RESUMEN
OBJECTIVE: To investigate the effects of the transabdominal functional magnetic stimulation (A-FMS) for constipation in stroke or brain-injured patients. METHODS: Twenty-four brain-injured patients (11 males and 13 females; median age, 65 years; 22 cases of stroke and 2 cases of traumatic brain injury) with constipation, who were admitted to the rehabilitation department, were enrolled and randomly divided into magnetic stimulation (MS) group and sham stimulation (Sham) group. Several parameters related with constipation such as total and segmental colon transit time (CTT), defecation frequency, and Bristol Stool Scale (BSS) before and after 2 weeks of A-FMS (5 times per week, total 10 times of A-FMS) were evaluated. The Korean version of the Modified Barthel Index (K-MBI) was also evaluated. RESULTS: A significant decrease in segmental CTT in the left colon (-8.2±3.9 vs. 4.1±2.5 hours; p<0.05 by paired sample t-test) and a significant increase in the frequency of defecation (1.5±0.2 vs 0.7±0.3; p<0.05 by paired sample t-test) were observed in the MS group compared with the Sham group. Stool hardness became significantly softer in the MS group compared with the Sham group (2.3-3.5 in the MS and 2.6-3.1 in the Sham; p<0.05 by chi-square test) as evaluated by BSS. No difference in the K-MBI was observed between the two groups. CONCLUSION: The present study suggests that A-FMS can be an additional therapeutic tool for managing constipation in brain-injured patients with abnormal bowel movement, defecation frequency, and stool hardness.
RESUMEN
Mitogen- and stress-activated kinase 1 (MSK1) is a chromatin kinase that facilitates activator-dependent transcription by altering chromatin structure through histone H3 phosphorylation. The kinase activity of MSK1 is activated by intramolecular autophosphorylation, which is initially triggered by the activation of upstream mitogen-activated protein kinases (MAPKs), such as p38 and ERK1/2. MSK1 has been implicated in the expression of p21, a p53 target gene; however, the precise connection between MSK1 and p53 has not been clearly elucidated. Here, using in vitro and cell-based transcription assays, we show that MSK1 functions as a transcriptional coactivator of p53 in p21 expression, an action associated with MAPK-dependent phosphorylation of MSK1 and elevated kinase activity. Of special significance, we show that MSK1 directly interacts with p53 and is recruited to the p21 promoter, where it phosphorylates histone H3 in a p53-dependent manner. In addition, phosphomimetic mutant analysis demonstrated that negative charges in the hydrophobic motif are critical for serine 212 phosphorylation in the N-terminal kinase domain, which renders MSK1 competent for histone kinase activity. These studies suggest that MSK1 acts through a direct interaction with p53 to function as a transcriptional coactivator and that MSK1 activation by upstream MAPK signaling is important for efficient p21 gene expression.
Asunto(s)
Inhibidor p21 de las Quinasas Dependientes de la Ciclina/genética , Regulación de la Expresión Génica , Proteínas Quinasas S6 Ribosómicas 90-kDa/metabolismo , Proteína p53 Supresora de Tumor/metabolismo , Sitios de Unión , Línea Celular , Cromatina/genética , Cromatina/metabolismo , Inhibidor p21 de las Quinasas Dependientes de la Ciclina/metabolismo , Histonas/metabolismo , Humanos , Modelos Biológicos , Mutación , Fosforilación , Regiones Promotoras Genéticas , Unión Proteica , Proteínas Quinasas S6 Ribosómicas 90-kDa/genética , Factores de Transcripción/metabolismoRESUMEN
OBJECTIVE: To evaluate the effects of electric cortical stimulation (ECS) and transcranial direct current stimulation (tDCS) on motor and cognitive function recovery and brain plasticity in focal traumatic brain injury (TBI) of rats model. METHODS: Forty rats were pre-trained to perform a single pellet reaching task (SPRT), rotarod test (RRT), and Y-maze test for 14 days, then a focal TBI was induced by a weight drop model on the motor cortex. All rats were randomly assigned to one of the three groups: anodal ECS (50 Hz and 194 µs) (ECS group), tDCS (0.1 mA, 50 Hz and 200 µs) (tDCS group), and no stimulation as a control group. Four-week stimulation, including rehabilitation, was started 3 days after the operation. SPRT, RRT, and Y-maze were measured from day 1 to day 28 after the TBI was induced. Histopathological and immunohistochemistry staining evaluations were performed at 4 weeks. RESULTS: SPRT was improved from day 7 to day 26 in ECS, and from day 8 to day 26 in tDCS compared to the control group (p<0.05). SPRT of ECS group was significantly improved on days 3, 8, 9, and 17 compared to the tDCS group. Y-maze was improved from day 8 to day 16 in ECS, and on days 6, 12, and 16 in the tDCS group compared to the control group (p<0.05). Y-maze of the ECS group was significantly improved on day 9 to day 15 compared to the tDCS group. The c-Fos protein expression was better in the ECS group and the tDCS group compared to the control group. CONCLUSION: Electric stimulation in rats modified with a focal TBI is effective for motor recovery and brain plasticity. ECS induced faster behavioral and cognitive improvements compared to tDCS during the recovery period of rats with a focal TBI.
RESUMEN
OBJECTIVE: To evaluate the association between progression of curvature of scoliosis, and correction for functional component in patients with juvenile idiopathic scoliosis (JIS). METHODS: We retrospectively reviewed medical data of patients prescribed custom molded foot orthosis (FO) to correct inequality of RCSPA (resting calcaneal stance position angle), and chose 52 patients (26 females, 26 males) with Cobb angle ≥10° in radiology and uneven pelvic level at iliac crest by different RCSPA (≥3°) as a factor of functional scoliosis. They had different hump angle ≥5° in forward bending test, for idiopathic scoliosis component. Their mean age and mean period of wearing FO were 79.5±10.6 months and 18.6±0.70 months. RESULTS: Cobb angle was reduced from 22.03°±4.39° initially to 18.86°±7.53° after wearing FO. Pelvis height difference and RCSPA difference, were reduced from 1.07±0.25 cm initially to 0.60±0.36, and from 4.25°±0.71° initially to 1.71°±0.75° (p<0.01). Cobb angle improved most in 9 months. However, there was no significant improvement for those with more than 25° of Cobb angle initially. Mean Cobb angle improved in all age groups, but patients less than 6 years had clinically significant improvement of more than 5°. CONCLUSION: JIS can have functional components, which should be identified and managed. Foot orthosis is useful in correcting functional factors, in the case of pelvic inequality caused by different RCSPA, for patients with juvenile idiopathic scoliosis.