7 research outputs found
Fatores de redução de resistĂȘncia de geotĂȘxtil tecido devido a danos mecĂąnicos causados por resĂduos de construção e demolição reciclados (RCDR)
O uso de resĂduos de construção e demolição reciclados (RCD-R) em obras com geossintĂ©ticos apresenta-se como uma interessante alternativa do ponto de vista econĂŽmico-ambiental. No entanto, para viabilizar esta proposta, um fator primordial deve ser investigado: os danos mecĂąnicos que os RCDR podem causar nos geossintĂ©ticos duranto os processos de lançamento e compactação. Diante disso, esta pesquisa buscou avaliar experimentalmente os danos mecĂąnicos em geotĂȘxtil tecido devido a danos mecĂąnicos causados por RCD-R. Com isso, espera-se obter paramentos de fatores de redução de resistĂȘncia Ă tração, que possam subsidiar a elaboração de projetos que contemplem o uso de RCD-R em obras de terra reforçadas com geossintĂ©ticos. Os resultados revelaram os RCD-R apresentam excelentes propriedades geotĂ©cnicas, com uma baixa variabilidade. Observou-se tambĂ©m que os danos provocados pelo lançamento do RCD-R foram influenciados pelo tipo de geotĂȘxtil tecido e a altura de lançamento
Oxidants, antioxidants and mitochondrial function in non-proliferative diabetic retinopathy
Background: Diabetic retinopathy (DR) is a preventable cause of visual disability. The aims of the present study were to investigate levels and behavior oxidative stress markers and mitochondrial function in non-proliferative DR (NPDR) and to establish the correlation between the severity of NPDR and markers of oxidative stress and mitochondrial function. Methods: In a transverse analysis, type 2 diabetes mellitus (T2DM) patients with mild, moderate and severe non-proliferative DR (NPDR) were evaluated for markers of oxidative stress (i.e. products of lipid peroxidation (LPO) and nitric oxide (NO) catabolites) and antioxidant activity (i.e. total antioxidant capacity (TAC), catalase, and glutathione peroxidase (GPx) activity of erythrocytes). Mitochondrial function was also determined as the fluidity of the submitochondrial particles of platelets and the hydrolytic activity of F0/F1-ATPase. Results: Levels of LPO and NO were significantly increased in T2DM patients with severe NPDR (3.19±0.05Όmol/mL and 45.62±1.27pmol/mL, respectively; P<0.007 and P<0.0001 vs levels in health volunteers, respectively), suggesting the presence of oxidative stress. TAC had significant decrease levels with minimum peak in severe retinopathy with 7.98±0.48mEq/mL (P<0.0001). In contrast with TAC, erythrocyte catalase and GPx activity was increased in patients with severe NPDR (139.4±4.4 and 117.13±14.84U/mg, respectively; P<0.0001 vs healthy volunteers for both), suggesting an imbalance between oxidants and antioxidants. The fluidity of membrane submitochondrial particles decreased significantly in T2DM patients with mild, moderate, or severe NPDR compared with that in healthy volunteers (P<0.0001 for all). Furthermore, there was a significant increase in the hydrolytic activity of the F0/F1-ATPase in T2DM patients with mild NPDR (265.07±29.55nmol/PO4; P<0.0001 vs healthy volunteers), suggesting increased catabolism. Conclusions: Patients with NPDR exhibit oxidative deregulation with decreased membrane fluidity of submitochondrial particles and increased systemic catabolism (mitochondrial dysfunction) with the potential for generalized systemic damage in T2DM. © 2013 The Authors. Journal of Diabetes published by Ruijin Hospital, Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
Interval-Based Diagnosis of Biological Systems - a Powerful Tool for Highly Uncertain Anaerobic Digestion Processes
Background: Diabetic retinopathy (DR) is a preventable cause of visual disability. The aims of the present study were to investigate levels and behavior oxidative stress markers and mitochondrial function in non-proliferative DR (NPDR) and to establish the correlation between the severity of NPDR and markers of oxidative stress and mitochondrial function. Methods: In a transverse analysis, type 2 diabetes mellitus (T2DM) patients with mild, moderate and severe non-proliferative DR (NPDR) were evaluated for markers of oxidative stress (i.e. products of lipid peroxidation (LPO) and nitric oxide (NO) catabolites) and antioxidant activity (i.e. total antioxidant capacity (TAC), catalase, and glutathione peroxidase (GPx) activity of erythrocytes). Mitochondrial function was also determined as the fluidity of the submitochondrial particles of platelets and the hydrolytic activity of F0/F1-ATPase. Results: Levels of LPO and NO were significantly increased in T2DM patients with severe NPDR (3.19 0.05?mol/mL and 45.62 1.27pmol/mL, respectively; P<0.007 and P<0.0001 vs levels in health volunteers, respectively), suggesting the presence of oxidative stress. TAC had significant decrease levels with minimum peak in severe retinopathy with 7.98 0.48mEq/mL (P<0.0001). In contrast with TAC, erythrocyte catalase and GPx activity was increased in patients with severe NPDR (139.4 4.4 and 117.13 14.84U/mg, respectively; P<0.0001 vs healthy volunteers for both), suggesting an imbalance between oxidants and antioxidants. The fluidity of membrane submitochondrial particles decreased significantly in T2DM patients with mild, moderate, or severe NPDR compared with that in healthy volunteers (P<0.0001 for all). Furthermore, there was a significant increase in the hydrolytic activity of the F0/F1-ATPase in T2DM patients with mild NPDR (265.07 29.55nmol/PO4; P<0.0001 vs healthy volunteers), suggesting increased catabolism. Conclusions: Patients with NPDR exhibit oxidative deregulation with decreased membrane fluidity of submitochondrial particles and increased systemic catabolism (mitochondrial dysfunction) with the potential for generalized systemic damage in T2DM. " 2013 The Authors. Journal of Diabetes published by Ruijin Hospital, Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd.",,,,,,"10.1111/1753-0407.12076",,,"http://hdl.handle.net/20.500.12104/43451","http://www.scopus.com/inward/record.url?eid=2-s2.0-84895071252&partnerID=40&md5=d3b0033aa6faf6f6a5e209b1a8f72b8