Effectiveness of the Integrated Dengue Education and Learning (iDEAL) module in improving the knowledge, attitude, practice, environmental cleanliness index, and dengue index among schoolchildren: A randomised controlled trial protocol.

BACKGROUND: Dengue is a mosquito-borne disease caused by four distinct, closely related dengue viruses (DENV). Global dengue incidence has markedly increased in the past decades. The World Health Organization reported that cases increased from 505,430 in 2000 to 5.2 million in 2019. Similarly, the total dengue cases in Malaysia increased from 7,103 in 2000 to a peak of 130,101 in 2019. Knowledge, attitude, and practice (KAP) remain the most effective dengue prevention and control tools. Furthermore, school-based health education is key to enhancing knowledge and raising awareness of the seriousness of dengue among schoolchildren and transferring knowledge and practice from classrooms to homes. Thus, it is necessary to plan an integrated module for the primary prevention of dengue infection, specifically among schoolchildren. AIMS: The present study intends to develop, implement, and evaluate the effectiveness of a theory-based integrated dengue education and learning (iDEAL) module in improving the KAP, environmental cleanliness index, and dengue index among schoolchildren in Selangor and Kuala Lumpur. METHODS: This study is a single-blinded, cluster randomised controlled trial to be conducted from 1 September 2023 to 31 August 2025. The study will involve 20 primary and 20 secondary schools in Selangor and Kuala Lumpur. The 1600 participants will be randomly allocated to intervention and control groups based on selected clusters to avoid contamination. A cluster is a comparable school that fulfils the inclusion and exclusion criteria. The intervention group will receive the iDEAL module, while the control group will receive standard education. The iDEAL module will be developed following a systematic procedure and delivered in-person by trained researchers to the participants. The outcome will be measured using validated, self-administered questionnaires at baseline (T0), immediately (T1), one month (T2), and three months (T3) post-intervention to measure the intervention module effectiveness. The data will be analysed using IBM Statistical Package for Social Science (SPSS) version 28 and descriptive and inferential statistics. Within-group changes over time will be compared using one-way repeated measure analysis of variance for continuous and normally distributed variables. Within-group analysis of categorical data will use Cochran's Q test. The main effect and interaction between and within the intervention and control groups at T0, T1, T2, and T3 will be tested using the generalised linear mixed model (GLMM). Hypothetically, the KAP, environmental cleanliness index, and dengue index among the intervention group will be significantly improved compared to the control group. The hypothesis will be tested using a significance level with a p-value of 0.05 and a confidence interval of 95%. CONCLUSIONS: The study protocol outlines developing and testing an iDEAL module for schoolchildren in Selangor and Kuala Lumpur, with no socio-demographic differences expected. The intervention aims to improve KAP, environmental cleanliness index, and dengue index, potentially reducing dengue risk. Results could inform public health policies, emphasizing school-based interventions' importance in combating diseases like dengue.

Effect of Carcinomas on Autosomal Trait Screening: A Review Article.

This review highlights the effect of carcinomas on the results of the examination of autosomal genetic traits for identification and paternity tests when carcinoid tissue is the only source and no other samples are available. In DNA typing or genetic fingerprinting, variable elements are isolated and identified within the base pair sequences that form the DNA. The person's probable identity can be determined by analysing nucleotide sequences in particular regions of DNA unique to everyone. Genetics plays an increasingly important role in the risk stratification and management of carcinoma patients. The available information from previous studies has indicated that in some incidents, including mass disasters and crimes such as terrorist incidents, biological evidence may not be available at the scene of the accident, except for some unknown human remains found in the form of undefined human tissues. If these tissues have cancerous tumours, it may affect the examination of the genetic traits derived from these samples, thereby resulting in a failure to identify the person. Pathology units, more often, verify the identity of the patients who were diagnosed with cancer in reference to their deceased tumorous relatives. Genetic fingerprinting (GF) is also used in paternity testing when the alleged parent disappeared or died and earlier was diagnosed and treated for cancer.

The Influence of Environmental Polycyclic Aromatic Hydrocarbons (PAHs) Exposure on DNA Damage among School Children in Urban Traffic Area, Malaysia.

