OBJECTIVES: This pilot study compared the motor evoked potential (MEP) changes using different settings of rTMS in the post-ischemic stroke patient. The goal of the study is to identify effect sizes for a further trial and evaluate safety aspects.
METHODS: Eight post-stroke patients with upper limb hemiparesis for at least six months duration were studied in a tertiary hospital in Northeast Malaysia. Quasi experimental design was applied and the participants were randomised into two groups using software generated random numbers. One of the two settings: i) inhibitory setting, or ii) facilitatory setting have been applied randomly during the first meeting. The motor evoked potential (MEP) were recorded before and after application of the rTMS setting. A week later, a similar procedure will be repeated but using different setting than the first intervention. Each patient will serve as their own control. Repeated measures ANOVA test was applied to determine the effect sizes for both intervention through the options of partial eta-squared (η2 p).
RESULT: The study observed large effect sizes (η2 p > 0.14) for both rTMS settings in the lesion and non-lesion sides. For safety aspects, no minor or major side effects associated with the rTMS was reported by the participants.
CONCLUSIONS: The partial eta square of MEP value for both rTMS settings (fascilitatory and inhibitory) in both lesion and non-lesion sides represents large effect sizes. We recommend further trial to increase number of sample in order to study the effectiveness of both settings in ischemic stroke patient. Our preliminary data showed both settings may improve the MEP of the upper extremity in the ischemic stroke patient. No significant improvement noted when comparing both settings.
MATERIALS AND METHODS: The SLs that were fermented and further characterized for their biochemical activities. Cytotoxicity study was performed to assess cytostatic properties. A series of in vitro and ex vivo angiogenesis assay was also carried out. The relative fold change in the expression of p53 mRNA by SLs was also studied.
RESULTS: Altogether, the data show that SLs derived from palm oil fermentation process inhibited neovascularization in the ex vivo tissue segments and also the endothelial cell proliferation between 50% and 65% inhibition as a whole. The palm oil derived SLs also caused downregulation of the suppression level of vascular endothelial growth factor and also upregulate the p53 mRNA level. The analytical studies revealed the presence of high amount of phenolic compounds but with relatively weak antioxidant activity. The gas chromatography-mass spectrometry studies revealed abundant amount of palmitic and oleic acid, the latter an established antiangiogenic agent, and the former being proangiogenic.
CONCLUSION: Therefore, it can be concluded from this study that SLs derived from fermented palm oil have potent antiangiogenic activity which may be attributed by its oleic acid component.
Methods: Freeze-dried pineapple vinegar was evaluated for its in vitro apoptosis and metastasis inhibitory potential using MTT, cell cycle, Annexin V and scratch assays. The in vivo test using BALB/c mice challenged with 4 T1 cells was further investigated by pre-treating the mice with 0.08 or 2 ml/kg body weight of freshly-prepared pineapple vinegar for 28 days. The tumor weight, apoptotic state of cells in tumor, metastasis and immune response of the untreated and pineapple vinegar treatment group were evaluated and compared.
Results: From the in vitro study, an IC50 value of 0.25 mg/mL after 48 h of treatment was established. Annexin V/PI and scratch closure assays showed that pineapple vinegar induced 70% of cell population to undergo apoptosis and inhibited 30% of wound closure of 4 T1 cells. High concentration of pineapple vinegar (2 ml/kg body weight) led to the reduction of tumor weight and volume by 45%as compared to the untreated 4 T1-challenged mice. This effect might have been contributed by the increase of T cell and NK cells population associated with the overexpression of IL-2 andIFN-γ cytokines and splenocyte cytotoxicity. Furthermore, fewer instances of metastasis events were recorded in the pineapple vinegar treatment group and this could be explained by the downregulation of inflammation related genes (iNOS, NF-kB and COX2), metastasis related genes (iCAM, VEGF and MMP9) and angeogenesis related genes (CD26, TIMP1, HGF, MMP3, IGFBP-1 and IGFBP-2).
Conclusion: The ability of pineapple vinegar to delay cancer progression portrayed its potential as chemopreventive dietry intervention for cancer therapy.