Examinando por Autor "Gonzalez, A."
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Ítem Eggshell membrane as a biodegradable bone regeneration inhibitor(WILEY, 2008-06-01) Arias, J. I.; Gonzalez, A.; Fernandez, M. S.; Gonzalez, C.; Saez, D.; Arias, J. L.The efficiency of chicken eggshell membranes combined with a minimally invasive small osteotomy procedure of the ulna to accomplish an efficient release of the radius so that it can continue to grow in an unstressed manner was tested in rabbits. Eggshell membranes were extracted from chicken eggs, rinsed, dried and sterilized with ethylene oxide for 24 h. For reactivity testing, four separate subcutaneous pockets were created in 10 rats in the paravertebral region by blunt dissection and eggshell membranes were implanted in two of them. After 1-16 weeks, the implants were retrieved with the surrounding soft tissues and submitted to histological examination. Subsequently, 10 rabbits were anaesthetized and a complete 0.5 mm. wide osteotomy was performed in both the right and the left distal ulna. A piece of eggshell membranes was interposed in the osteotomy site of one ulna. The opposite osteotomized ulna was left as a negative control. The rabbits were injected with oxytetracycline at the time of surgery and this was repeated every 7 days for labelling new bone formation. After 1-16 weeks, ulnar osteotomized regions were histologically examined. After histological, fluorescence microcopy and radiological evaluation, we demonstrate here for the first time that eggshell membranes as interpositional material in rabbit osteotomized ulnar experiments acted as an active barrier against bone bridging. The degradation of the eggshell membrane, due to host reaction, appeared sufficiently late to cause the desirable delay of bone healing that is compatible with the time needed for a corrective response. Copyright (C) 2008 John Wiley & Sons, Ltd.Ítem Impact of exercise training on the sarcopenia criteria in non-alcoholic fatty liver disease: A systematic review and meta-analysis(Page Press Publications, 2021-03) Gonzalez, A.; Valero-Breton, M.; Huerta-Salgado, C.; Achiardi, O.; Simon, F.; Cabello-Verrugio, C.Sarcopenia is a highly prevalent complication of non-alcoholic fatty liver disease (NAFLD). We aimed to conduct a systematic review and meta-analyses to elucidate the exercise training (ET)'s efficacy on NAFLD adult patients' sarcopenia criteria. We identified relevant randomized controlled trials (RCT) in electronic databases PubMed, CINAHL, and Scopus. We selected seven RCT from 66 screened studies. The ET programs included endurance or combined (endurance and resistance) training. No study performed resistance training alone. The physical function improved with endurance or combined training (mean differences [MD] 8.26 mL/Kg*min [95% CI 5.27 to 11.24 mL/Kg*min], p < 0.0001); Muscle mass showed no evidence of the beneficial effects of endurance or combined training (MD 1.01 Kg [95% CI -1.78 to 3.80 Kg], p = 0.48). None of the selected studies evaluated muscle strength. Endurance and combined training increase physical function criteria but do not improve muscle mass criteria on sarcopenia in NAFLD patients. These results must be interpreted with caution for the small number of patients included in the RCTs analyzed, the different characteristics of the ET carried out, the non-use of resistance training, which prevents assess its effect on sarcopenia despite the evidence that recommends it and does not assessment muscle strength criteria in RCT include. Future research should include muscle strength assessments and resistance training to evaluate the effects in this condition. Exercise training is beneficial for sarcopenia in NAFLD but is necessary more experimental evidence to define the best type of training that positively affects the three criteria of sarcopenia. PROSPERO reference number CRD42020191471. © 2021 PAGEPress Publications. All rights reserved.Ítem Lymphoid B cells induce NF-κB activation in high endothelial cells from human tonsils(Oxford University Press [University Publisher] Japanese Society for Immunology [Associate Organisation], 2006-02) Naves, R.; Reyes, L.; Rosemblatt, M.; Jacobelli, S.; Gonzalez, A.; Bono, M.Immune surveillance depends on still poorly understood lymphocyte-endothelium interactions required for lymphocyte transendothelial migration into secondary lymphoid organs. The nuclear factor κB (NF-κB) regulatory system and its inhibitory IκB proteins control the inducible expression of adhesion molecules, cytokines and chemokines involved in endothelial activation and lymphocyte transmigration. Here we present results showing the activation of this system in response to the interaction