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Background: Pesticides manage pests and diseases in agriculture, but they harm the health of agricultural workers. Concentrations of thirteen pesticides were determined in personal air and blood serum of 85 paddy farmers and 85 non-farmers, thereafter associated with health symptoms. Method: Samples were analyzed using ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS). Results: The median concentration of pesticides in personal air samples ranged from 10.69 to 188.49 ng/m3 for farmers and from 5.79 to 73.66 ng/m3 for non-farmers. The median concentration of pesticides in blood serum was from 58.27 to 210.12 ng/mL for farmers and 47.83 to 62.74 ng/mL for non-farmers. Concentration of eleven pesticides in personal air and twelve pesticides in blood serum were significantly higher in farmers than non-farmers (p < 0.05). All pesticides detected in personal air correlated significantly with concentration in the blood serum of farmers (p < 0.05). Health symptoms reported by farmers were dizziness (49.4%), nausea (47.1%), cough (35.3%), chest pain (30.6%), breathing difficulty (23.5%), sore throat (22.4%), vomiting (18.8%), phlegm (16.5%), and wheezing (15.3%). Concentration of pesticides in personal air, blood serum, and health symptoms were not significantly associated. Conclusion: Occupational exposure to pesticides significantly contaminates blood serum of farmers compared to non-farmers.

Prostate cancer (PCa) is a challenging polygenic disease because the genes that cause PCa remain largely elusive and are affected by several causal factors. Consequently, research continuously strives to identify a genetic marker which could be used as an indicator to predict the most vulnerable (i.e., predisposed) segments of the population to the disease or for the gene which may be directly responsible for PCa. To enhance the genetic etiology of PCa, this research sought to discover the key studies conducted in this field using data from the main journal publication search engines, as it was hoped that this could shed light on the main research findings from these studies, which in turn could assist in determining these genes or markers. From the research highlighted, the studies primarily used two kinds of markers: short tandem repeats or single-nucleotide polymorphisms. These markers were found to be quite prevalent in all the chromosomes within the research carried out. It also became apparent that the studies differed in both quantity and quality, as well as being conducted in a variety of societies. Links were also determined between the degree and strength of the relationship between these markers and the occurrence of the disease. From the studies identified, most recommended a larger and more diverse survey for the parameters which had not been studied before, as well as an increase in the size of the community (i.e., the population) being studied. This is an indication that work in this field is far from complete, and thus, current research remains committed toward finding genetic markers that can be used clinically for the diagnosis and screening of patients with PCa.

Background: Type II diabetes mellitus (T2DM) is a polygenic disorder that can be prevented or delayed in case of the adoption of proper interventions. The identification of susceptible genes and novel biomarkers of T2DM could be of great help in the early detection of high-risk individuals. First-degree relatives of T2DM patients have a high risk of this disease, even when they have no major abnormalities in glucose metabolism. The present study was conducted to examine the status of the expression of two genes, namely toll-like receptor 4 (TLR4) and insulin receptor substrate (IRS1), involved in glucose metabolism in peripheral blood, in individuals genetically predisposed to T2DM development. Methods: Blood samples were collected from 54 participants in three research groups, including Malay subjects with T2DM, first-degree relatives of T2DM patients, and healthy controls. The measurement of gene expression was accomplished using a quantitative real-time polymerase chain reaction. Result: The results were indicative of the significant upregulation and downregulation of TLR4 in patients with T2DM and their first-degree relatives, respectively (P<0.05). With regard to IRS1, the data revealed a decreased expression in T2DM patients as compared to that in the healthy controls (p<0.05). Conclusion: The results indicated that TLR4 and IRS1 might be involved in the pathogenesis of T2DM. Moreover,the altered expression of TLR4 in the first-degree relatives of diabetic patients is an important marker showing a genetic predisposition to T2DM. Therefore, the two investigated genes could be used as a diagnostic tool for the prediction of T2DM in this population.

