Search for triboson W±W±W∓ production in pp collisions at √s=8 TeV with the ATLAS detector

This paper reports a search for triboson $W^{\pm}W^{\pm}W^{\mp}$ production in two decay channels ($W^{\pm}W^{\pm}W^{\mp}\rightarrow \ell^{\pm}\nu\ell^{\pm}\nu\ell^{\mp}\nu$ and $W^{\pm}W^{\pm}W^{\mp}\rightarrow \ell^{\pm}\nu\ell^{\pm}\nu{}jj$ with $\ell=e, \mu$) in proton-proton collision data corresponding to an integrated luminosity of 20.3 fb$^{-1}$ at a centre-of-mass energy of 8 TeV with the ATLAS detector at the Large Hadron Collider. Events with exactly three charged leptons, or two leptons with the same electric charge in association with two jets, are selected. The total number of events observed in data is consistent with the Standard Model (SM) predictions. The observed 95 % confidence level upper limit on the SM $W^{\pm}W^{\pm}W^{\mp}$ production cross section is found to be 730 fb with an expected limit of 560 fb in the absence of SM $W^{\pm}W^{\pm}W^{\mp}$ production. Limits are also set on $WWWW$ anomalous quartic gauge couplings.Comment: Comments: 39 pages in total, author list starting page 23, 5 figures, 7 tables, submitted to European Physics Journal C, All figures including auxiliary figures are available at https://atlas.web.cern.ch/Atlas/GROUPS/PHYSICS/PAPERS/STDM-2015-07

Effects of ACE2 deficiency on physical performance and physiological adaptations of cardiac and skeletal muscle to exercise

The renin-angiotensin system (RAS) is related to physiological adaptations induced by exercise. Angiotensin-converting enzyme (ACE) 2 is a major regulator of the RAS in tissues, as it metabolizes angiotensin (Ang) II to Ang-(1-7). The aim of this study was to determine the effects of ACE2 deficiency on physical performance and physiological adaptations induced by voluntary running. Physical performance, body composition and plasma angiotensin levels, as well as tissue morphology and gene expression of RAS components in the left ventricle (LV) and skeletal muscle (gastrocnemius), were evaluated in ACE2-deficient (ACE2(-/y)) and wild-type (ACE2(+/y)) mice after 6 weeks of voluntary wheel running. ACE2(-/y) mice run less than ACE2(+/y) mice (19+/-4.7 vs. 26+/-12.6 revolutions per day x 100, P<0.01). The ACE2(+/y) group presented a lower fat mass (15+/-1.1%) and higher muscle mass (76.6+/-1.6%) after 6 weeks of voluntary running compared with the sedentary control group (fat mass: 18.3+/-2.1%; muscle mass: 72.7+/-2.2). However, no change in body composition was observed in ACE2(-/y) mice after exercise. Heart and skeletal muscle hypertrophy was observed only in trained ACE2(+/y) mice. Besides a small decrease in Ang I in ACE2(-/y) mice, plasma levels of angiotensin peptides remained unchanged by exercise or ACE2 deficiency. In the LV of trained animals, AT2 gene expression was higher in ACE2(+/y) compared with ACE2(-/y) mice. ACE2 deficiency leads to an increase in AT1 gene expression in skeletal muscle. ACE expression in soleus was increased in all exercised groups. ACE2 deficiency affects physical performance and impairs cardiac and skeletal muscle adaptations to exercise

Downregulated bone morphogenetic protein signaling in nitrofen-induced congenital diaphragmatic hernia.

Bone morphogenetic proteins (BMP) have been shown to play crucial roles in not only lung and heart development, but also in the pathogenesis of pulmonary vascular remodeling in pulmonary hypertension (PH). We therefore hypothesized that BMP signaling could be altered in nitrofen-induced congenital diaphragmatic hernia (CDH) and associated PH.Journal ArticleResearch Support, Non-U.S. Gov'tSCOPUS: ar.jinfo:eu-repo/semantics/publishe

Genetic models

Genetically altered rat and mouse models have been instrumental in the functional analysis of genes in a physiological context. In particular, studies on the renin-angiotensin system (RAS) have profited from this technology in the past. In this review, we summarize the existing animal models for the protective axis of the RAS consisting of angiotensin-converting enzyme 2 (ACE2), angiotensin-(1-7)(Ang-(1-7), and its receptor Mas. With the help of models with altered expression of the components of this axis in the brain and cardiovascular organs, its physiological and pathophysiological functions have been elucidated. Thus, novel opportunities for therapeutic interventions in cardiovascular diseases were revealed targeting ACE2 or Mas