Impact of physical exercise in cardiovascular and metabolic parameters in post-menopausal women / Impacto do exercício físico nos parâmetros cardiovasculares e metabólicos em mulheres na pós-menopausa

Backgound: understanding how physical exercise changes vascular and metabolic health of women with hormonal changes resulting from the menopausal period is essential for better discernment of therapeutic anti-sedentary indications. Besides that, the effects of physical exercise in post-menopause women is not entirely understood.Objectives: the aim of the present study was to investigate the effect of physical exercise on specific parameters in post-menopause women’s cardiovascular and metabolic health.Design: a total of 31 participants, assisted in a primary health care were included. Twenty (20) women from a program promoted by the health service were assigned to the physically active group (AG), in which they performed many types of exercise, including stretching, aerobic and resistance training of varying intensities. Eleven (11) women on the control group (CG) were recruited at the same service and attended the institution for other ends related to their health.Results: arterial pressure had a significant diference between AG adn CG: mean systolic blood pressure (SBP) in the AG was 111±6mmHg versus 118mmHg in the CG; mean diastolic blood pressure (DBP) was 71mmHg in the AG versus 82mmHg in the CG. The fact that the majority of women in the AG (60%) had more than 8 years of formal education versus 37% in the CG drew attention. In both groups, most women had less than 3 children. Most women in the CG reported formal work while domestic work prevailed in the AG. Despite this, per capita income showed no difference.Conclusion: blood pressure, an important cardiovascular risk factor, is significantly lower in post-menopause women that practised regular physical exercises; in addition, socioeconomic factors is very close influencer in physical exercise engagement. Other studies are necessary to evaluate more cardiovascular variables.Backgound: understanding how physical exercise changes vascular and metabolic health of women with hormonal changes resulting from the menopausal period is essential for better discernment of therapeutic anti-sedentary indications. Besides that, the effects of physical exercise in post-menopause women is not entirely understood.Objectives: the aim of the present study was to investigate the effect of physical exercise on specific parameters in post-menopause women’s cardiovascular and metabolic health.Design: a total of 31 participants, assisted in a primary health care were included. Twenty (20) women from a program promoted by the health service were assigned to the physically active group (AG), in which they performed many types of exercise, including stretching, aerobic and resistance training of varying intensities. Eleven (11) women on the control group (CG) were recruited at the same service and attended the institution for other ends related to their health.Results: arterial pressure had a significant diference between AG adn CG: mean systolic blood pressure (SBP) in the AG was 111±6mmHg versus 118mmHg in the CG; mean diastolic blood pressure (DBP) was 71mmHg in the AG versus 82mmHg in the CG. The fact that the majority of women in the AG (60%) had more than 8 years of formal education versus 37% in the CG drew attention. In both groups, most women had less than 3 children. Most women in the CG reported formal work while domestic work prevailed in the AG. Despite this, per capita income showed no difference.Conclusion: blood pressure, an important cardiovascular risk factor, is significantly lower in post-menopause women that practised regular physical exercises; in addition, socioeconomic factors is very close influencer in physical exercise engagement. Other studies are necessary to evaluate more cardiovascular variables

Intravital Microscopic Evaluation of the Effects of a CXCR2 Antagonist in a Model of Liver Ischemia Reperfusion Injury in Mice

BackgroundIschemia–reperfusion (IR) is a major contributor to graft rejection after liver transplantation. During IR injury, an intense inflammatory process occurs in the liver. Neutrophils are considered central players in the events that lead to liver injury. CXC chemokines mediate hepatic inflammation following reperfusion. However, few studies have demonstrated in real-time the behavior of recruited neutrophils. We used confocal intravital microscopy (IVM) to image neutrophil migration in the liver and to analyze in real-time parameters of neutrophil recruitment in the inflamed tissue in animals treated or not with reparixin, an allosteric antagonist of CXCR1/2 receptors.Materials and methodsWT and LysM-eGFP mice treated with reparixin or saline were subjected to 60 min of ischemia followed by different times of reperfusion. Mice received Sytox orange intravenously to show necrotic DNA in IVM. The effect of reparixin on parameters of local and systemic reperfusion-induced injury was also investigated.ResultsIR induced liver injury and inflammation, as evidenced by high levels of alanine aminotransferase and myeloperoxidase activity, chemokine and cytokine production, and histological outcome. Treatment with reparixin significantly decreased neutrophil influx. Moreover, reparixin effectively suppressed the increase in serum concentrations of TNF-α, IL-6, and CCL3, and the reperfusion-associated tissue damage. The number of neutrophils in the liver increased between 6 and 24 h of reperfusion, whereas the distance traveled, velocity, neutrophil size and shape, and cluster formation reached a maximum 6 h after reperfusion and then decreased gradually. In vivo imaging revealed that reparixin significantly decreased neutrophil infiltration and movement and displacement of recruited cells. Moreover, neutrophils had a smaller size and less elongated shape in treated mice.ConclusionImaging of the liver by confocal IVM was successfully implemented to describe neutrophil behavior in vivo during liver injury by IR. Treatment with reparixin decreased not only the recruitment of neutrophils in tissues but also their activation state and capacity to migrate within the liver. CXCR1/2 antagonists may be a promising therapy for patients undergoing liver transplantation