This study aimed to investigate the association between particulate PAHs exposure and DNA damage in Malaysian schoolchildren in heavy traffic (HT) and low traffic (LT) areas. PAH samples at eight schools were collected using a low volume sampler for 24 h and quantified using Gas Chromatography-Mass Spectrometry. Two hundred and twenty-eight buccal cells of children were assessed for DNA damage using Comet Assay. Monte-Carlo simulation was performed to determine incremental lifetime cancer risk (ILCR) and to check the uncertainty and sensitivity of the estimated risk. Total PAH concentrations in the schools in HT area were higher than LT area ranging from 4.4 to 5.76 ng m-3 and 1.36 to 3.79 ng m-3, respectively. The source diagnostic ratio showed that PAHs in the HT area is pyrogenic, mainly from diesel emission. The 95th percentile of the ILCR for children in HT and LT area were 2.80 × 10-7 and 1.43 × 10-7, respectively. The degree of DNA damage was significantly more severe in children in the HT group compared to LT group. This study shows that total indoor PAH exposure was the most significant factor that influenced the DNA damage among children. Further investigation of the relationship between PAH exposure and genomic integrity in children is required to shed additional light on potential health risks.

The Influence of Traffic-Related Air Pollution (TRAP) in Primary Schools and Residential Proximity to Traffic Sources on Histone H3 Level in Selected Malaysian Children.

This study aimed to investigate the association between traffic-related air pollution (TRAP) exposure and histone H3 modification among school children in high-traffic (HT) and low-traffic (LT) areas in Malaysia. Respondents' background information and personal exposure to traffic sources were obtained from questionnaires distributed to randomly selected school children. Real-time monitoring instruments were used for 6-h measurements of PM10, PM2.5, PM1, NO2, SO2, O3, CO, and total volatile organic compounds (TVOC). Meanwhile, 24-h measurements of PM2.5-bound black carbon (BC) were performed using air sampling pumps. The salivary histone H3 level was captured using an enzyme-linked immunosorbent assay (ELISA). HT schools had significantly higher PM10, PM2.5, PM1, BC, NO2, SO2, O3, CO, and TVOC than LT schools, all at p < 0.001. Children in the HT area were more likely to get higher histone H3 levels (z = -5.13). There were positive weak correlations between histone H3 level and concentrations of NO2 (r = 0.37), CO (r = 0.36), PM1 (r = 0.35), PM2.5 (r = 0.34), SO2 (r = 0.34), PM10 (r = 0.33), O3 (r = 0.33), TVOC (r = 0.25), and BC (r = 0.19). Overall, this study proposes the possible role of histone H3 modification in interpreting the effects of TRAP exposure via non-genotoxic mechanisms.

Exposure to Particulate PAHs on Potential Genotoxicity and Cancer Risk among School Children Living Near the Petrochemical Industry.

This study aimed to assess the association of exposure to particle-bound (PM2.5) polycyclic aromatic hydrocarbons (PAHs) with potential genotoxicity and cancer risk among children living near the petrochemical industry and comparative populations in Malaysia. PM2.5 samples were collected using a low-volume sampler for 24 h at three primary schools located within 5 km of the industrial area and three comparative schools more than 20 km away from any industrial activity. A gas chromatography-mass spectrometer was used to determine the analysis of 16 United States Environmental Protection Agency (USEPA) priority PAHs. A total of 205 children were randomly selected to assess the DNA damage in buccal cells, employing the comet assay. Total PAHs measured in exposed and comparative schools varied, respectively, from 61.60 to 64.64 ng m-3 and from 5.93 to 35.06 ng m-3. The PAH emission in exposed schools was contributed mainly by traffic and industrial emissions, dependent on the source apportionment. The 95th percentiles of the incremental lifetime cancer risk estimated using Monte Carlo simulation revealed that the inhalation risk for the exposed children and comparative populations was 2.22 × 10-6 and 2.95 × 10-7, respectively. The degree of DNA injury was substantially more severe among the exposed children relative to the comparative community. This study reveals that higher exposure to PAHs increases the risk of genotoxic effects and cancer among children.

Deoxyribonucleic acid (DNA) methylation in children exposed to air pollution: a possible mechanism underlying respiratory health effects development.

