Nanodomains in cardiopulmonary disorders and the impact of air pollution

Air pollution is a major environmental threat and each year about 7 million people reported to die as a result of air pollution. Consequently, exposure to air pollution is linked to increased morbidity and mortality world-wide. Diesel automotive engines are a major source of urban air pollution in the western societies encompassing particulate matter and diesel exhaust particles (DEP). Air pollution is envisioned as primary cause for cardiovascular dysfunction, such as ischemic heart disease, cardiac dysrhythmias, heart failure, cerebrovascular disease and stroke. Air pollution also causes lung dysfunction, such as chronic obstructive pulmonary disease (COPD), asthma, idiopathic pulmonary fibrosis (IPF), and specifically exacerbations of these diseases. DEP induces inflammation and reactive oxygen species production ultimately leading to mitochondrial dysfunction. DEP impair structural cell function and initiate the epithelial-to-mesenchymal transition, a process leading to dysfunction in endothelial as well as epithelial barrier, hamper tissue repair and eventually leading to fibrosis. Targeting cyclic adenosine monophosphate (cAMP) has been implicated to alleviate cardiopulmonary dysfunction, even more intriguingly cAMP seems to emerge as a potent regulator of mitochondrial metabolism. We propose that targeting of the mitochondrial cAMP nanodomain bear the therapeutic potential to diminish air pollutant - particularly DEP - induced decline in cardiopulmonary function

Dimethyl Fumarate Attenuates Lung Inflammation and Oxidative Stress Induced by Chronic Exposure to Diesel Exhaust Particles in Mice

Air pollution is mainly caused by burning of fossil fuels, such as diesel, and is associated with increased morbidity and mortality due to adverse health effects induced by inflammation and oxidative stress. Dimethyl fumarate (DMF) is a fumaric acid ester and acts as an antioxidant and anti-inflammatory agent. We investigated the potential therapeutic effects of DMF on pulmonary damage caused by chronic exposure to diesel exhaust particles (DEPs). Mice were challenged with DEPs (30 µg per mice) by intranasal instillation for 60 consecutive days. After the first 30 days, the animals were treated daily with 30 mg/kg of DMF by gavage for the remainder of the experimental period. We demonstrated a reduction in total inflammatory cell number in the bronchoalveolar lavage (BAL) of mice subjected to DEP + DMF as compared to those exposed to DEPs alone. Importantly, DMF treatment was able to reduce lung injury caused by DEP exposure. Intracellular total reactive oxygen species (ROS), peroxynitrite (OONO), and nitric oxide (NO) levels were significantly lower in the DEP + DMF than in the DEP group. In addition, DMF treatment reduced the protein expression of kelch-like ECH-associated protein 1 (Keap-1) in lung lysates from DEP-exposed mice, whereas total nuclear factor κB (NF-κB) p65 expression was decreased below baseline in the DEP + DMF group compared to both the control and DEP groups. Lastly, DMF markedly reduced DEP-induced expression of nitrotyrosine, glutathione peroxidase-1/2 (Gpx-1/2), and catalase in mouse lungs. In summary, DMF treatment effectively reduced lung injury, inflammation, and oxidative and nitrosative stress induced by chronic DEP exposure. Consequently, it may lead to new therapies to diminish lung injury caused by air pollutants

Music therapy in nursing care in intensive care

Objective: To analyze studies nationally published that discuss the use of music in nursing care in intensive care. Method: Descriptive study, systematic review of literature type, having as object the studies published about music therapy in the intensive care unit (ICU), in national journals accessed during the month of March, 2011. Results: Most of the publications were focused on pediatric care, not directed to the ICU, indexed in the LILACS database, predominantly literature review. Conclusion: With further study and dissemination of knowledge in the scientific community, health workers and nursing satisfaction can implement music therapy in health services

The scientific production about occupational health of nursing

Objective: To know the scientific literature about the nursing worker's health. Method: Bibliography review of literature published from 2005 to 2010. It was used the databases LILACS and SCIELO and BDENF, with intersection between the descriptors nursing and worker's health, 20 studies were selected. Results: Most publications on nursing worker's health discuss biosecurity, exposure to biohazards, occupational stress and its prevention and control measures. There are still few published studies about this issue in primary care or family health strategy, with most studies conducted in hospitals, mainly in university hospitals. Conclusion: The research on occupational health of nursing is important because it can contribute significantly to the improved quality of life of nursing staff

