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1.
J Bodyw Mov Ther ; 24(1): 47-55, 2020 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-31987562

RESUMEN

BACKGROUND: Patellofemoral pain syndrome (PFPS), characterized by retropatellar and peripatellar pain, is a common disorder affecting young women. Treatment has included exercise-based therapy and taping techniques for rapid reduction of symptoms and pain. Although Kinesio Taping® (KT) has been studied as adjunctive therapy, evidence on its effectiveness is limited and conflicting. OBJECTIVE: To determine the feasibility of performing a double-blind randomized controlled trial (RCT) using KT® for PFPS treatment and to determine an ideal sample size. DESIGN: Double-blind, randomized, controlled pilot study. METHOD: Forty-three women (aged 18-45 years) with at least a 3-month history of PFPS were randomized based on the mechanical correction techniques: using KT® for patellar medialization (KT-PM), using KT® for lateral rotation of the femur and tibia (KT-LRFT), and the control group (CG). All groups underwent the same muscle strengthening and motor control procedures for 12 weeks. Knee pain and function were evaluated at baseline, at 6 weeks, at treatment completion (12 weeks), and during the 12-week follow-up using the numerical pain rating scale (NPRS) at rest and during effort, Anterior Knee Pain Scale (AKPS), and single jump hop test. RESULTS: There were clinically significant differences between the KT-LRFT and the CG in terms of AKPS and NPRS scores during effort at the 6-week and 12-week follow-ups. All groups (within group) showed a significant improvement in pain and function. CONCLUSIONS: A complete RCT using KT® for the treatment of PFPS is feasible with some changes regarding outcome measures and treatment protocols.


Asunto(s)
Cinta Atlética , Terapia por Ejercicio/métodos , Fuerza Muscular/fisiología , Síndrome de Dolor Patelofemoral/terapia , Adulto , Método Doble Ciego , Femenino , Humanos , Persona de Mediana Edad , Dimensión del Dolor , Proyectos Piloto , Rango del Movimiento Articular/fisiología , Resultado del Tratamiento , Adulto Joven
2.
Nat Chem Biol ; 11(5): 347-354, 2015 May.
Artículo en Inglés | MEDLINE | ID: mdl-25848931

RESUMEN

Huntington's disease (HD) is a currently incurable neurodegenerative condition caused by an abnormally expanded polyglutamine tract in huntingtin (HTT). We identified new modifiers of mutant HTT toxicity by performing a large-scale 'druggable genome' siRNA screen in human cultured cells, followed by hit validation in Drosophila. We focused on glutaminyl cyclase (QPCT), which had one of the strongest effects on mutant HTT-induced toxicity and aggregation in the cell-based siRNA screen and also rescued these phenotypes in Drosophila. We found that QPCT inhibition induced the levels of the molecular chaperone αB-crystallin and reduced the aggregation of diverse proteins. We generated new QPCT inhibitors using in silico methods followed by in vitro screening, which rescued the HD-related phenotypes in cell, Drosophila and zebrafish HD models. Our data reveal a new HD druggable target affecting mutant HTT aggregation and provide proof of principle for a discovery pipeline from druggable genome screen to drug development.


Asunto(s)
Aminoaciltransferasas/efectos de los fármacos , Aminoaciltransferasas/genética , Enfermedad de Huntington/tratamiento farmacológico , Enfermedad de Huntington/genética , ARN Interferente Pequeño , Aminoaciltransferasas/antagonistas & inhibidores , Animales , Células Cultivadas , Biología Computacional , Drosophila , Evaluación Preclínica de Medicamentos , Inhibidores Enzimáticos/farmacología , Inhibidores Enzimáticos/uso terapéutico , Proteínas Fluorescentes Verdes/metabolismo , Humanos , Proteína Huntingtina , Ratones , Ratones Endogámicos C57BL , Mutación/genética , Proteínas del Tejido Nervioso/genética , Proteínas del Tejido Nervioso/metabolismo , Neuronas/efectos de los fármacos , Neuronas/metabolismo , Pez Cebra , Cadena B de alfa-Cristalina/metabolismo
3.
Int J Biochem Cell Biol ; 40(9): 1775-91, 2008.
Artículo en Inglés | MEDLINE | ID: mdl-18289917

RESUMEN

The peroxisome proliferator-activated receptor alpha (PPARalpha) has been known to play a pivotal role in maintaining the energy balance during fasting; however, the battery of PPARalpha target genes involved in this metabolic response is still not fully characterized. Here, we report the identification and characterization of Ppsig (for PPARalpha-regulated and starvation-induced gene) with unknown biological function from mouse liver. Multiple Ppsig cDNAs which differed in the 3'-untranslated regions were identified. The open reading frame of Ppsig cDNA is 1830 bp which encodes a protein of 67.33 kDa. Ppsig contains 11 exons spanning at least 10 kb. Although the exact biological function of Ppsig is still not known, we found that Ppsig mRNA transcript was dramatically up-regulated during 72 h fasting and following treatment with a potent PPARalpha agonist, in a tissue-specific and PPARalpha-dependent manner. A functional peroxisome proliferator-response element was found in the intron 1 of Ppsig, thus confirming that Ppsig is a novel direct mouse PPARalpha target gene. This finding might help in elucidating the transcriptional regulatory mechanism of Ppsig in the cellular response to fasting.


Asunto(s)
Oxidorreductasas actuantes sobre Donantes de Grupo CH-CH/genética , Oxidorreductasas actuantes sobre Donantes de Grupo CH-CH/metabolismo , PPAR alfa/metabolismo , Inanición/genética , Animales , Secuencia de Bases , Clonación Molecular , ADN Complementario/genética , Ayuno/metabolismo , Genómica , Humanos , Intrones/genética , Metabolismo de los Lípidos , Masculino , Ratones , Ratones Noqueados , Datos de Secuencia Molecular , Oxidorreductasas actuantes sobre Donantes de Grupo CH-CH/biosíntesis , Regiones Promotoras Genéticas/genética , ARN Mensajero/genética , Regulación hacia Arriba
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