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1.
J Phys Ther Sci ; 26(7): 1033-6, 2014 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-25140090

RESUMO

[Purpose] We investigated the effect of low-intensity pulsed ultrasound and cryotherapy on joint function recovery and C-reactive protein (CRP) levels of patients with total knee replacement. [Subjects] Forty-six patients with total knee replacement were recruited and allocated to either low-intensity pulsed ultrasound therapy (n=15), cryotherapy (n=15), or a combination of both (n=16). Therapy was administered once a day, 5 times a week for 3 weeks. To determine functional joint recovery and reduction of inflammation, changes in the Korean Western Ontario and McMaster Universities Arthritis Index (K-WOMAC), range of motion (ROM), and CRP were assessed postsurgically and four times over a 3-week period. Using one-way analysis of variance (ANOVA), homogeneity tests were performed based on participants' general characteristics. To recognize changes in time-variant K-WOMAC, ROM, and CRP values between groups, repeated measures ANOVA was performed, and Tukey's test was used for post-test analysis. Values at α=0.05 were considered significant. [Results] We found a difference between groups and times, and the group that received the combined therapies showed greater changes in outcomes than the group that received low-intensity pulsed ultrasound therapy alone. [Conclusion] Applying both low-intensity pulsed ultrasound and cryotherapy can relieve inflammation and enhance joint function in patients who undergo total knee replacement.

2.
Prog Neuropsychopharmacol Biol Psychiatry ; 38(2): 116-20, 2012 Aug 07.
Artigo em Inglês | MEDLINE | ID: mdl-22449478

RESUMO

BACKGROUND: It has been suggested that Alzheimer's disease (AD) is mediated by pathological angiogenesis. Vascular endothelial growth factor (VEGF), transforming growth factor ß (TGF-ß), and tumor necrosis factor α (TNF -α) may play important roles in inflammation and angiogenesis through effects on inflammatory cell infiltration or neovascularization in AD pathogenesis. A few studies on the roles of VEGF in AD have been reported recently. But, the results were inconsistent. Angiogenin, which is suspected to have a similar function as VEGF, however, has not yet been studied in patients with AD. OBJECTIVE: This study was performed to investigate the levels of angiogenin and vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptorI (VEGFR I), and vascular endothelial growth factor receptor II (VEGFR II) in serums of patients with AD, to compare their levels with control subjects, and to determine whether serum angiogenin, VEGF, VEGFR I, and VEGFR II levels are associated with Alzheimer's disease (AD). METHODS: Serum angiogenin, VEGF, VEGFR I, and VEGFR II levels were quantified at the time of diagnosis in 20 patients with definite AD, and 18 healthy controls, using a commercial ELISA kit. RESULTS: Patients with AD exhibited lower serum angiogenin (p=0.003) and higher VEGF (p=0.008) levels than control subjects. No difference in serum VEGFR I and VEGFR II concentrations was observed between AD patients and controls. There was a correlation between serum levels of angiogenin and cognitive function (MMSE-KC and CDR) in AD patients. CONCLUSION: The increased serum level of VEGF and decreased serum angiogenin level were founded. Cognitive function was correlated with serum levels of angiogenin. Angiogenin may be involved in the pathogenesis of AD. Further study should be needed to evaluate the possibility of serum angiogenin as a biomarker of AD and as a predictor of disease progression.


Assuntos
Doença de Alzheimer/sangue , Cognição/fisiologia , Ribonuclease Pancreático/sangue , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , Neovascularização Patológica/fisiopatologia , Testes Neuropsicológicos , Fator A de Crescimento do Endotélio Vascular/sangue , Receptor 1 de Fatores de Crescimento do Endotélio Vascular/sangue , Receptor 2 de Fatores de Crescimento do Endotélio Vascular/sangue
3.
Nanotechnology ; 22(24): 245602, 2011 Jun 17.
Artigo em Inglês | MEDLINE | ID: mdl-21508466

RESUMO

We present a novel and straightforward approach to fabricate large-scale and robust free-standing TiO(2) nanotube (TNT) membranes. Simply by blowing N(2) gas onto as-anodized TNTs that are wetted with methanol, free-standing TNT membranes are produced. The approach also provides homogeneous and honeycomb-like Ti substrates after the detachment of TNT membranes. Through the second anodization of the honeycomb-like Ti substrates following the N(2) blowing, TNT membranes comprising hexagonally close-packed and regularly ordered TNTs with clear open ends can be achieved. Characterization of the free-standing TNT membranes using Raman spectroscopy and a high-resolution transmission electron microscope reveals that anatase TiO(2) and crystalline graphitic carbon are embedded in the bottom surface of the free-standing TNT membranes.

4.
J Pharmacol Exp Ther ; 327(3): 610-9, 2008 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-18776065

RESUMO

P38alpha is a protein kinase that regulates the expression of inflammatory cytokines, suggesting a role in the pathogenesis of diseases such as rheumatoid arthritis (RA) or systemic lupus erythematosus. Here, we describe the preclinical pharmacology of pamapimod, a novel p38 mitogen-activated protein kinase inhibitor. Pamapimod inhibited p38alpha and p38beta enzymatic activity, with IC(50) values of 0.014 +/- 0.002 and 0.48 +/- 0.04 microM, respectively. There was no activity against p38delta or p38gamma isoforms. When profiled across 350 kinases, pamapimod bound only to four kinases in addition to p38. Cellular potency was assessed using phosphorylation of heat shock protein-27 and c-Jun as selective readouts for p38 and c-Jun NH(2)-terminal kinase (JNK), respectively. Pamapimod inhibited p38 (IC(50), 0.06 microM), but inhibition of JNK was not detected. Pamapimod also inhibited lipopolysaccharide (LPS)-stimulated tumor necrosis factor (TNF) alpha production by monocytes, interleukin (IL)-1beta production in human whole blood, and spontaneous TNFalpha production by synovial explants from RA patients. LPS- and TNFalpha-stimulated production of TNFalpha and IL-6 in rodents also was inhibited by pamapimod. In murine collagen-induced arthritis, pamapimod reduced clinical signs of inflammation and bone loss at 50 mg/kg or greater. In a rat model of hyperalgesia, pamapimod increased tolerance to pressure in a dose-dependent manner, suggesting an important role of p38 in pain associated with inflammation. Finally, an analog of pamapimod that has equivalent potency and selectivity inhibited renal disease in lupus-prone MRL/lpr mice. Our study demonstrates that pamapimod is a potent, selective inhibitor of p38alpha with the ability to inhibit the signs and symptoms of RA and other autoimmune diseases.


Assuntos
Inibidores de Proteínas Quinases/farmacologia , Inibidores de Proteínas Quinases/uso terapêutico , Piridonas/farmacologia , Pirimidinas/farmacologia , Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores , Animais , Artrite Reumatoide/tratamento farmacológico , Avaliação Pré-Clínica de Medicamentos , Humanos , Inflamação/tratamento farmacológico , Concentração Inibidora 50 , Interleucina-1beta/antagonistas & inibidores , Interleucina-6/antagonistas & inibidores , Nefropatias/prevenção & controle , Camundongos , Monócitos/imunologia , Monócitos/metabolismo , Osteoporose/prevenção & controle , Isoformas de Proteínas , Piridonas/uso terapêutico , Pirimidinas/uso terapêutico , Líquido Sinovial/imunologia , Líquido Sinovial/metabolismo , Resultado do Tratamento , Fator de Necrose Tumoral alfa/antagonistas & inibidores
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