METHODS: All-cause and cause-specific mortality estimates were obtained from the 2013 Global Burden of Disease Study. Data were extracted from 1990 to 2013 for the developmental age range from 1 to 24 years, for both sexes. Trends in all-cause and cause-specific mortality for the major epidemiological causes were estimated.
RESULTS: From 1990 to 2013, all-cause mortality decreased in all age groups. Reduction of all-cause mortality was greatest in 1- to 4-year-olds (2.4% per year reduction) and least in 20- to 24-year-olds (.9% per year reduction). Accordingly, in 2013, all-cause mortality was highest in 20- to 24-year-old males (129 per 100,000 per year). In 1990, the principal cause of death for 1- to 9-year boys and girls was vaccine preventable diseases. By 2013, neoplasms had become the major cause of death in 1-9 year olds of both sexes. The major cause of death in 10- to 24-year-old females was typhoid in 1990 and neoplasms in 2013, whereas the major cause of death in 10- to 24-year-old males remained road traffic injuries.
CONCLUSIONS: The reduction in mortality across the epidemiological transition in Malaysia has been much less pronounced for adolescents than younger children. The contribution of injuries and noncommunicable diseases to adolescent mortality suggests where public health strategies should focus.
METHODS: This cross-sectional study involved children aged 4-12 years old with moderate to severe AD. Age and sex-matched healthy children were recruited as the comparison group. The Children's Sleep Habits Questionnaire (CSHQ) and the Strengths and Difficulties Questionnaire (SDQ) were used to assess sleep disturbance and behavioral problems, respectively. Higher scores in both questionnaires signify more disturbance.
RESULTS: Seventy patients and 141 controls were recruited. Median (interquartile range) age of patients was 5 (4,8) years. Patients had later sleep time (p
OBJECTIVE: The present study seeks to determine the mutation spectrum of the AGL gene in Malaysian population.
METHODS: A total of eleven patients (eight Malay, two Chinese and one Bajau) were investigated. Genomic DNA was extracted and subsequently the AGL gene was amplified using specific primers and sequenced. Mutations found were screened in 150 healthy control samples either by restriction enzyme digestion assay or TaqMan® SNP Genotyping assay.
RESULTS: We identified six unreported mutations (c.1423+1G>T, c.2914_2915delAA, c.3814_3815delAG, c.4333T>G, c.4490G>A, c.4531_4534delTGTC) along with three previously reported mutations (c.99C>T, c.1783C>T, c.2681+1G>A). One of the six unreported mutation causes abnormal splicing and results in retention of intron 12 of the mature transcript, while another is a termination read-through. One of the reported mutation c.2681+1G>A was recurrently found in the Malay patients (n = 7 alleles; 31.8%).
CONCLUSION: The mutation spectrum of the AGL gene in Malaysian patients has shown considerable heterogeneity, and all unreported mutations were absent in all 150 healthy control samples tested.
METHOD: This cross-sectional study was carried out to measure salivary cotinine concentrations among 1064 schoolchildren (10-11 years) attending 24 schools in Malaysia following recent partial smoke-free restrictions. Parents completed questionnaires and schoolchildren provided saliva samples for cotinine assay.
RESULTS: The geometric mean (GM) salivary cotinine concentrations for 947 non-smoking schoolchildren stratified by household residents' smoking behaviour were: for children living with non-smoking parents 0.32 ng/ml (95% CI 0.28-0.37) (n = 446); for children living with a smoker father 0.65 ng/ml (95% CI 0.57-0.72) (n = 432); for children living with two smoking parents 1.12 ng/ml (95% CI 0.29-4.40) (n = 3); for children who live with an extended family member who smokes 0.62 ng/ml (95% CI 0.42-0.89) (n = 33) and for children living with two smokers (father and extended family member) 0.71 ng/ml (95% CI 0.40-0.97) (n = 44). Parental-reported SHS exposures showed poor agreement with children's self-reported SHS exposures. Multiple linear regression demonstrated that cotinine levels were positively associated with living with one or more smokers, urban residence, occupation of father (Armed forces), parental-reported exposure to SHS and education of the father (Diploma/Technical certificate).
CONCLUSIONS: This is the first study to characterise exposures to SHS using salivary cotinine concentrations among schoolchildren in Malaysia and also the first study documenting SHS exposure using salivary cotinine as a biomarker in a South-East Asian population of schoolchildren. Compared to other populations of similarly aged schoolchildren, Malaysian children have higher salivary cotinine concentrations. The partial nature of smoke-free restrictions in Malaysia is likely to contribute to these findings. Enforcement of existing legislation to reduce exposure in public place settings and interventions to reduce exposure at home, especially to implement effective home smoking restriction practices are required.