Air pollution is a substantial environmental threat to children and acts as acute and chronic disease risk factors alike. Several studies have previously evaluated epigenetic modifications concerning its exposure across various life stages. However, findings on epigenetic modifications as the consequences of air pollution during childhood are rather minimal. This review evaluated highly relevant studies in the field to analyze the existing literature regarding exposure to air pollution, with a focus on epigenetic alterations during childhood and their connections with respiratory health effects. The search was conducted using readily available electronic databases (PubMed and ScienceDirect) to screen for children's studies on epigenetic mechanisms following either pre- or post-natal exposure to air pollutants. Studies relevant enough and matched the predetermined criteria were chosen to be reviewed. Non-English articles and studies that did not report both air monitoring and epigenetic outcomes in the same article were excluded. The review found that epigenetic changes have been linked with exposure to air pollutants during early life with evidence and reports of how they may deregulate the epigenome balance, thus inducing disease progression in the future. Epigenetic studies evolve as a promising new approach in deciphering the underlying impacts of air pollution on deoxyribonucleic acid (DNA) due to links established between some of these epigenetic mechanisms and illnesses.

Ethnicity as predictor of immune reconstitution among Malaysian HIV-positive patients treated with highly active antiretroviral therapy.

The impact of sociodemographic and clinical factors on immune recovery and viral load suppression among HIV-1 positive patients treated with HAART particularly in Malaysia is largely unknown. This cross-sectional study enrolled 170 HIV-1-infected individuals of three major ethnicities who attended three HIV outpatient clinics in Malaysia. Questionnaire was used to obtain sociodemographic data while CD4 count and viral load data were gathered from hospital's record. Multiple factors were assessed for their predictive effects on CD4 count recovery (≥500 cells/mm3 ) and viral load suppression (≤50 copies/mL) using binary logistic regression. Most of the subjects were male (149/87.6%), in the age group 30 to 39 years old (78/45.9%) and got infected via homosexual contact (82/48.2%). Indians were associated with 11 times higher chance for CD4 recovery as compared to Malays at 8 to 12 months of HAART (adjusted OR: 10.948, 95% CI: 1.873, 64.001, P = .008). Viral load suppression was positively influenced by intravenous drug use (IVDU) status (adjusted OR: 35.224, 95% CI: 1.234, 1000.489, P = .037) at 4 to 6 months of HAART. Higher pretreatment CD4 count was a positive predictor for both initial immunological and virological responses while higher pretreatment viral load was a negative predictor for virological suppression only. In conclusion, ethnicity plays a significant role in determining early immune reconstitution in Malaysia, besides pretreatment CD4 count. Further studies are needed to identify possible biological factors underlying this association.

Channa striatus cream down-regulates tumour necrosis factor (TNF)-alpha gene expression and alleviates chronic-like dermatitis in mouse model.

ETHNOPHARMACOLOGICAL RELEVANCE: Haruan, Channa striatus, is a freshwater fish which has been well-known locally to accelerate wound healing during post-operative and post-partum periods. The fish extract also has potent anti-inflammatory and analgesic properties. AIM OF THE STUDY: To assess topical anti-inflammatory effect of Haruan cream on 12-0-tetradecanoylphorbol-13-acetate (TPA)-induced chronic-like dermatitis in mice. MATERIALS AND METHODS: Male ICR mice were randomized into six groups of five mice each: acetone (vehicle), TPA alone (negative control), three Haruan treatment groups (Haruan 1%, Haruan 5% and Haruan 10%) and hydrocortisone 1% (positive control). Briefly, both surfaces of mouse ears were applied with TPA (2.5µg/20µl acetone) for five times on alternate days and with Haruan or hydrocortisone 1% cream for the last three days. Mouse ear thickness was measured 24h after final treatment with the cream and the ears were harvested for further histological analysis and gene expression studies of TNF-α by real-time reverse transcriptase-polymerase chain reaction (RT-qPCR). RESULTS: Topical application of Haruan cream had reduced the mouse ear thickness 18.1-28%) with comparable effect to the positive control. In addition, histopathological comparison had shown evident reduction in various parameters of cutaneous inflammation including dermal oedema, inflammatory cells infiltration and proliferation of epidermal keratinocytes. Furthermore, TPA application had resulted in the up-regulation of TNF-α gene expression by 353-fold, which was subsequently down-regulated by the Haruan cream (34- to 112-fold). CONCLUSION: Haruan is an effective topical anti-inflammatory agent in this mouse model of chronic-like dermatitis, thus suggesting its potential as a non-steroidal treatment option for chronic inflammatory dermatoses.

A comparison of assays for accurate copy number measurement of the low-affinity Fc gamma receptor genes FCGR3A and FCGR3B.

