520 research outputs found

    SU(2) Kinetic Mixing Terms and Spontaneous Symmetry Breaking

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    The non-abelian generalization of the Holdom model --{\it i.e.} a theory with two gauge fields coupled to the kinetic mixing term gtr(Fμν(A)Fμν(B))g {tr}(F_{\mu \nu} (A) F_{\mu \nu} (B))-- is considered. Contrarily to the abelian case, the group structure G×GG\times G is explicitly broken to GG. For SU(2) this fact implies that the residual gauge symmetry as well as the Lorentz symmetry is spontaneusly broken. We show that this mechanism provides of masses for the involved particles. Also, the model presents instanton solutions with a redefined coupling constant.Comment: 9pp. typos and clarifications are adde

    Primary pleural liposarcoma, pleomorphic variant

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    Primary pleural liposarcoma (PPL) is a rare tumor derived from primitive mesenchymal tissue. We report a case of a 49-year-old female patient complaining of thoracic pain and dyspnea for 3 months. The chest X-ray showed a left basal opacity of lobulated contours and the thoracic computer tomography (CT) scan revealed a left pleural collection/mass, of 18 HU density and passive pulmonary atelectasis. The patient was taken to surgery and the cytologic examination of the gelatinous mass found in the procedure confirmed the diagnosis of a pleomorphic variant of pleural liposarcoma. We emphasise in the importance of careful inspection of the origin of the tumor in the diagnostic images to allow accurate diagnosis. © Pioneer Bioscience Publishing Company

    Physical activity and bone health in schoolchildren: the mediating role of fitness and body fat

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    This is the final version of the article. Available from Public Library of Science via the DOI in this record.BACKGROUND: The relationship between physical activity (PA) and bone health is well known, although the role of percent body fat (%BF) and fitness as confounders or mediators in this relationship remains uncertain. OBJECTIVE: To examine whether the association between PA and bone mineral content (BMC) is mediated by %BF and cardiorespiratory fitness (CRF). METHODS: In this cross sectional study, BMC, total %BF (by DXA), vigorous PA (VPA), CRF, age and height were measured in 132 schoolchildren (62 boys, aged 8-11 years). ANCOVA was used to test differences in BMC by %BF, CRF and VPA, controlling for different sets of confounders. Simple mediation analyses and serial multiple mediation analyses were fitted to examine whether the relationship between PA and BMC is mediated by %BF and fitness. RESULTS: Children with high %BF had higher total body BMC than their peers after controlling for all sets of confounders. Children with good CRF or VPA had significantly less total body BMC after controlling for age and sex but in children with good CRF this inverse relation disappeared after adjusting by %BF. %BF and CRF both act as a full mediator in the association between VPA and BMC, after inclusion of the potential confounders in the models. CONCLUSION: Fitness and %BF seem to have a mediator role on the relationship between physical activity and bone mass.This study was funded by grant numbers PII1I09-0259-9898 and POII10-0208-5325 from the Ministry of Education and Science - Junta de Comunidades de Castilla-La Mancha, and Ministry of Health (FIS grant number PI081297). Additional funding was provided by the Research Network on Preventative Activities and Health Promotion (RD06/0018/0038)

    Influence of ligand structure and molecular geometry on the properties of d6 polypyridinic transition metal complexes

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    Different strategies to improve the excited state properties of polypyridinic complexes by varying ligand structure and molecular geometry are described. Bidentate and tetradentate ligands based on fragments as dipyrido[3,2-a:2′,3′-c]phenazine, dppz, and pyrazino[2,3-f][1,10]-phenanthroline, ppl, have been used. Quinonic residues were fused to these basic units to improve acceptor properties. Photophysical studies were performed in order to test theoretical predictions

    Barley-Ăź-glucans reduce systemic inflammation, renal injury and aortic calcification through ADAM17 and neutral-sphingomyelinase2 inhibition

