Water from 15 sampling stations in Tasik Chini (Chini Lake), Peninsular Malaysia were sampled for 12 months from September 2004 until August 2005 and analyzed for 11 metals including iron (Fe), aluminum (Al), manganese (Mn), barium (Ba), zinc (Zn), lead (Pb), copper (Cu), cadmium (Cd), nickel (Ni), chromium (Cr) and cobalt (Co). Results showed that the mean (min-max) metal concentrations (in micrograms per liter) in Tasik Chini waters for the 12 months sampling based on 15 sampling stations (in descending order) for Fe, Al, Mn, Ba, Zn, Pb, Cu and Cd were 794.84 (309.33-1609.07), 194.53 (62.37-665.93), 29.16 (16.68-79.85), 22.07 (15.64-29.71), 5.12 (2.224-6.553), 2.36 (1.165-4.240), 0.832 (0.362-1.443) and 0.421 (0.254-0.696) respectively. Concentration for three metals i.e. Ni, Cr and Co were too low and not detected by the graphite furnace Atomic Absorption Spectrophotometry (AAS). Comparison with various water quality standards showed that the mean metals concentration in surface water of Tasik Chini were low and within the range of natural background except for Fe and Al. In general, metal concentrations in Tasik Chini water varied temporally and spatially. The main factors influencing these metal concentrations in the water were the raining season and mining activities. Stations located at Tanjung Jerangking and Melai areas were the most effected due to those factors.
A study of the water quality changes of Chini Lake was conducted for 12 months, which began in May 2004 and ended in April 2005. Fifteen sampling stations were selected representing the open water body in the lake. A total of 14 water quality parameters were measured and Malaysian Department of Environment Water Quality Index (DOE-WQI) was calculated and classified according to the Interim National Water Quality Standard, Malaysia (INWQS). The physical and chemical variables were temperature, dissolved oxygen (DO), conductivity, pH, total dissolved solid (TDS), turbidity, chlorophyll-a, biochemical oxygen demand (BOD), chemical oxygen demand (COD), total suspended solid (TSS), ammonia-N, nitrate, phosphate and sulphate. Results show that base on Malaysian WQI, the water in Chini Lake is classified as class II, which is suitable for recreational activities and allows body contact. With respect to the Interim National Water Quality Standard (INWQS), temperature was within the normal range, conductivity, TSS, nitrate, sulphate and TDS are categorized under class I. Parameters for DO, pH, turbidity, BOD, COD and ammonia-N are categorized under class II. Comparison with eutrophic status indicates that chlorophyll-a concentration in the lake was in mesotrophic condition. In general water quality in Chini Lake varied temporally and spatially, and the most affected water quality parameters were TSS, turbidity, chlorophyll-a, sulphate, DO, ammonia-N, pH and conductivity.
MYB proteins are highly conserved DNA-binding domains (DBD) and mutations in MYB oncoproteins have been reported to cause aberrant and augmented cancer progression. Identification of MYB molecular biomarkers predictive of cancer progression can be used for improving cancer management. To address this, a biomarker discovery pipeline was employed in investigating deleterious non-synonymous single nucleotide polymorphisms (nsSNPs) in predicting damaging and potential alterations on the properties of proteins. The nsSNP of the MYB family; MYB, MYBL1, and MYBL2 was extracted from the NCBI database. Five in silico tools (PROVEAN, SIFT, PolyPhen-2, SNPs&GO and PhD-SNP) were utilized to investigate the outcomes of nsSNPs. A total of 45 nsSNPs were predicted as high-risk and damaging, and were subjected to PMut and I-Mutant 2.0 for protein stability analysis. This resulted in 32 nsSNPs with decreased stability with a DDG score lower than - 0.5, indicating damaging effect. G111S, N183S, G122S, and S178C located within the helix-turn-helix (HTH) domain were predicted to be conserved, further posttranslational modifications and 3-D protein analysis indicated these nsSNPs to shift DNA-binding specificity of the protein thus altering the protein function. Findings from this study would help in the field of pharmacogenomic and cancer therapy towards better intervention and management of cancer.
Dysregulation of fibroblast growth factors is linked to the pathogenesis of bladder cancer. The role of FGF1 and FGF3 is evident in bladder cancer; however, the role of FGF4 is vague. Despite being reported that FGF4 interacts with FGF1 and FGF3 in MAPK pathways, its pathogenesis and mechanism of action are yet to be elucidated. Therefore, this study aimed to elucidate pathogenic nsSNPs and their role in the prognosis of bladder cancer by employing in-silico analysis. The nsSNPs of FGF4 were retrieved from the NCBI database. Different in silico tools, PROVEAN, SIFT, PolyPhen-2, SNPs&GO, and PhD-SNP, were used for predicting the pathogenicity of the nsSNPs. Twenty-seven nsSNPs were identified as “damaging”, and further stability analysis using I-Mutant 2.0 and MUPro indicated 22 nsSNPs to cause decreased stability (DDG scores < −0.5). Conservation analysis predicted that Q97K, G106V, N164S, and N167S were highly conserved and exposed. Biophysical characterisation indicated these nsSNPs were not tolerated, and protein-protein interaction analysis showed their involvement in the GFR-MAPK signalling pathway. Furthermore, Kaplan Meier bioinformatics analyses indicated that the FGF4 gene deregulation affected the overall survival rate of patients with bladder cancer, leading to prognostic significance. Thus, based on these analyses, our study suggests that the reported nsSNPs of FGF4 may serve as potential targets for diagnoses and therapeutic interventions focusing on bladder cancer.