Introduction: Metabolic syndrome is associated with low-grade, chronic inflammation. Our study aimed to evaluate the effects of tocotrienols supplementation on cytokines and lipid profile in adults with metabolic syndrome. Method: In a 16-week randomised, double-blind, placebo-controlled trial, 70 adults with metabolic syndrome aged 20-60 years were randomly assigned to a mixed tocotrienols group (n=35) that received 400mg/day of mixed tocotrienols or a placebo group (n=35) that received capsules containing soy bean oil. At baseline, week 8 and week 16, anthropometric, body composition and blood pressure measurements were conducted. At baseline and week 16 only, serum levels of total cholesterol (TC) and high density lipoprotein (HDL)-cholesterol, plasma levels of fasting plasma glucose (FPG), interleukin-6 (IL-6), tumouxr necrosis factor- a (TNF-a), leptin, adiponectin and high sensitivity C-reactive protein were also determined. Changes in dietary intake and physical activity level between baseline, week 8 and week 16 were also assessed. Results:In the tocotrienols group, significant reductions from baseline were found in diastolic blood pressure (p=0.001), TC (p=0.008), LDL-cholesterol (p=0.022), HDL-cholesterol (p<0.001), IL-6 (p=0.024) and TNF-a (p=0.013) at week sixteen. However, the changes in the tocotrienols group were not significantly different from those of the placebo group. Conclusion: The 16-week mixed tocotrienols supplementation exerted potential beneficial effects on cytokines and lipid profile in adults with metabolic syndrome. The results might have been confounded by the physiological effects produced by the soy bean oil in the placebo capsule.

Introduction: Statins have several pleiotropic effects including its primary effect of lipid lowering that is important to prevent cardiovascular disease (CVD). Subjects often have heterogeneous responses to statin. This study aims to determine the biochemical effects of statins on lipid parameters among newly diagnosed dyslipidaemia subjects. Methods: This was a prospective observational study involving 118 newly diagnosed adults with dyslipidaemia from three government health clinics in Selangor, Malaysia. Biochemical analyses including fasting lipid profile [triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C)] and apolipoproteins (apoA1, apoB) were taken at baseline and follow-up after a month on statin. Results: Majority of subjects (61.9%) were prescribed with lovastatin, with the rest on simvastatin. At baseline, the median values for all lipid profile parameters (TC, LDL-C, HDL-C) and non-conventional lipid parameters (LDL-C:HDL-C ratio, non-HDL-C, TC:HDL-C ratio, apoB:apoA1 ratio) were deranged except for TG and apoA1. On follow up, all parameters showed median values within the reference range except for HDL-C, non-HDL-C and TC:HDL-C ratio. There was significant difference in the effect of statins on lipid parameters including predictors of cardiovascular risk, simvastatin having better effects. Conclusions: Different statinshave varying effects on lipid parameters. Simvastatin showed significantly better effects compared to lovastatin. Non-HDL value should be included in the standard lipid profile report given its ease of use and implementation as it’s both a marker of coronary artery disease (CAD) risk stratification as well as an established determinant of goal attainment during therapy.

Introduction: One of the commonly used techniques for mutation screening is High Resolution Melting (HRM) analysis. HRM is a post PCR method that relies on the detection of the fluorescent signals acquired due to the release of DNA intercalated dyes upon the melting of dsDNA to ssDNA. The method is simple, inexpensive and does not require post PCR-handling, making it suitable for high throughput screening. Methods: This study aimed to develop and validate HRM technique for the screening of two disease-associated single nucleotide polymorphisms (SNPs) namely BDNF rs6265 and DAT1 rs40184 using a total of 30 gDNA samples. The obtained results were confirmed and validated by sequencing. Results: HRM analysis showed that the predicted genotypes of BDNF rs6265 and DAT1 rs40184 among all the gDNA samples were in 100% concordance with the sequencing results, making it an accurate and sensitive method for the detection of SNPs. Conclusions: The application of HRM can accurately determine the genotype of BDNF rs6265 and DAT1 rs40184 SNPs, making it a promising tool for rapid and high-throughput screening of targeted SNPs in a large population study.

Objective: To determine the lead bioactive compound in kernel extract of Mangifera pajang and its anti-cancer activity against human breast cancer cell lines with positive estrogen receptor (MCF-7). Methods: The methanolic extract of dried powder kernel of Mangifera pajang was exposed to column chromatography for isolation. The structural elucidation of the isolated compound was characterized using infrared, nuclear magnetic resonance, mass spectrometry. Furthermore, cytotoxicity, morphological changes, flow cytometry and cell cycle arrest analyses were performed to examine the mechanism of anti-proliferation and apoptosis induced by methyl gallate against MCF-7. Results: One compound was isolated from the methanolic extract of Mangifera pajang kernel and identified as methyl gallate. The flow cytometric results demonstrated induction of apoptosis in MCF-7 cells by three concentrations of methyl gallate. The cell cycle arrest showed a significant (P<0.05) decrease in cell progression at G 2/M phase of MCF-7 after treatment with 100 μM of methyl gallate. The cell percentage of early and late apoptosis was significant at 10 and 100 μM of methyl gallate. Also, methyl gallate treatment induced up-regulation of reactive oxygen species levels in MCF-7 cells with a reduction in superoxide dismutase levels. Conclusions: These findings indicate that isolated methyl gallate from Mangifera pajang kernel extracts induces growth inhibition and apoptosis in MCF-7 cells via up-regulating oxidative stress pathway.