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    In chronic kidney disease (CKD), hyperphosphatemia-induced inflammation aggravates vascular calcification (VC) by increasing vascular smooth muscle cell (VSMC) osteogenic differentiation, ADAM17-induced renal and vascular injury, and TNFα-induction of neutral-sphingomyelinase2 (nSMase2) to release pro-calcifying exosomes. This study examined anti-inflammatory β-glucans efficacy at attenuating systemic inflammation in health, and renal and vascular injury favoring VC in hyperphosphatemic CKD. In healthy adults, dietary barley β-glucans (Bβglucans) reduced leukocyte superoxide production, inflammatory ADAM17, TNFα, nSMase2, and pro-aging/pro-inflammatory STING (Stimulator of interferon genes) gene expression without decreasing circulating inflammatory cytokines, except for γ-interferon. In hyperphosphatemic rat CKD, dietary Bβglucans reduced renal and aortic ADAM17-driven inflammation attenuating CKD-progression (higher GFR and lower serum creatinine, proteinuria, kidney inflammatory infiltration and nSMase2), and TNFα-driven increases in aortic nSMase2 and calcium deposition without improving mineral homeostasis. In VSMC, Bβglucans prevented LPS- or uremic serum-induced rapid increases in ADAM17, TNFα and nSMase2, and reduced the 13-fold higher calcium deposition induced by prolonged calcifying conditions by inhibiting osteogenic differentiation and increases in nSMase2 through Dectin1-independent actions involving Bβglucans internalization. Thus, dietary Bβglucans inhibit leukocyte superoxide production and leukocyte, renal and aortic ADAM17- and nSMase2 gene expression attenuating systemic inflammation in health, and renal injury and aortic calcification despite hyperphosphatemia in CKD.A grant to A.S.D. and M.J.M. from IRBLleida and Agrotecnio Research collaborative projects from the Consell Social at Lleida University supported initial work, Instituto de Salud Carlos III and co-funded by European Union (ERDF/FEDER) (FIS PI11/00259, PI14/01452, PI17/02181), Plan de Ciencia, Tecnología e Innovación 2013–2017 y 2018–2022 del Principado de Asturias (GRUPIN14-028, IDI-2018-000152), RedInRen from ISCIII (ISCIII-RETIC REDINREN RD16/0009). Investigator support included: NC-L by GRUPIN14-028 and IDI-2018-000152, LM-A by GRUPIN14-028, SP by FICYT; MVA and PV by Educational Grant 2 A/2015 from ERA-EDTA CKD-MBD Working Group; PV and AC by ERA-EDTA fellowships 2011 and 2012; JR-C by MINECO (“Juan de la Cierva” program, FJCI-2015-23849); A.S.D. by Asociación Investigación de Fisiología Aplicada. A.S.D. and M.J.M. are members of the Campus Iberus (Ebro Valley Campus of International Excellence)

    Fibrosis in chronic kidney disease: Pathogenesis and consequences

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    Fibrosis is a process characterized by an excessive accumulation of the extracellular matrix as a response to different types of tissue injuries, which leads to organ dysfunction. The process can be initiated by multiple and different stimuli and pathogenic factors which trigger the cascade of reparation converging in molecular signals responsible of initiating and driving fibrosis. Though fibrosis can play a defensive role, in several circumstances at a certain stage, it can progressively become an uncontrolled irreversible and self-maintained process, named pathological fibrosis. Several systems, molecules and responses involved in the pathogenesis of the pathological fibrosis of chronic kidney disease (CKD) will be discussed in this review, putting special attention on inflammation, renin-angiotensin system (RAS), parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), Klotho, microRNAs (miRs), and the vitamin D hormonal system. All of them are key factors of the core and regulatory pathways which drive fibrosis, having a great negative kidney and cardiac impact in CKD

    Stability and enzymatic studies with omeprazole: hydroxypropyl-β-cyclodextrin

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    The original publication is available at www.springerlink.com. A publicação original está disponível em www.springerlink.comOmeprazole (OME) exhibits low stability to light, heat and humidity. In stress conditions OME stability should improve under inclusion complex form with hydroxypropyl-b-cyclodextrin (HPbCD). Stability of OME, its physical mixture (PM) with HPbCD and OME:HPbCD inclusion complex was assessed during 60 days. The inclusion complexes were prepared by kneading and freezedrying techniques and characterized by differential scanning calorimetry (DSC) and Fourier transform infrared spectroscopy (FTIR). A molecular modelling was also held to predict the most probable tridimensional conformation of inclusion complex OME:HPbCD. The inhibitory activity of free and complexed OME on selected enzymes, namely, papain (protease model of the proton pump) and acetylcholinesterase (enzyme present in cholinergic neurons and also involved in Alzheimer’s disease) was compared. The results obtained show that HPbCD do not protect against OME degradation, in any prepared powder, in the presence of light, heat and humidity. This may indicate that the reactive group of OME is not included in the HPbCD cavity. This fact is supported by molecular modelling data, which demonstrated that 2-pyridylmethyl group of OME is not included into the cyclodextrin cavity. In relation to enzymatic assays it was observed that free OME and OME in the binary systems showed identical inhibitory activity on papain and acethylcolinesterase, concluding that HPbCD do not affect OME activity on these two enzymes
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