How do the year's seasons and specific weather indices affect physical activity and the patterns of use of public open spaces in the Brazilian context?

BACKGROUND: Public open spaces (POS) can offer various resources to promote visitation and engagement in moderate-to-vigorous physical activity (MVPA). However, the influence of seasonal variations and specific meteorological conditions on this relationship remains unclear. Thus, this study aims to investigate the effect of seasonal variations and specific meteorological elements on different days of the week and times of day on POS use and POS-based MVPA in the Brazilian context. METHODS: In 2018, repeated measurements carried out in Southern Brazil used a systematic observation to identify the presence of users in the POS and their engagement in MVPA. The meteorological elements (temperature, thermal sensation, and relative humidity), as well as seasonality (summer, autumn, winter, and spring), were aggregated into the observations. RESULTS: A total of 19,712 systematic observations were conducted across nine POS. During these observations, a total of 59,354 users were identified. Out of theses, 39,153 (66.0%) were engaged in POS-based MVPA. The presence of users was found to be more frequent during the spring season (38.7%) and on weekends (ranging from 37.6 to 50.1% across seasons). Additionally, user presence was higher in the late afternoon (ranging from 36.4 to 58.2% across seasons) and at higher temperatures with lower relative humidity (p-value < 0.001). Regarding POS-based MVPA, it was more frequent during the winter season (36.4%) and on weekdays (ranging from 73.2 to 79.9% across seasons). Similarly, MVPA was higher in the late afternoon (ranging from 58.3 to 67.5% across seasons) and at lower temperatures and thermal sensations (p-value < 0.005). CONCLUSIONS: Higher presence of users in POS, as well as their visiting, to practice POS-based MVPA, depending on the seasons and specific meteorological elements. By creating infrastructure and conducive conditions, cities can encourage individuals to adopt more active and healthy behaviors. These findings emphasize the importance of designing urban spaces that promote physical activity and contribute to overall well-being.

Perspectives on urban mobility in promoting physical activity in the context of commuting in Brazil / Perspectivas sobre mobilidade urbana na promoção da atividade física no contexto dos deslocamentos no Brasil

Despite Brazil's important advances in regulatory aspects related to city planning, the disorder-ly growth of Brazilian cities makes it difficult to implement changes that would result in greater opportunities for the active commuting of the population. This essay was designed to reflect on opportunities for improvement in the urban environment to promote physical activity in the context of commuting in Brazil. From this perspective, the study identified policies that promote orderly growth and support active commuting in cities. It also suggested the use of indicators to evaluate and monitor development, with a particular emphasis on active commuting. Furthermore, it is essential to adapt and improve the urban planning process to meet the needs of Brazilian municipalities and foster closer collaboration with civil society. Thus, it will be possible to verify the changes in the urban environment and their impact on the active commuting, promoting the development of healthy and sustainable cities

Apesar do Brasil apresentar importante avanço em aspectos regulatórios relacionados ao planejamento das cidades, o crescimento desordenado das cidades brasileiras dificulta a realização de mudanças que reflitam em maiores oportunidades no deslocamento ativo da população. Este ensaio foi elaborado com objetivo de refletir sobre as oportunidades para melhorias no ambiente urbano para a promoção da atividade física no contexto do deslocamento no Brasil. Nessa perspectiva, o estudo identificou políticas que permitem o crescimento ordenado e favoreça o deslocamento ativo nas cidades, além de sugerir o uso de indicadores para avaliação e monitoramento do desenvolvimento, com especial foco no deslocamento ativo. Ademais, é imprescindível que o processo de planejamento urbano seja adaptado e aprimorado considerando as necessidades dos municípios brasileiros e com aproximação da sociedade civil. Assim, será possível verificar as modificações no ambiente urbano e seu impacto no deslocamento ativo da população, estimulando a criação de cidades saudáveis e sustentáveis

Neuroprotective effects of thromboxane receptor antagonist SQ 29,548 after pilocarpine-induced status epilepticus in mice.