Introduction: Association studies between single nucleotide polymorphisms (SNPs) and type 2 diabetes mellitus (T2DM) have been abundant. However, there are limited reports on copy number variations (CNVs) of beta-defensins (DEFB) gene in relation to T2DM. In this study, DEFB copy numbers were quantified in T2DM with nephropathy, T2DM without nephropathy and non-diabetic control groups to investigate its influence in chronic inflammation in Malaysian individuals. Methods: DEFB copy number in Malaysian individuals were quantified by using paralogue ratio tests (PRT) which allow direct quantification of gene copy number by using PRT107A and HSPD21 PRT primers. The copy number generated was then validated from insertion/deletion ratio measurement 5DEL (rs5889219) and two microsatellite analyses (EPEV-1 and EPEV-3). Results: DEFB copy number was found extending from 2 to 8 copies in the non-diabetic group (n=146), while in T2DM group (n=392), copy numbers were more extensive, ranging between 1 and 12 copies; with 1, 10 and 12 copies detected in T2DM with nephropathy group (n=202). Statistically, there is no significant difference in DEFB copy number between T2DM and the non-diabetic group (p=0.209) as well as between diabetic nephropathy and without nephropathy of the T2DM group (p=0.522). However, significant white blood cell (WBC) count was found between T2DM groups with and without diabetic nephropathy (p=0.000). Conclusion: Extreme DEFB copy numbers in T2DM with nephropathy group suggest future studies with bigger sample size are necessary to elucidate the true impact of CNVs of DEFB gene in promoting early onset of nephropathy in T2DM.

Type 2 diabetes mellitus (T2DM) is associated with a high incidence of nephropathy. The aim of this study was to investigate the association of a genetic polymorphism of carnosinase (CNDP1-D18S880 and -rs2346061), endothelial nitric oxide synthase (NOS3-rs1799983), and manganese superoxide dismutase (MnSOD-rs4880) genes with the development of diabetic nephropathy among Malaysian type 2 diabetic patients. A case-control association study was performed using 652 T2DM patients comprising 227 Malays (without nephropathy = 96 and nephropathy = 131), 203 Chinese (without nephropathy = 95 and nephropathy = 108), and 222 Indians (without nephropathy = 136 and nephropathy = 86). DNA sequencing was performed for the D18S880 of CNDP1, while the rest were tested using DNA Sequenom MassARRAY to identify the polymorphisms. DNA was extracted from the secondary blood samples taken from the T2DM patients. The alleles and genotypes were tested using four genetic models, and the best mode of inheritance was chosen based on the least value. The rs2346061 of CNDP1 was significantly associated with diabetic nephropathy among the Indians only with OR = 1.94 and 95% CI = (1.76–3.20) and fitted best the multiplicative model, while D18S880 was associated among all the three major races with the Malays having the strongest association with OR = 2.46 and 95% CI = (1.48–4.10), Chinese with OR = 2.26 and 95% CI = (1.34–3.83), and Indians with OR = 1.77 and 95% CI = (1.18–2.65) in the genotypic multiplicative model. The best mode of inheritance for both MnSOD and NOS3 was the additive model. For MnSOD-rs4880, the Chinese had OR = 2.8 and 95% CI = (0.53–14.94), Indians had OR = 2.4 and 95% CI = (0.69–2.84), and Malays had OR = 2.16 and 95% CI = (0.54–8.65), while for NOS3-rs1799983, the Indians had the highest risk with OR = 3.16 and 95% CI = (0.52–17.56), followed by the Chinese with OR = 3.55 and 95% CI = (0.36–35.03) and the Malays with OR = 2.89 and 95% CI = (0.29–28.32). The four oxidative s

Age-related macular degeneration (AMD) is the most widely recognised cause of irreversible vision loss and previous studies have suggested that the advancement of wet AMD is influenced by both modifiable and non-modifiable elements. Single nucleotide polymorphism (SNPs) and copy number of variations (CNVs) have been associated with AMD in various populations, however the results are conflicting. Our aim is to determine the CNVs of Complement Factor H-Related genes among Malaysian subjects with wet AMD. 130 patients with wet AMD and 120 healthy controls were included in this research. DNA was extracted from all subjects and CNVs of CFH, CFHR1 and CFHR3 genes; determined using quantitative real-time PCR and were compared between the two groups. A consistent association was observed between CFH gene and wet AMD susceptibility (P < 0.05). The age-adjusted data suggests a possible increased risk of AMD disease (P < 0.05). No correlation was detected between CNVs and wet AMD for the remaining genes after we compared the frequencies of mean for that gene. An association was observed between CFH CNVs and wet AMD in the Malaysian population, however, strong evidence of a link with wet AMD was not found. Further investigative studies are needed using larger sample sizes to elucidate the role of CNVs in AMD pathogenesis.