METHODOLOGY: CT coronary angiography was performed on patients with Kawasaki disease diagnosed with coronary aneurysm or suspected to have coronary stenosis. Studies were performed using electrocardiogram-gated protocols. General anaesthesia was used in patients who were not cooperative for breathing control. Heart rate, image quality, and effective radiation dose were documented.
RESULTS: Fifty-two Kawasaki patients underwent CT coronary angiography to assess coronary artery lesions. Median heart rate was 88 beats per minute (range 50-165 beats/minute). Image quality was graded as excellent in 34 (65%) patients, good in 17 (32%), satisfactory in 1, and poor in 1 patient. Coronary artery aneurysm was found in 25 (bilateral = 6, unilateral = 19, multiple = 11). Thrombus was found in 11 patients resulting in partial and total occlusion in 8 and 3 patients, respectively. Coronary stenosis was noted in 2 patients. The effective radiation dose was 1.296 millisievert (median 0.81 millisievert). Better diagnostic imaging quality was significantly related to lower heart rate (p = 0.007).
CONCLUSION: Electrocardiogram-triggered CT coronary angiography provides a good diagnostic assessment of coronary artery lesions in children with Kawasaki disease.
METHODS: This is a retrospective cohort study utilizing data from the National Cardiovascular Disease (NCVD)-PCI registry. The data collected (N = 28,007) were split into training set (n = 24,409) and testing set (n = 3598). Four predictive models (logistic regression [LR], random forest method, support vector machine [SVM], and artificial neural network) were developed and validated. The outcome on risk prediction were compared.
RESULTS: The demographic and clinical features of patients in the training and testing cohorts were similar. Patients had mean age ± standard deviation of 58.15 ± 10.13 years at admission with a male majority (82.66%). In over half of the procedures (50.61%), patients had chronic stable angina. Within 1 year of follow up mortality, target vessel revascularization (TVR), and composite event of mortality and TVR were 3.92%, 9.48%, and 12.98% respectively. LR was the best model in predicting mortality event within 1-year post-PCI (AUC: 0.820). SVM had the highest discrimination power for both TVR event (AUC: 0.720) and composite event of mortality and TVR (AUC: 0.720).
CONCLUSIONS: This study successfully identified optimal prediction models with the good discriminatory ability for mortality outcome and good discrimination ability for TVR and composite event of mortality and TVR with a simple machine learning framework.
METHODS: HepG2 cells were treated with different concentrations of KMF and 0.5 mM palmitate (PA) for 24 h. The mRNA and protein levels of genes involved in lipid metabolism were evaluated using real-time PCR and western blot. The expression of Nrf2 was silenced using siRNA.
RESULTS: Data indicated that KMF (20 μM) reversed PA-induced increased triglyceride (TG) levels and total lipid content. These effects were accompanied by down-regulation of the mRNA and protein levels of lipogenic genes (FAS, ACC and SREBP1), and up-regulation of genes related to fatty acid oxidation (CPT-1, HADHα and PPARα). Kaempferol significantly decreased the levels of the oxidative stress markers (ROS and MDA) and enhanced the activities of antioxidant enzymes SOD and GPx in PA-challenged cells. Luciferase analysis showed that KMF increased the transactivation of Nrf2 in hepatocytes. The results also revealed that KMF-mediated activation of Nrf2 target genes was suppressed by Nrf2 siRNA. Furthermore, Nrf2 siRNA abolished the KMF-induced reduction in ROS and MDA levels in PA treated cells. In addition, the inhibitory effect of KMF on TG levels and the mRNA and protein levels of FAS, ACC and SREPB-1 were significantly abolished by Nrf2 inhibition. Nrf2 inhibition also suppressed the KMF-induced activation of genes involved in β oxidation (CPT-1 and PPAR-α).
CONCLUSION: The results suggest that KMF protects HepG2 cells from PA-induced lipid accumulation via activation of the Nrf2 signaling pathway.
OBJECTIVES: This study examined the speech and hearing status of Malay-speaking children with CLP residing in Kuala Lumpur.
METHODS: Parents whose children were between the age of 5 and 7 years were recruited via the Cleft Lip and Palate Association of Malaysia (CLAPAM) registry. Parents completed a survey and the children completed a speech and hearing assessment at the Audiology and Speech Sciences Clinic, Universiti Kebangsaan Malaysia.
OUTCOMES: Speech measures include nasality rating, nasalance scores, articulation errors and speech intelligibility rating, while hearing measures include hearing thresholds and tympanometry results for each child.
RESULTS: Out of 118 registered members who fulfilled the inclusion criteria, 21 agreed to participate in the study. The overall speech and hearing status of children in this sample were poor. Only four (19%) participants had normal speech intelligibility rating and normal hearing bilaterally. In terms of overall cleft management, only four (19%) participants were seen by a cleft team while seven (33%) had never had their hearing tested prior to this study.
CONCLUSION: Participants in this sample had poor outcomes in speech and hearing and received uncoordinated and fragmented cleft care. This finding calls for further large scale research and collaborative efforts into improving and providing centralised, multidisciplinary care for children born with CLP.