Thromboxane A2 (TXA2) is an important eicosanoid in the cardiovascular system, and increasing evidence suggests that TXA2 receptors (TPs) and their ligands may constitute valuable tools for the development of neuroprotective drugs. However, the role of TPs on seizure-induced damage has not been investigated. Therefore, we evaluated the effects of SQ 29,548, a potent and selective TP antagonist-on neuromotor performance, neurodegeneration, reactive astrocytosis, and c-Fos protein immunoreactivity after pilocarpine-induced status epilepticus (SE) in mice. Adult C57BL/6 mice received intracerebroventricular SQ 29,548 injections 90 min and 24 h after pilocarpine-induced SE. We found that SQ 29,548 prevented the impairment of neuromotor performance (Neuroscore test) 48 h after pilocarpine-induced SE. Data analysis suggested the existence of two subgroups of SQ 29,548-treated post-SE animals. Eight out of 12 SQ 29,548-treated animals displayed Neuroscore values identical to those of vehicle-treated controls, and were considered SQ 29,548 responders. However, 4 out of 12 SQ 29,548-treated animals did not show any improvement in Neuroscore values, and were considered SQ 29,548 non-responders. Treatment with SQ 29,548 attenuated SE-induced increase in the number of FJC- or GFAP-positive cells in the hippocampus of SQ 29,548 responders. In addition, SQ 29,548 prevented the SE-elicited increase of c-Fos immunoreactivity in the hippocampus. In summary, our results suggest that the TP antagonist (SQ 29,548) improves neurological outcome after pilocarpine-induced SE in mice. The existence of SQ 29,548 responders and non-responders was suggested by results from the Neuroscore test. Additional studies are needed to understand the mechanisms underlying these findings, as well as the potential uses of TP antagonists in the treatment of seizure-induced damage.

Potential therapeutic implications of ergogenic compounds on pathophysiology induced by traumatic brain injury: A narrative review.

Traumatic brain injury (TBI) is a devastating condition that often triggers a sequel of neurological disorders that can last throughout lifespan. From a metabolic viewpoint, the compromising of the energy metabolism of the brain has produced evidence linking the severity of brain injury to the extent of disturbances in the cerebral metabolism. The cerebral metabolic crisis, however, displays that regional heterogeneity varies temporally post-injury. It is important to note that energy generation and mitochondrial function are closely related and interconnected with delayed secondary manifestations of brain injury, including early neuromotor dysfunction, cognitive impairment, and post-traumatic epilepsy (PTE). Given the extent of post-traumatic changes in neuronal function and the possibility of amplifying secondary cascades, different therapies designed to minimize damage and retain/restore cellular function after TBI are currently being studied. One of the possible strategies may be the inclusion of ergogenic compounds, which is a class of supplements that typically includes ingredients used by athletes to enhance their performance. The combination of these compounds offers specific physiological advantages, which include enhanced energy availability/metabolism and improved buffering capacity. However, the literature on their effects in certain biological systems and neurological diseases, such as TBI, has yet to be determined. Thus, the present review aims to discuss the role of ergogenic compounds popularly used in secondary damage induced by this neurological injury. In this narrative review, we also discuss how the results from animal studies can be applied to TBI clinical settings.

Galangin Prevents Increased Susceptibility to Pentylenetetrazol-Stimulated Seizures by Prostaglandin E2.

Epilepsy is one of the most common chronic neurological diseases. It is characterized by recurrent epileptic seizures, where one-third of patients are refractory to existing treatments. Evidence revealed the association between neuroinflammation and increased susceptibility to seizures since there is a pronounced increase in the expression of key inflammatory mediators, such as prostaglandin E2 (PGE2), during seizures. The purpose of this study was to investigate whether PGE2 increases susceptibility to pentylenetetrazol-induced (PTZ) seizures. Subsequently, we evaluated if the flavonoid isolated from the plant Piper aleyreanum (galangin) presented any anticonvulsive effects. Our results demonstrated that the group treated with PGE2 increased susceptibility to PTZ and caused myoclonic and generalized seizures, which increased seizure duration and electroencephalographic wave amplitudes. Furthermore, treatment with PGE2 and PTZ increased IBA-1 (microglial marker), GFAP (astrocytic marker), 4-HNE (lipid peroxidation marker), VCAM-1 (vascular cell adhesion molecule 1), and p-PKAIIα (phosphorylated cAMP-dependent protein kinase) immunocontent. Indeed, galangin prevented behavioral and electroencephalographic seizures, reactive species production, decreased microglial and astrocytic immunocontent, as well as decreased VCAM-1 immunocontent and p-PKA/PKA ratio induced by PGE2/PTZ. Therefore, this study suggests galangin may have an antagonizing role on PGE2-induced effects, reducing cerebral inflammation and protecting from excitatory effects evidenced by administrating PGE2 and PTZ. However, further studies are needed to investigate the clinical implications of the findings and their underlying mechanisms.

Delayed creatine supplementation counteracts reduction of GABAergic function and protects against seizures susceptibility after traumatic brain injury in rats.