The scientific literature on nursing audit and quality of records

Objectives: To know about the scientific production about nursing audit and to identify the importance of the nursing record in medical records for the audit. Method: Narrative literature review, it was selected articles related to nursing audit and nursing records in the electronic databases Scientific Electronic Library Online, and Latin American Literature and Caribbean Health Sciences, published between 2000 and 2010. Results: The articles analyzed indicated that there are few studies about this subject. It was identified that nursing audit is currently conducted by the retrospective method in the medical records and it is facing the accounting framework, and that nursing records are unsatisfactory quality as a tool to collect data. Conclusion: There are prospects that pass the audit to investigate the quality of care and to have an educational character that will enable the quality of care

Redox markers and inflammation are differentially affected by atorvastatin, pravastatin or simvastatin administered before endotoxin-induced acute lung injury

AbstractStatins are standard therapy for the treatment of lipid disorders, and the field of redox biology accepts that statins have antioxidant properties. Our aim in this report was to consider the pleiotropic effects of atorvastatin, pravastatin and simvastatin administered prior to endotoxin-induced acute lung injury. Male mice were divided into 5 groups and intraperitoneally injected with LPS (10mg/kg), LPS plus atorvastatin (10mg/kg/day; A+LPS group), LPS plus pravastatin (5mg/kg/day; P+LPS group) or LPS plus simvastatin (20mg/kg/day; S+LPS group). The control group received saline. All mice were sacrificed one day later. There were fewer leukocytes in the P+LPS and S+LPS groups than in the LPS group. MCP-1 cytokine levels were lower in the P+LPS group, while IL-6 levels were lower in the P+LPS and S+LPS groups. TNF-α was lower in all statin-treated groups. Levels of redox markers (superoxide dismutase and catalase) were lower in the A+LPS group (p<0.01). The extent of lipid peroxidation (malondialdehyde and hydroperoxides) was reduced in all statin-treated groups (p<0.05). Myeloperoxidase was lower in the P+LPS group (p<0.01). Elastance levels were significantly greater in the LPS group compared to the statin groups. Our results suggest that atorvastatin and pravastatin but not simvastatin exhibit anti-inflammatory and antioxidant activity in endotoxin-induced acute lung injury

Critical role for CCR2 and HMGB1 in induction of experimental endotoxic shock

AbstractOur aim was to investigate CCR2 and HMGB1 involvement in a murine model of endotoxic shock. We used C57BL/6 CCR2 knockout (KO) mice and wild-type (WT) littermates to establish an optimal dose of LPS. CCR2 KO mice survived more frequently than WT mice after 80, 40 and 20mg/kg of LPS i.p. Inflammation and redox markers were high in WT mice than in CCR2 KO mice. HMGB1 expression was reduced in CCR2 KO mice in parallel to ERK 1/2 activation. Therefore, we used glycyrrhizic acid (50mg/kg), an HMGB1 inhibitor in WT mice injected with LPS, and mortality was fully abolished. Thus, drugs targeting CCR2 and HMGB1 could represent future resources for sepsis treatment

Resposta ao exercício físico aeróbico tipo natação sobre o estado oxidativo cardíaco induzido por inalação de fumaça de cigarro em ratos Wistar

Introdução: O estresse oxidativo (EO) é o desequilíbrio no balanço pró-oxidante e antioxidante que pode ser desencadeado por diversos fatores, sendo um deles o hábito de fumar, uma vez que aumenta a concentração de espécies reativas de oxigênio (ERO). A realização do exercício físico de forma regular é capaz de melhorar o sistema de defesa antioxidante. Objetivo: Assim, este estudo teve como objetivo avaliar a resposta ao exercício físico aeróbico, como a natação, sobre o estado oxidativo cardíaco, induzido por inalação de fumaça de cigarro no coração de ratos. Metodologia: utilizaram-se ratos Wistar machos, divididos em quatro grupos: treinado fumante (TF), treinado não fumante (TNF), sedentário fumante (SF) e sedentário não fumante (SNF). O protocolo de treinamento utilizado foi de 16 semanas, sendo associado à administração passiva de fumaça de cigarro. Ao final do protocolo, o coração foi coletado para análises bioquímicas pró e antioxidantes. Resultado: Os resultados demonstraram aumento da atividade da enzima CAT nos animais treinados, em relação aos sedentários, e uma diminuição na concentração das TBARS, quando se compara os sedentários aos treinados. Ao comparar os animais fumantes com os não fumantes, percebeu-se diminuição significativa na atividade da CAT dos animais fumantes em relação aos não fumantes, bem como a concentração do FOX (

