RESUMEN
O objetivo deste estudo foi caracterizar os óbitos em acidentes de trânsito com motociclistas e analisar a tendência da mortalidade por série temporal. Assim, trata-se de estudo de série temporal realizada com dados sobre óbitos de motociclistas em acidentes de trânsito no Estado de Goiás entre 2000 e 2015, fornecidos pelo Sistema de Informação sobre Mortalidade. Foram analisadas variáveis sociodemográficas, dados sobre a frota de motocicletas e as taxas de mortalidade anuais, por meio de estatística descritiva e inferencial. Verificou-se aumento na taxa de mortalidade de motociclistas por 100.000 habitantes durante a série temporal em 152,27%, passando de 3,09 para 8,30 mortes a cada 100.000 habitantes, entre as mulheres o aumento foi 268,84%. Porém, os homens jovens são os que mais morrem em acidentes com motocicletas em Goiás, com 88,09% dos óbitos (n = 5.417). Além disso, houve tendência crescente na taxa de mortalidade entre 2000 e 2015. Tendo isso em vista, é possível constatar que houve aumento nas taxas de mortalidade por acidente de motocicleta no Estado de Goiás, confirmando ser um problema de saúde pública que carece de medidas efetivas para reduzir os prejuízos causados à comunidade.
Current paper characterizes deaths by accidents with motorcycles and analyzes mortality trends by time series retrieved from data on deaths of motorcycles drivers in traffic accidents in the state of Goiás, Brazil, between 2000 and 2015, provided by the Mortality Information System. Social and demographic variables, data on number of motorcycles and yearly annual death rates were analyzed by descriptive and inferential statistics. There was a 152.27% increase in mortality rates of motorcycles drivers per 100,000 inhabitants during the period, with 3.09 going to 8.30 deaths per 100,000 inhabitants; in the case of females, increase reached 268.84%. However, young men die more frequently in motorcycle accidents in Goiás, with 88.09% of deaths (n=5.417). Further, death rate increased between 2000 and 2015 and death rates increased per motorcycle accident, characterizing the event as an issue of public health which fails in effective measures to reduce harm to the community.
RESUMEN
Sepsis induces organ dysfunction due to overexpression of the inflammatory host response, resulting in cardiopulmonary and autonomic dysfunction, thus increasing the associated morbidity and mortality. Wharton's jelly-derived mesenchymal stem cells (WJ-MSCs) express genes and secrete factors with anti-inflammatory properties, neurological and immunological protection, as well as improve survival in experimental sepsis. The cholinergic anti-inflammatory pathway (CAP) is mediated by α7-nicotinic acetylcholine receptors (α7nAChRs), which play an important role in the control of systemic inflammation. We hypothesized that WJ-MSCs attenuate sepsis-induced organ injury in the presence of an activated CAP pathway. To confirm our hypothesis, we evaluated the effects of WJ-MSCs as a treatment for cardiopulmonary injury and on neuroimmunomodulation. Male Wistar rats were randomly divided into four groups: control (sham-operated); cecal ligation and puncture (CLP) alone; CLP+WJ-MSCs (1 × 106 cells, at 6 h post-CLP); and CLP+methyllycaconitine (MLA)+WJ-MSCs (5 mg/kg body wt, at 5.5 h post-CLP, and 1 × 106 cells, at 6 h post-CLP, respectively). All experiments, including the assessment of echocardiographic parameters and heart rate variability, were performed 24 h after CLP. WJ-MSC treatment attenuated diastolic dysfunction and restored baroreflex sensitivity. WJ-MSCs also increased cardiac sympathetic and cardiovagal activity. WJ-MSCs reduced leukocyte infiltration and proinflammatory cytokines, effects that were abolished by administration of a selective α7nAChR antagonist (MLA). In addition, WJ-MSC treatment also diminished apoptosis in the lungs and spleen. In cardiac and splenic tissue, WJ-MSCs downregulated α7nAChR expression, as well as reduced the phospho-STAT3-to-total STAT3 ratio in the spleen. WJ-MSCs appear to protect against sepsis-induced organ injury by reducing systemic inflammation, at least in part, via a mechanism that is dependent on an activated CAP.