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Objective:To observe the effect of warm joint needling plus rehabilitation techniques on the balance function and quality of life (QOL) of patients with spastic hemiplegia after ischemic cerebral stroke.Methods:Ninety patients with spastic hemiplegia after ischemic cerebral stroke were randomized into a rehabilitation group,a warm joint needling group and an observation group,with 30 cases in each group.The rehabilitation group was intervened by Bobath therapy,the warm joint needling group was treated with joint needling on the affected side plus warm needling,and the observation group was given the same rehabilitation treatment as the rehabilitation group together with the same warm joint needling as the warm joint needling group.The three groups were treated once another day,1 month as a treatment course for 6 months.Before the treatment,and respectively after 2-week,1-month,3-month,and 6-month treatment,the modified Ashworth scale (MAS) was used to measure the anti-spasm ability of the lower limb,the Berg balance scale (BBS) was adopted to evaluate the balance function,and the stroke-specific quality of life scale (SS-QOL)was employed to estimate the QOL.Results:After 3-month and 6-month treatment,the lower-limb MAS scores in the observation group were significantly better than those in the rehabilitation group and the warm joint needling group (all P＜0.05).After 1-month,3-month and 6-month treatment,the BBS scores in the observation group were significantly better than those in the rehabilitation group and the warm joint needling group (all P＜0.05).After 2-week,1-month,3-month and 6-month treatment,the SS-QOL scores in the observation group were markedly better than those in the rehabilitation group and the warm joint needling group (all P＜0.05).Conclusion:Warm joint needling plus rehabilitation can effectively improve the lower-limb spasticity state,balance function and QOL in patients with spastic hemiplegia after ischemic cerebral stroke.
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<p><b>OBJECTIVE</b>To investigate the effects of T-2 toxin on expressions of Fas, p53, Bcl-xL, Bcl-2, Bax and caspase-3 on human chondrocytes.</p><p><b>METHODS</b>Human chondrocytes were treated with T-2 toxin (1-20 ng/ml) for 5 d. Fas, p53 and other apoptosis-related proteins such as Bax, Bcl-2, Bcl-xL, caspase-3 were determined by Western blot analysis and their mRNA expressions were determined by reverse transcriptase-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>Increases in Fas, p53 and the pro-apoptotic factor Bax protein and mRNA expressions and a decrease of the anti-apoptotic factor Bcl-xL were observed in a dose-dependent manner after exposures to 1-20 ng/ml T-2 toxin, while the expression of the anti-apoptotic factor Bcl-2 was unchanged. Meanwhile, T-2 toxin could also up-regulate the expressions of both pro-caspase-3 and caspase-3 in a dose-dependent manner.</p><p><b>CONCLUSION</b>These data suggest a possible underlying molecular mechanism for T-2 toxin to induce the apoptosis signaling pathway in human chondrocytes by regulation of apoptosis-related proteins.</p>
Subject(s)
Humans , Apoptosis , Base Sequence , Blotting, Western , Caspase 3 , Genetics , Metabolism , Cell Proliferation , Cells, Cultured , Chondrocytes , Cell Biology , Metabolism , DNA Primers , Genetics , Gene Expression , Proto-Oncogene Proteins c-bcl-2 , Genetics , Metabolism , RNA, Messenger , Genetics , Metabolism , Reverse Transcriptase Polymerase Chain Reaction , Signal Transduction , T-2 Toxin , Toxicity , Tumor Suppressor Protein p53 , Genetics , Metabolism , bcl-2-Associated X Protein , Genetics , Metabolism , bcl-X Protein , Genetics , Metabolism , fas Receptor , Genetics , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To study the inhibitory effect of T-2 toxin on the expression of aggrecan and collagen II in chondrocytes and the protection of selenium against this effect.</p><p><b>METHODS</b>Human chondrocytes cultured in vitro were treated with T-2 toxin at different concentrations for varied time periods (1-5 days), and the cell viability was measured by MTT assay. Aggrecan expression was detected by toluidine blue staining and collagen II expression by immunostaining using monoclonal antibody of collagen. Aggrecan and collagen II mRNA expressions were measured by semiquantitative RT-PCR.</p><p><b>RESULTS</b>T-2 toxin dose- and time-dependently affected chondrocyte viability within the concentration range of 0.001-2 mg/L, the prolonged treatment time further enhanced the dose dependence of the inhibitory effect. T-2 toxin lowered aggrecan and collagen II synthesis in the chondrocytes and reduced their mRNA expressions. Selenium could partly attenuate the inhibitory effects of T-2 toxin on aggrecan mRNA expression, but showed no such effect against T-2-induced collagen II expression.</p><p><b>CONCLUSION</b>T-2 toxin can obviously inhibit aggrecan and collagen II synthesis in human chondrocytes, and selenium can partly antagonize the inhibitory effects of T-2 toxin on aggrecan.</p>
Subject(s)
Humans , Aggrecans , Genetics , Cells, Cultured , Chondrocytes , Cell Biology , Metabolism , Collagen Type II , Genetics , Dose-Response Relationship, Drug , Fetus , Protective Agents , Pharmacology , RNA, Messenger , Genetics , Selenium , Pharmacology , T-2 Toxin , ToxicityABSTRACT
0.05).(4) Significant differences between CC and CIN Ⅰ for p16,CDH1,RASSF1A and TIMP3 genes(P