METHOD: Between November 2009 and July 2010, outpatients from 45 countries who met the criteria for stable CAD were recruited into the registry. Baseline characteristics were documented at enrolment, and patients were reassessed during their annual visits over a five-year follow-up period. Key outcomes measured were sudden death and cardiovascular (CV) death, non-CV death and CV morbidity.
RESULTS: At baseline, 33,283 patients were available for analysis within the registry; 380 and 27 were Malaysians and Bruneians, respectively. The mean ages of Malaysian/Bruneian patients and the rest of the world (RoW) were 57.83 ±9.98 years and 64.23 ± 10.46 years, respectively (p<0.001). The median body mass index values were 26.6 (24.4-29.6) kg/m2 and 27.3 (24.8-30.3) kg/m2, respectively (p=0.014). Malaysian/Bruneian patients had lower rates of myocardial infarction (54.55% versus 59.76%, p=0.033) and higher rates of diabetes (43.24% versus 28.99%, p<0.001) and dyslipidaemia (90.42% versus 74.66%, p<0.001) compared with the RoW. Measured clinical outcomes in Malaysian and Bruneian patients at 2-years follow-up were low and generally comparable to the RoW.
CONCLUSION: Malaysian/Bruneian patients with stable CAD tend to be younger with poorer diabetic control compared with the RoW. However, they had similar outcomes as the main registry following two years of treatment.
METHODS: This randomized trial was conducted in Malaysia in 232 term multiparous women with balloon catheter-ripened cervixes (dilatation ≥3 cm), singleton fetus, cephalic presentation with intact membranes, and reassuring fetal heart rate tracing. They were randomized to immediate titrated intravenous oxytocin infusion and early amniotomy (116) or delayed amniotomy after 4 h of oxytocin (116). Primary outcome was intervention (oxytocin initiation)-to-delivery interval.
RESULTS: Oxytocin-to-delivery intervals were a median of 4.99 h (interquartile range [IQR], 3.21-7.82 h) versus 6.23 h (IQR, 4.50-8.45 h) (P
Methods: In this study, type 2 diabetes model mice were induced by streptozotocin and high-fat diet (HFD) and used to evaluate the antihyperglycemic and anti-inflammatory effects of FFP. Mice were fed with HFD and challenged with 30 mg/kg body weight (BW) of streptozotocin for 1 month followed by 6 weeks of supplementation with 0.1 and 1.0 g/kg BW of FFP. Metformin was used as positive control treatment.
Results: Xeniji™-supplemented hyperglycemic mice were recorded with lower glucose level after 6 weeks of duration. This effect was contributed by the improvement of insulin sensitivity in the hyperglycemic mice indicated by the oral glucose tolerance test, insulin tolerance test, and end point insulin level. In addition, gene expression study has shown that the antihyperglycemic effect of FFP is related to the improvement of lipid and glucose metabolism in the mice. Furthermore, both 0.1 and 1 g/kg BW of FFP was able to reduce hyperglycemia-related inflammation indicated by the reduction of proinflammatory cytokines, NF-kB and iNOS gene expression and nitric oxide level.
Conclusion: FFP potentially demonstrated in vivo antihyperglycemic and anti-inflammatory effects on HFD and streptozotocin-induced diabetic mice.