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1.
PLoS One ; 16(8): e0255160, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-34358238

RESUMEN

OBJECTIVE: Irritable bowel syndrome (IBS) affects children's quality of life and learning. The purpose of this research was to systematically evaluate the efficacy of probiotic adjuvant therapy for IBS in children. METHODS: The Web of Science, PubMed, Cochrane Library, EMBASE and Clinical Trials databases were electronically searched for randomized controlled trials (RCTs) published prior to January 2021 exploring the use of probiotic adjuvant therapy for IBS in children. Strict screening and quality evaluations of the eligible articles were performed independently by 2 researchers. Outcome indexes were extracted, and a meta-analysis of the data was performed using RevMan 5.4.1 and STATA 16 software. Finally, the risk of bias in the included studies was assessed with the RCT bias risk assessment tool recommended in the Cochrane Handbook for Systematic Reviews of Interventions (5.1.0). RESULTS: A total of nine RCTs were included. In children, probiotics significantly reduced the abdominal pain score (I2 = 95%, SMD = -1.15, 95% (-2.05, -0.24), P = 0.01) and Subject's Global Assessment of Relief (SGARC) score (I2 = 95%, MD = -3.84, 95% (-6.49, -1.20), P = 0.004), increased the rate of abdominal pain treatment success (I2 = 0%, RR = 3.44, 95% (1.73, 6.87), P = 0.0005) and abdominal pain relief (I2 = 40%, RR = 1.48, 95% (0.96, 2.28), P = 0.08), and reduced the frequency of abdominal pain (I2 = 2%, MD = -0.82, 95% (-1.57, -0.07), P = 0.03). However, we found that it might not be possible to relieve abdominal pain by increasing the daily intake of probiotics. CONCLUSIONS: Probiotics are effective at treating abdominal pain caused by IBS in children, however, there was no significant correlation between abdominal pain and the amount of probiotics ingested. More attention should be given to IBS in children, and a standardized evaluation should be adopted.


Asunto(s)
Adyuvantes Farmacéuticos/uso terapéutico , Síndrome del Colon Irritable/tratamiento farmacológico , Probióticos/uso terapéutico , Dolor Abdominal/tratamiento farmacológico , Dolor Abdominal/etiología , Adyuvantes Farmacéuticos/efectos adversos , Niño , Humanos , Placebos , Probióticos/administración & dosificación , Probióticos/efectos adversos , Probióticos/farmacología , Sesgo de Publicación , Medición de Riesgo , Resultado del Tratamiento
2.
Kaohsiung J Med Sci ; 35(7): 401-407, 2019 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-31001918

RESUMEN

Ubiquitin specific peptidase 49 (USP49) has been reported as a tumor suppressor in several tumors, but its function and molecular mechanism in non-small cell lung cancer (NSCLC) are still unknown. In this study, USP49 was found downregulated in NSCLC primary tissues and cell lines, and high USP49 predicted a positive index for the overall survival of NSCLC patients. Overexpression of USP49 downregulated the expression levels of Cyclin D1, and upregulated p53 expression. Further flow cytometry analysis showed that overexpressed USP49 induced cell cycle arrest at G0/G1 phase. As a result, overexpression of USP49 significantly inhibited cell growth of NSCLC cells. In mechanism, overexpression of USP49 inhibited PI3K/AKT signaling, but knockdown of USP49 enhanced this signaling. Further studies indicated that USP49 deubiquitinated PTEN and stabilized PTEN protein, which suggested that USP49 inhibited PI3K/AKT signaling by stabilizing PTEN in NSCLC cells. In conclusion, we demonstrated that USP49 was functional in NSCLC cells, and inhibited NSCLC cell growth by suppressing PI3K/AKT signaling, suggesting that USP49 could be as a novel target for NSCLC therapy.


Asunto(s)
Carcinoma de Pulmón de Células no Pequeñas/genética , Regulación Neoplásica de la Expresión Génica , Neoplasias Pulmonares/genética , Fosfatidilinositol 3-Quinasas/genética , Proteínas Proto-Oncogénicas c-akt/genética , Ubiquitina Tiolesterasa/genética , Carcinoma de Pulmón de Células no Pequeñas/metabolismo , Carcinoma de Pulmón de Células no Pequeñas/mortalidad , Carcinoma de Pulmón de Células no Pequeñas/patología , Puntos de Control del Ciclo Celular/genética , Línea Celular Tumoral , Proliferación Celular , Ciclina D1/genética , Ciclina D1/metabolismo , Células HEK293 , Humanos , Pulmón/metabolismo , Pulmón/patología , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/mortalidad , Neoplasias Pulmonares/patología , Fosfohidrolasa PTEN/genética , Fosfohidrolasa PTEN/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , ARN Interferente Pequeño/genética , ARN Interferente Pequeño/metabolismo , Fase de Descanso del Ciclo Celular , Transducción de Señal , Análisis de Supervivencia , Proteína p53 Supresora de Tumor/genética , Proteína p53 Supresora de Tumor/metabolismo , Ubiquitina Tiolesterasa/antagonistas & inhibidores , Ubiquitina Tiolesterasa/metabolismo
3.
Int J Clin Exp Pathol ; 8(9): 11847-53, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-26617939

RESUMEN

OBJECTIVE: To explore the special significances in advantages of using anti-inflammatory drugs, such as amelioration of growing conditions and the promotion of cell growth. METHODS: Utilizing anti-adhesive effects of synthetic E-selectins, we observed the changes of inflammatory cytokines (TNF-α, IL-1ß) contented in brain tissues and rat serums in rats hind cerebral ischemia-reperfusion models. Both growth and expression of endogenetic/exogenous neurological stem cells were detected after ameliorated local microenvironment. RESULTS: The contents of TNF-α and IL-1ß were decreased in brain tissues and rat serums after applying synthetic E-selectins. Expression of exogenous neurological stem cells was enhanced. Animal neurological functions improved. CONCLUSION: Anti-inflammatory therapy in early stage could enhance proliferation of stem cells so that it has vital significations in treating cerebrovascular diseases.


Asunto(s)
Antiinflamatorios/farmacología , Isquemia Encefálica/tratamiento farmacológico , Encéfalo/efectos de los fármacos , Selectina E/farmacología , Células-Madre Neurales/efectos de los fármacos , Fármacos Neuroprotectores/farmacología , Daño por Reperfusión/prevención & control , Nicho de Células Madre , Animales , Antiinflamatorios/síntesis química , Encéfalo/metabolismo , Encéfalo/patología , Encéfalo/fisiopatología , Isquemia Encefálica/sangre , Isquemia Encefálica/patología , Isquemia Encefálica/fisiopatología , Proliferación Celular/efectos de los fármacos , Citoprotección , Modelos Animales de Enfermedad , Femenino , Interleucina-1beta/sangre , Masculino , Células-Madre Neurales/metabolismo , Células-Madre Neurales/patología , Fármacos Neuroprotectores/síntesis química , Ratas Sprague-Dawley , Recuperación de la Función , Daño por Reperfusión/sangre , Daño por Reperfusión/patología , Daño por Reperfusión/fisiopatología , Factores de Tiempo , Factor de Necrosis Tumoral alfa/sangre
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