of high endothelial cells from human tonsils (HUTEC) with human B and T lymphoid cell lines and primary tonsillar lymphocytes. Western blot and electrophoretic mobility shift assays show that adhesion of different lymphoid cells induce varying levels of NF-κB activation in HUTEC, with Daudi cells, tonsil-derived B cell line 10 (TBCL-10) and primary tonsillar B lymphocytes causing the strongest activation. The main NF-κB protein complexes translocated to the nucleus were p65/p50 and p50/p50. Results from reverse transcription-PCR and flow cytometry analysis of HUTEC indicate that the interaction with Daudi cells induce an increased expression of IL-6 and IL-8 mRNA and cell-surface expression of intercellular adhesion molecule-1, all of which were prevented by sodium salicylate, an inhibitor of NF-κB activation. Transwell experiments show that NF-κB activation and the response of HUTEC to the interaction of Daudi cells does not depend on direct cell-cell contact but rather on the production of soluble factors that require the presence of both cell types. These results suggest that lymphocytes and high endothelium establish a cross talk leading to NF-κB-mediated expression of cytokines and adhesion molecules, inducing endothelial cell activation.Ítem Protective effect of angiotensin 1–7 on sarcopenia induced by chronic liver disease in mice(MDPI AG, 2020-04) Aguirre, F.; Abrigo, J.; Gonzalez, F.; Gonzalez, A.; Simon, F.; Cabello-Verrugio, C.Sarcopenia associated with chronic liver disease (CLD) is one of the more common extrahepatic features in patients with these pathologies. Among the cellular alterations observed in the muscle tissue under CLD is the decline in the muscle strength and function, as well as the increased fatigue. Morphological changes, such as a decrease in the fiber diameter and transition in the fiber type, are also reported. At the molecular level, sarcopenia for CLD is characterized by: (i) a decrease in the sarcomeric protein, such as myosin heavy chain (MHC); (ii) an increase in the ubiquitin–proteasome system markers, such as atrogin-1/MAFbx1 and MuRF-1/TRIM63; (iii) an increase in autophagy markers, such as LC3II/LC3I ratio. Among the regulators of muscle mass is the renin-angiotensin system (RAS). The non-classical axis of RAS includes the Angiotensin 1–7 [Ang-(1-7)] peptide and its receptor Mas, which in skeletal muscle has anti-atrophic effect in models of muscle wasting induced by immobilization, lipopolysaccharide, myostatin or angiotensin II. In this paper, we evaluated the effect of Ang-(1-7) on the sarcopenia by CLD in a murine model induced by the 5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) hepatotoxin administered through diet. Our results show that Ang-(1-7) administration prevented the decline of the function and strength of muscle and increased the fatigue detected in the DDC-fed mice. Besides, we observed that the decreased fiber diameter and MHC levels, as well as the transition of fiber types, were all abolished by Ang-(1-7) in mice fed with DDC. Finally, Ang-(1-7) can decrease the atrogin-1 and MuRF-1 expression as well as the autophagy marker in mice treated with DDC. Together, our data support the protective role of Ang-(1-7) on the sarcopenia by CLD in mice. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.Ítem Role of Oxidative Stress in Hepatic and Extrahepatic Dysfunctions during Nonalcoholic Fatty Liver Disease (NAFLD)(Hindawi, 2020) Gonzalez, A.; Huerta-Salgado, C.; Orozco-Aguilar, J.; Aguirre, F.; Tacchi, F.; Simon, F.; Cabello-Verrugio, C.Nonalcoholic fatty liver disease (NAFLD) is a pathology that contains a broad liver dysfunctions spectrum. These alterations span from noninflammatory isolated steatosis until nonalcoholic steatohepatitis (NASH), a more aggressive form of the disease characterized by steatosis, inflammatory status, and varying liver degrees fibrosis. NAFLD is the most prevalent chronic liver disease worldwide. The causes of NAFLD are diverse and include genetic and environmental factors. The presence of NASH is strongly associated with cirrhosis development and hepatocellular carcinoma, two conditions that require liver transplantation. The liver alterations during NAFLD are well described. Interestingly, this pathological condition also affects other critical tissues and organs, such as skeletal muscle and even the cardiovascular, renal, and nervous systems. Oxidative stress (OS) is a harmful state present in several chronic diseases, such as NAFLD. The purpose of this review is to describe hepatic and extrahepatic dysfunctions in NAFLD. We will also review the influence of OS on the physiopathological events that affect the critical function of the liver and peripheral tissues.