Stroke is associated with a high rate of disability and mortality, and survivors are usually accompanied with dysphagia, aphasia, motor dysfunction, cognitive impairment, depression, and other complications. In the past decades, many studies have been conducted to reveal the pathogenesis and pathological mechanisms of stroke. Furthermore, treatment methods have been developed that contribute to the elevated survival rate of stroke patients. Early rehabilitation poststroke is starting to be recognized as important and has been receiving increasing attention in order to further improve the quality of life of the patients. As an emerging method of poststroke rehabilitation, music therapy can help attenuate dysphagia and aphasia, improve cognition and motor function, alleviate negative moods, and accelerate neurological recovery in stroke patients. This review helps summarize the recent progress that has been made using music therapy in stroke rehabilitation and is aimed at providing clinical evidence for the treatment of stroke patients.

Subarachnoid hemorrhage (SAH) is a common cerebrovascular disease with high mortality and disability rates. Despite progressive advances in drugs and surgical techniques, neurological dysfunction in surviving SAH patients have not improved significantly. Traditionally, vasospasm has been considered the main cause of death and disability following SAH, but anti-vasospasm therapy has not benefited clinical prognosis. Many studies have proposed that early brain injury (EBI) may be the primary factor influencing the prognosis of SAH. Melatonin is an indole hormone and is the main hormone secreted by the pineal gland, with low daytime secretion levels and high nighttime secretion levels. Melatonin produces a wide range of biological effects through the neuroimmune endocrine network, and participates in various physiological activities in the central nervous system, reproductive system, immune system, and digestive system. Numerous studies have reported that melatonin has extensive physiological and pharmacological effects such as anti-oxidative stress, anti-inflammation, maintaining circadian rhythm, and regulating cellular and humoral immunity. In recent years, more and more studies have been conducted to explore the molecular mechanism underlying melatonin-induced neuroprotection. The studies suggest beneficial effects in the recovery of intracerebral hemorrhage, cerebral ischemia-reperfusion injury, spinal cord injury, Alzheimer’s disease, Parkinson’s disease and meningitis through anti-inflammatory, antioxidant and anti-apoptotic mechanisms. This review summarizes the recent studies on the application and mechanism of melatonin in SAH.

BRAF mutations have been found in gliomas which exhibit abnormal electrophysiological activities, implying their potential links with the ion channel functions. In this study, we identified the Drosophila potassium channel, Slowpoke (Slo), the ortholog of human KCNMA1, as a critical factor involved in dRafGOF glioma progression. Slo was upregulated in dRafGOF glioma. Knockdown of slo led to decreases in dRafGOF levels, glioma cell proliferation, and tumor-related phenotypes. Overexpression of slo in glial cells elevated dRaf expression and promoted cell proliferation. Similar mutual regulations of p-BRAF and KCNMA1 levels were then recapitulated in human glioma cells with the BRAF mutation. Elevated p-BRAF and KCNMA1 were also observed in HEK293T cells upon the treatment of 20 mM KCl, which causes membrane depolarization. Knockdown KCNMA1 in these cells led to a further decrease in cell viability. Based on these results, we conclude that the levels of p-BRAF and KCNMA1 are co-dependent and mutually regulated. We propose that, in depolarized glioma cells with BRAF mutations, high KCNMA1 levels act to repolarize membrane potential and facilitate cell growth. Our study provides a new strategy to antagonize the progression of gliomas as induced by BRAF mutations.