Traumatic brain injury (TBI) is a devastating disease frequently followed by behavioral disabilities including post-traumatic epilepsy (PTE). Although reasonable progress in understanding its pathophysiology has been made, treatment of PTE is still limited. Several studies have shown the neuroprotective effect of creatine in different models of brain pathology, but its effects on PTE is not elucidated. Thus, we decided to investigate the impact of delayed and chronic creatine supplementation on susceptibility to epileptic seizures evoked by pentylenetetrazol (PTZ) after TBI. Our experimental data revealed that 4 weeks of creatine supplementation (300 mg/kg, p.o.) initiated 1 week after fluid percussion injury (FPI) notably increased the latency to first myoclonic and tonic-clonic seizures, decreased the time spent in tonic-clonic seizure, seizure intensity, epileptiform discharges and spindle oscillations induced by a sub-convulsant dose of PTZ (35 mg/kg, i.p.). Interestingly, this protective effect persists for 1 week even when creatine supplementation is discontinued. The anticonvulsant effect of creatine was associated with its ability to reduce cell loss including the number of parvalbumin positive (PARV+) cells in CA3 region of the hippocampus. Furthermore, creatine supplementation also protected against the reduction of GAD67 levels, GAD activity and specific [3H]flunitrazepam binding in the hippocampus. These findings showed that chronic creatine supplementation may play a neuroprotective role on brain excitability by controlling the GABAergic function after TBI, providing a possible new strategy for the treatment of PTE.

Involvement of the Cholinergic Parameters and Glial Cells in Learning Delay Induced by Glutaric Acid: Protection by N-Acetylcysteine.

Dysfunction of basal ganglia neurons is a characteristic of glutaric acidemia type I (GA-I), an autosomal recessive inherited neurometabolic disease characterized by deficiency of glutaryl-CoA dehydrogenase (GCDH) and accumulation of glutaric acid (GA). The affected patients present clinical manifestations such as motor dysfunction and memory impairment followed by extensive striatal neurodegeneration. Knowing that there is relevant striatal dysfunction in GA-I, the purpose of the present study was to verify the performance of young rats chronically injected with GA in working and procedural memory test, and whether N-acetylcysteine (NAC) would protect against impairment induced by GA. Rat pups were injected with GA (5 µmol g body weight-1, subcutaneously; twice per day; from the 5th to the 28th day of life) and were supplemented with NAC (150 mg/kg/day; intragastric gavage; for the same period). We found that GA injection caused delay procedural learning; increase of cytokine concentration, oxidative markers, and caspase levels; decrease of antioxidant defenses; and alteration of acetylcholinesterase (AChE) activity. Interestingly, we found an increase in glial cell immunoreactivity and decrease in the immunoreactivity of nuclear factor-erythroid 2-related factor 2 (Nrf2), nicotinic acetylcholine receptor subunit alpha 7 (α7nAChR), and neuronal nuclei (NeuN) in the striatum. Indeed, NAC administration improved the cognitive performance, ROS production, neuroinflammation, and caspase activation induced by GA. NAC did not prevent neuronal death, however protected against alterations induced by GA on Iba-1 and GFAP immunoreactivities and AChE activity. Then, this study suggests possible therapeutic strategies that could help in GA-I treatment and the importance of the striatum in the learning tasks.

Subtle improvement of seizure susceptibility by atorvastatin treatment during epileptogenesis.

BACKGROUND: The process by which a brain insult elicits epilepsy is termed epileptogenesis and it is characterized by numerous molecular and functional alterations. Statins are first-line drugs for hypercholesterolemia and related diseases, and display neuroprotective properties in clinical and experimental studies. Considering the importance in developing therapeutic strategies to prevent or modify epileptogenesis, we aimed the present study to test the hypothesis that atorvastatin modifies seizure susceptibility of mice after status epilepticus (SE). METHODS: Male and female C57BL/6 mice were submitted to the pilocarpine-induced SE and then treated with atorvastatin (10 or 100mg/kg, once daily by gavage) for 14days. At days 7 and 14 post SE we evaluated the susceptibility of mice to the convulsant effects of a low dose of PTZ (30mg/kg). Cell loss in the hilus of dentate gyrus was evaluated by Giemsa staining. RESULTS: Latencies to myoclonic jerks and to tonic-clonic seizures decreased between baseline (before SE) and days 7 and 14 after SE, confirming the development of seizure susceptibility. Atorvastatin protected against PTZ-induced tonic-clonic seizures in both sexes at day 14 post-SE. Protective effects were similar in both female and male mice, except that a high dose of atorvastatin was required for females (protection at 100mg/kg versus 10mg/kg in males). Giemsa staining did not reveal neuroprotective effects of atorvastatin. CONCLUSIONS: Atorvastatin treatment during epileptogenesis had slight beneficial effects on seizure susceptibility. These seem not related to neuroprotection. Further studies are needed to determine the disease-modifying potential of atorvastatin in epilepsy.