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        Effect of Pectin on the Expression of Proteins Associated with Mitochondrial Biogenesis and Cell Senescence in HT29-Human Colorectal Adenocarcinoma Cells

        Jose Javier Zamorano-Leon,Sandra Ballesteros,Natalia de las Heras,Luis Alvarez-Sala,Mariano de la Serna-Soto,Khaoula Zekri-Nechar,Gala Freixer,Bibiana Calvo-Rico,Zhengguang Yang,Jose Manuel Garcia-Gar 한국식품영양과학회 2019 Preventive Nutrition and Food Science Vol.24 No.2

        Mitochondria dynamic is regulated by different proteins, maintaining a balance between fission and fusion. An imbalance towards mitochondrial fission has been associated with tumor cell proliferation. The aim of this study was to analyze whether pectin modifies the viability of human colon cancer cells and the expression of proteins involved in mitochondrial fusion and fission. The human colon carcinoma cell line HT29 cells was growth in 10% fetal bovine serum in the absence and presence of pectin. Pectin reduced HT29 cell viability in a concentration-dependent manner, reaching a plateau at 150∼300 μ㏖/L pectin. The presence of 200 μ㏖/L pectin reduced the expression of dynamin-related protein-1 and increased expression of the mitochondrial fusion-associated proteins mitofusin-1 and 2. Expression of cyclin B1, a protein involved in G2/M transition, was found decreased in pectin-incubated HT29 cells. Moreover, expression of p53 protein, the amount of p53 in the nucleous and β-galactosidase activity, which are all biomarkers for cellular senescence, were significantly higher in pectin-incubated HT29 cells than in HT29 cells incubated without pectin. Expression of the protein B-cell lymphoma 2 (Bcl-2) homologous antagonist/killer was increased in response to incubation with pectin. However, incubation with pectin did not affect expression of Bcl-2-associated X protein or Bcl-2, or the caspase-3 activity. Overall, we concluded that pectin reduces the viability of human HT29 colon cancer cells, which is accompanied with a shift in the expression of proteins associated with mitochondrial dynamics towards mitochondrial fusion. Moreover, incubation with pectin favors cellular senescence over apoptosis in HT29 cells.

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        A Study on the Effects of Dry Needling in Multiple Sclerosis Patients with Spasticity: Protocol of a Randomized Waitlist-Controlled Trial

        Omid Motamedzadeh,Noureddin Nakhostin Ansari,Soofia Naghdi,Amirreza Azimi,Ashraf Mahmoudzadeh,Sandra Calvo,Pablo Herrero 사단법인약침학회 2021 Journal of Acupuncture & Meridian Studies Vol.14 No.2

        Background: Spasticity is a common symptom in multiple sclerosis (MS). Dry needling (DN) has been considered a useful method for the treatment of spasticity; however, there are no studies on the effects of DN on spasticity in patients with MS. We propose a study protocol aiming to investigate the effects of DN on spasticity in patients with MS. Methods: MS patients with plantar flexor spasticity will be recruited. Participants will be randomly assigned to the DN group, where they will be receiving a single session of DN, one minute for each head of gastrocnemius muscle, or to the waiting list control group with no intervention. Primary outcome measures are the Modified Ashworth Scale (MAS) for gastrocnemius spasticity, passive resistive torque, and podography for foot pressure distribution. The ankle active and passive range of dorsiflexion and Timed Up and Go tests are the secondary outcome measures. All outcomes will be measured at baseline, immediately after the intervention, and one week later. A mixed-model, general linear model, and two-way repeated-measures ANOVA will be used to compare the quantitative variables between groups and within groups at the measurement time points. The MAS ordinal measure of spasticity will be compared between groups using the Kruskal-Wallis test, and both the Friedman test and Wilcoxon test will be used for within-group changes. Discussion: This study will provide primary evidence on the effects of DN on gastrocnemius muscle spasticity and gait in patients with MS. Trial registration: Iranian Registry of Clinical Trials (IRCT): IRCT20190617043918N1.

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