, as tissue-specific overexpression of single autophagy genes is sufficient to extend lifespan. Second, selective types of autophagy may be crucial for longevity by specifically targeting dysfunctional cellular components and preventing their accumulation. And third, autophagy can influence organismal health and ageing even non-cell autonomously, and thus, autophagy stimulation in select tissues can have beneficial, systemic effects on lifespan. Understanding these mechanisms will be important for the development of approaches to improve human healthspan that are based on the modulation of autophagy

Characteristics of buckbrush shrubs exposed to herbivores after seven years of protection

In dense ponderosa pine (Pinus ponderosa Laws.) forests of northern Arizona, forage limitations may lead to severe herbivory by large ungulates on certain plant species. In 1999, we fenced 76 buckbrush (Ceanothus fendleri Gray) shrubs to protect them from herbivores and study growth and reproduction in response to forest restoration treatments implemented on the Fort Valley Experimental Forest. After seven years, we removed fences from around half the plants and examined herbivore impacts on vegetative characteristics. In spring, and again in fall, we measured stem heights and took photographs of exposed shrubs and protected controls. In fall, we also collected stems to analyze size, biomass, and leaf area. Plants exposed to herbivores had significantly less leaf area and total leaf weight than protected control plants. Stem length, diameter, and weight were statistically similar between exposed and control groups. Results from this study suggest that temporary protection from herbivores during the early stages of forest restoration may enhance rates of development and persistence of native plants such as buckbrush

Rethinking learning for a digital age : how learners are shaping their experiences Rhona Sharpe, Helen Beetham and Sara de Freitas London:Routledge(2010)pp.256 Pbk.£24.99 ISBN 9781415785431

Peer reviewedPublisher PD

The Value of Information Technology-Enabled Diabetes Management

Reviews different technologies used in diabetes disease management, as well as the costs, benefits, and quality implications of technology-enabled diabetes management programs in the United States

Short-term genome stability of serial Clostridium difficile ribotype 027 isolates in an experimental gut model and recurrent human disease

Copyright: © 2013 Eyre et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are creditedClostridium difficile whole genome sequencing has the potential to identify related isolates, even among otherwise indistinguishable strains, but interpretation depends on understanding genomic variation within isolates and individuals.Serial isolates from two scenarios were whole genome sequenced. Firstly, 62 isolates from 29 timepoints from three in vitro gut models, inoculated with a NAP1/027 strain. Secondly, 122 isolates from 44 patients (2–8 samples/patient) with mostly recurrent/on-going symptomatic NAP-1/027 C. difficile infection. Reference-based mapping was used to identify single nucleotide variants (SNVs).Across three gut model inductions, two with antibiotic treatment, total 137 days, only two new SNVs became established. Pre-existing minority SNVs became dominant in two models. Several SNVs were detected, only present in the minority of colonies at one/two timepoints. The median (inter-quartile range) [range] time between patients’ first and last samples was 60 (29.5–118.5) [0–561] days. Within-patient C. difficile evolution was 0.45 SNVs/called genome/year (95%CI 0.00–1.28) and within-host diversity was 0.28 SNVs/called genome (0.05–0.53). 26/28 gut model and patient SNVs were non-synonymous, affecting a range of gene targets.The consistency of whole genome sequencing data from gut model C. difficile isolates, and the high stability of genomic sequences in isolates from patients, supports the use of whole genome sequencing in detailed transmission investigations.Peer reviewe