Oxidative damage induced by cigarette smoke exposure in mice : impact on lung tissue and diaphragm muscle

Objetivo: Avaliar o dano oxidativo (oxidação lipídica, oxidação proteica, thiobarbituric acid-reactive substances [TBARS, substâncias reativas ao ácido tiobarbitúrico], e carbonilação) e inflamação (expressão de phosphorylated AMP-activated protein kinase e de phosphorylated mammalian target of rapamycin (p-AMPK e p-mTOR, respectivamente) em tecido pulmonar e músculos do diafragma em camundongos C57BL/6 machos expostos à fumaça de cigarro (FC) por 7, 15, 30, 45 ou 60 dias. Métodos: Trinta e seis camundongos machos da espécie C57BL/6 foram divididos em seis grupos (n = 6/grupo): grupo controle e 5 grupos expostos a FC por 7, 15, 30, 45 e 60 dias, respectivamente. Resultados: Comparados aos camundongos controle, os camundongos expostos à FC apresentaram menor peso corporal em 30 dias. Nos camundongos expostos à FC (comparados aos controle) as maiores diferenças (aumentos) nos níveis de TBARS foram observados no dia 7 no músculo diafragma, comparado ao dia 45 em tecido pulmonar; as maiores diferenças (aumentos) nos níveis de carbonilas foram observados no dia 7 em ambos os tipos de tecido; e os níveis de sulfidrilas foram menores, nos dois tipos de tecidos, em todos os tempos. No tecido pulmonar e no músculo diafragma, a expressão de p-AMPK exibiu um comportamento semelhante ao dos níveis de TBARS. A expressão de p-mTOR foi maior que o valor controle nos dias 7 e 15 no tecido pulmonar, assim como no dia 45 no músculo diafragma. Conclusões: Nossos dados demonstram que a exposição à FC produz dano oxidativo tanto no tecido pulmonar quanto (primariamente) no tecido muscular, tendo um efeito adicional no músculo respiratório, como é frequentemente observado em fumantes com DPOC.Objective: To evaluate oxidative damage (lipid oxidation, protein oxidation, thiobarbituric acid-reactive substances [TBARS], and carbonylation) and inflammation (expression of phosphorylated AMP-activated protein kinase and mammalian target of rapamycin [p-AMPK and p-mTOR, respectively]) in the lung parenchyma and diaphragm muscles of male C57BL-6 mice exposed to cigarette smoke (CS) for 7, 15, 30, 45, or 60 days. Methods: Thirty-six male C57BL-6 mice were divided into six groups (n = 6/group): a control group; and five groups exposed to CS for 7, 15, 30, 45, and 60 days, respectively. Results: Compared with control mice, CS-exposed mice presented lower body weights at 30 days. In CS-exposed mice (compared with control mice), the greatest differences (increases) in TBARS levels were observed on day 7 in diaphragm-muscle, compared with day 45 in lung tissue; the greatest differences (increases) in carbonyl levels were observed on day 7 in both tissue types; and sulfhydryl levels were lower, in both tissue types, at all time points. In lung tissue and diaphragm muscle, p-AMPK expression exhibited behavior similar to that of TBARS. Expression of p-mTOR was higher than the control value on days 7 and 15 in lung tissue, as it was on day 45 in diaphragm muscle. Conclusion: Our data demonstrate that CS exposure produces oxidative damage, not only in lung tissue but also (primarily) in muscle tissue, having an additional effect on respiratory muscle, as is frequently observed in smokers with COPD

2 nd Brazilian Consensus on Chagas Disease, 2015

Abstract Chagas disease is a neglected chronic condition with a high burden of morbidity and mortality. It has considerable psychological, social, and economic impacts. The disease represents a significant public health issue in Brazil, with different regional patterns. This document presents the evidence that resulted in the Brazilian Consensus on Chagas Disease. The objective was to review and standardize strategies for diagnosis, treatment, prevention, and control of Chagas disease in the country, based on the available scientific evidence. The consensus is based on the articulation and strategic contribution of renowned Brazilian experts with knowledge and experience on various aspects of the disease. It is the result of a close collaboration between the Brazilian Society of Tropical Medicine and the Ministry of Health. It is hoped that this document will strengthen the development of integrated actions against Chagas disease in the country, focusing on epidemiology, management, comprehensive care (including families and communities), communication, information, education, and research