The FCGR3 locus encoding the low affinity activating receptor FcγRIII, plays a vital role in immunity triggered by cellular effector and regulatory functions. Copy number of the genes FCGR3A and FCGR3B has previously been reported to affect susceptibility to several autoimmune diseases and chronic inflammatory conditions. However, such genetic association studies often yield inconsistent results; hence require assays that are robust with low error rate. We investigated the accuracy and efficiency in estimating FCGR3 CNV by comparing Sequenom MassARRAY and paralogue ratio test-restriction enzyme digest variant ratio (PRT-REDVR). In addition, since many genetic association studies of FCGR3B CNV were carried out using real-time quantitative PCR, we have also included the evaluation of that method's performance in estimating the multi-allelic CNV of FCGR3B. The qPCR assay exhibited a considerably broader distribution of signal intensity, potentially introducing error in estimation of copy number and higher false positive rates. Both Sequenom and PRT-REDVR showed lesser systematic bias, but Sequenom skewed towards copy number normal (CN = 2). The discrepancy between Sequenom and PRT-REDVR might be attributed either to batch effects noise in individual measurements. Our study suggests that PRT-REDVR is more robust and accurate in genotyping the CNV of FCGR3, but highlights the needs of multiple independent assays for extensive validation when performing a genetic association study with multi-allelic CNVs.

Association of insertion/deletion polymorphism of angiotensin-converting enzyme gene among Malay male hypertensive subjects in response to ACE inhibitors.

INTRODUCTION: Several studies show that the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been associated with hypertension in various populations. The present study sought to determine the association of the I/D gene polymorphism among Malay male essential hypertensive subjects in response to ACE inhibitors (enalapril and lisinopril). MATERIALS AND METHODS: A total of 72 patients with newly diagnosed hypertension and 72 healthy subjects were recruited in this study. Blood pressure was recorded from 0 to 24 weeks of treatment with enalapril or lisinopril. Genotyping of the I/D polymorphism was carried out using a standard PCR method. RESULTS: Statistically significant association of the D allele of the ACE gene was observed between the case and control subjects (p < 0.01). There was a decrease in blood pressure in the patients carrying the DD genotype (SBP=18.5±8.1 mmHg, DBP=15.29±7.1 mmHg) rather than the ID (SBP=4.1±3.3 mmHg, DBP=9.1±3.5 mmHg) and II genotypes (SBP= 3.0±0.2 mmHg, DBP 0.11±6.1 mmHg) of the ACE gene. CONCLUSION: Patients carrying the DD genotype had higher blood pressure-lowering response when treated with ACE inhibitors enalapril or lisinopril than those carrying ID and II genotypes, suggesting that the D allele may be a possible genetic marker for essential hypertension among Malay male subjects.

Measurement methods and accuracy in copy number variation: failure to replicate associations of beta-defensin copy number with Crohn's disease.

The copy number variation in beta-defensin genes on human chromosome 8 has been proposed to underlie susceptibility to inflammatory disorders, but presents considerable challenges for accurate typing on the scale required for adequately powered case-control studies. In this work, we have used accurate methods of copy number typing based on the paralogue ratio test (PRT) to assess beta-defensin copy number in more than 1500 UK DNA samples including more than 1000 cases of Crohn's disease. A subset of 625 samples was typed using both PRT-based methods and standard real-time PCR methods, from which direct comparisons highlight potentially serious shortcomings of a real-time PCR assay for typing this variant. Comparing our PRT-based results with two previous studies based only on real-time PCR, we find no evidence to support the reported association of Crohn's disease with either low or high beta-defensin copy number; furthermore, it is noteworthy that there are disagreements between different studies on the observed frequency distribution of copy number states among European controls. We suggest safeguards to be adopted in assessing and reporting the accuracy of copy number measurement, with particular emphasis on integer clustering of results, to avoid reporting of spurious associations in future case-control studies.

Allelic recombination between distinct genomic locations generates copy number diversity in human beta-defensins.

Beta-defensins are small secreted antimicrobial and signaling peptides involved in the innate immune response of vertebrates. In humans, a cluster of at least 7 of these genes shows extensive copy number variation, with a diploid copy number commonly ranging between 2 and 7. Using a genetic mapping approach, we show that this cluster is at not 1 but 2 distinct genomic loci approximately 5 Mb apart on chromosome band 8p23.1, contradicting the most recent genome assembly. We also demonstrate that the predominant mechanism of change in beta-defensin copy number is simple allelic recombination occurring in the interval between the 2 distinct genomic loci for these genes. In 416 meiotic transmissions, we observe 3 events creating a haplotype copy number not found in the parent, equivalent to a germ-line rate of copy number change of approximately 0.7% per gamete. This places it among the fastest-changing copy number variants currently known.