Effects of inspiratory muscle training on the severity of obstructive sleep apnea in individuals after stroke: a protocol for a randomized controlled trial.

BACKGROUND: Obstructive sleep apnea (OSA) is the most common form of sleep-disordered breathing in cerebrovascular diseases, requiring a multidisciplinary approach. There are few studies evaluating the effects of inspiratory muscle training (IMT) in individuals with OSA and the findings regarding the possible effect on apnea hypopnea index (AHI) reduction are controversial. OBJECTIVE: This protocol for a randomized clinical trial will assess the effects of IMT on the severity of obstructive sleep apnea, sleep quality, and daytime sleepiness in individuals after stroke participating in a rehabilitation program. METHODS: This study will be a randomized controlled trial with blinded assessors. Forty individuals after stroke will randomized to two groups. For 5 weeks, both groups will participate in the rehabilitation program activities, including aerobic exercise, resistance training, and educational class when they will receive guidance on the behavioral management of OSA. The experimental group will also perform high-intensity IMT 5 times a week, for 5 weeks, consisting initially of five sets of five repetitions achieving 75% of the maximal inspiratory pressure, increasing one set each week, totaling nine sets at the end of training. The primary outcome will be the severity of OSA measured as AHI at 5 weeks. Secondary outcomes will include sleep quality measured by the Pittsburgh Sleep Quality Index (PSQI) and daytime sleepiness measured by Epworth Sleepiness Scale (ESS). Outcomes will be collected by a researcher blinded to group allocation at baseline (week 0), after intervention (week 5), and 1 month beyond intervention (week 9). TRIAL REGISTRATION: Clinical Trials Register: NCT05135494.

Effects of photobiomodulation therapy (PBMT) on the management of pain intensity and disability in plantar fasciitis: systematic review and meta-analysis.

To review the effects of photobiomodulation therapy (PBMT) on pain intensity and disability in people with plantar fasciitis (PF) when compared with control conditions, other interventions, and adjunct therapies. Systematic searches were conducted in five database randomized controlled trials (RCT). We only included randomized controlled trials (RCTs) in adults with PF that compared PBMT to placebo, as well as RCTs that compared PBMT to other interventions; and as an adjunct to other therapies. The methodological quality and certainty were assessed through PEDro Scale and GRADE approach, respectively. The data of comparison were pooled and a meta-analysis was conducted when possible. Nineteen RCTs involving 1089 participants were included in this review. PBMT alone (MD = - 22.02 [- 35.21 to - 8.83]) or with exercise (MD = - 21.84 [- 26.14 to - 17.54]) improved pain intensity in short-term treatment. PBMT was superior to (extracorporeal shock wave therapy) EWST for relief of pain (MD = - 20.94 [- 32.74 to - 9.13]). In the follow-up, PBMT plus exercise had a superior to exercise therapy alone (MD = - 18.42 [- 26.48 to - 10.36]). PBMT may be superior to (ultrasound therapeutic) UST in medium- and long-term follow-ups for disability, but can be not clinically relevant. There is uncertainty that PBMT is capable of promoting improvement in disability. PBMT when used with adjuvant therapy does not enhance outcomes of interest. PBMT improves pain intensity with or without exercise. PBMT has been shown to be superior to ESWT for pain relief, but not superior to other interventions for pain intensity and disability. The evidence does not support PBMT as an adjunct to other electrotherapeutic modalities.

Astrocyte-induced synaptogenesis is mediated by transforming growth factor ß signaling through modulation of D-serine levels in cerebral cortex neurons.

Assembly of synapses requires proper coordination between pre- and postsynaptic elements. Identification of cellular and molecular events in synapse formation and maintenance is a key step to understand human perception, learning, memory, and cognition. A key role for astrocytes in synapse formation and function has been proposed. Here, we show that transforming growth factor ß (TGF-ß) signaling is a novel synaptogenic pathway for cortical neurons induced by murine and human astrocytes. By combining gain and loss of function approaches, we show that TGF-ß1 induces the formation of functional synapses in mice. Further, TGF-ß1-induced synaptogenesis involves neuronal activity and secretion of the co-agonist of the NMDA receptor, D-serine. Manipulation of D-serine signaling, by either genetic or pharmacological inhibition, prevented the TGF-ß1 synaptogenic effect. Our data show a novel molecular mechanism that might impact synaptic function and emphasize the evolutionary aspect of the synaptogenic property of astrocytes, thus shedding light on new potential therapeutic targets for synaptic deficit diseases.

Characterization of TGF-beta1 type II receptor expression in cultured cortical astrocytes.

The transforming growth factor-betas (TGF-betas) comprise a family of pleiotropic members that signal through two types of serine/threonine kinase receptors, named TGFRI (TGF-beta type I receptor) and TGFRII (TGF-beta type II receptor). We previously demonstrated that cortical neurons increase the astrocyte maturation marker, glial fibrillary acidic protein (GFAP), and thus, astrocyte differentiation, by inducing TGF-beta1 secretion by astrocytes in vitro. Although TGF-beta receptor expression has been described in different brain regions and cell types, their localization is still a subject of discussion. In the present work, we analyzed TGFRII expression in cultured cortical astrocytes from embryonic and newborn animals by immunocytochemistry, Western blot, and reverse transcriptase-polymerase chain reaction (RT-PCR). We report for the first time expression of TGFRII in embryonic glia. TGFRII immunostaining was punctual and spread throughout the cellular membrane of embryonic and newborn astrocytes. Western blot and RT-PCR assays revealed similar levels of the receptor in astrocytes from different ages. Identification of TGFRII in embryonic astrocytes is novel and might point to the multipotent precursor cell, radial glia, as a potential target for TGFbeta1 during astrocyte development.