Neutrophils: a cornerstone of liver ischemia and reperfusion injury

Ischemia-reperfusion injury (IRI) is the main cause of morbidity and mortality due to graft rejection after liver transplantation. During IRI, an intense inflammatory process occurs in the liver. This hepatic inflammation is initiated by the ischemic period but occurs mainly during the reperfusion phase, and is characterized by a large neutrophil recruitment to the liver. Production of cytokines, chemokines, and danger signals results in activation of resident hepatocytes, leukocytes, and Kupffer cells. The role of neutrophils as the main amplifiers of liver injury in IRI has been recognized in many publications. Several studies have shown that elimination of excessive neutrophils or inhibition of their function leads to reduction of liver injury and inflammation. However, the mechanisms involved in neutrophil recruitment during liver IRI are not well known. In addition, the molecules necessary for this type of migration are poorly defined, as the liver presents an atypical sinusoidal vasculature in which the classical leukocyte migration paradigm only partially applies. This review summarizes recent advances in neutrophil-mediated liver damage, and its application to liver IRI. Basic mechanisms of activation of neutrophils and their unique mechanisms of recruitment into the liver vasculature are discussed. In particular, the role of danger signals, adhesion molecules, chemokines, glycosaminoglycans (GAGs), and metalloproteinases is explored. The precise definition of the molecular events that govern the recruitment of neutrophils and their movement into inflamed tissue may offer new therapeutic alternatives for hepatic injury by IRI and other inflammatory diseases of the liver.status: publishe

Intravital microscopic evaluation of the effects of a CXCR2 antagonist in a model of liver ischemia reperfusion injury in mice

Ischemia-reperfusion (IR) is a major contributor to graft rejection after liver transplantation. During IR injury, an intense inflammatory process occurs in the liver. Neutrophils are considered central players in the events that lead to liver injury. CXC chemokines mediate hepatic inflammation following reperfusion. However, few studies have demonstrated in real-time the behavior of recruited neutrophils. We used confocal intravital microscopy (IVM) to image neutrophil migration in the liver and to analyze in real-time parameters of neutrophil recruitment in the inflamed tissue in animals treated or not with reparixin, an allosteric antagonist of CXCR1/2 receptors.status: publishe

USO DE DROGAS E DESEMPENHO ESCOLAR ENTRE JOVENS E ADOLESCENTES DO ENSINO MÉDIO DE UMA ESCOLA PÚBLICA DE PIRES DO RIO – GO

Este estudo teve como objetivo estimar a prevalência do uso de drogas por discentes de uma escola da rede estadual de Pires do Rio, Goiás, associando-a ao desempenho escolar dos mesmos. Participaram da pesquisa 371 discentes do ensino médio, com idade entre 14 e 34 anos, dos turnos matutino e noturno que responderam a um questionário anônimo coletivamente em sala de aula. As drogas mais consumidas, alguma vez na vida, foram: álcool (95,8%), tabaco (46,1%), maconha (3,5%), solventes (4%), cocaína (4%) e crack (0,5%). A partir deste estudo, foi possível perceber que os índices de reprovação apresentados, nos períodos investigados, foi elevado, quando associado aos discentes que já tiveram contato com algum tipo de droga, o que reforça a hipótese de que o uso de tais substâncias pode interferir no desempenho escolar dos alunos. Considera-se necessário a implantação de políticas de intervenção contra o uso de drogas, a fim de minimizar o problema

Paradoxical role of matrix metalloproteinases in liver injury and regeneration after sterile acute hepatic failure

Acetaminophen (APAP) poisoning is one of the leading causes of acute hepatic failure and liver transplantation is often the only lifesaving alternative. During the course of hepatocyte necrosis, an intense accumulation of neutrophils is often observed within the liver microenvironment. Despite the classic idea that neutrophil accumulation in tissues causes collateral tissue damage, there is a growing body of evidence showing that neutrophils can also orchestrate the resolution of inflammation. In this work, drug-induced liver injury was induced by oral administration of APAP and pharmacological intervention was made 12 h after this challenge. Liver injury and repair kinetics were evaluated by a novel combination of enzyme quantifications, ELISA, specific antagonists of neutrophil enzymes and confocal intravital microscopy. We have demonstrated that neutrophil infiltration is not only involved in injury amplification, but also in liver tissue repair after APAP-induced liver injury. In fact, while neutrophil depletion led to reduced hepatic necrosis during APAP poisoning, injury recovery was also delayed in neutropenic mice. The mechanisms underlying the neutrophil reparative role involved rapid degranulation and matrix metalloproteinases (MMPs) activity. Our data highlights the crucial role of neutrophils, in particular for MMPs, in the resolution phase of APAP-induced inflammatory response

Paradoxical Role of Matrix Metalloproteinases in Liver Injury and Regeneration after Sterile Acute Hepatic Failure

Acetaminophen (APAP) poisoning is one of the leading causes of acute hepatic failure and liver transplantation is often the only lifesaving alternative. During the course of hepatocyte necrosis, an intense accumulation of neutrophils is often observed within the liver microenvironment. Despite the classic idea that neutrophil accumulation in tissues causes collateral tissue damage, there is a growing body of evidence showing that neutrophils can also orchestrate the resolution of inflammation. In this work, drug-induced liver injury was induced by oral administration of APAP and pharmacological intervention was made 12 h after this challenge. Liver injury and repair kinetics were evaluated by a novel combination of enzyme quantifications, ELISA, specific antagonists of neutrophil enzymes and confocal intravital microscopy. We have demonstrated that neutrophil infiltration is not only involved in injury amplification, but also in liver tissue repair after APAP-induced liver injury. In fact, while neutrophil depletion led to reduced hepatic necrosis during APAP poisoning, injury recovery was also delayed in neutropenic mice. The mechanisms underlying the neutrophil reparative role involved rapid degranulation and matrix metalloproteinases (MMPs) activity. Our data highlights the crucial role of neutrophils, in particular for MMPs, in the resolution phase of APAP-induced inflammatory response.status: publishe