Monosodium methylarsonate (MSMA) is an organic arsenical pesticide widely used in agriculture. Humans are exposed to arsenic through drinking water and anthropogenic activities. Exposure to inorganic arsenic has been linked with multiple health problems. However, studies focusing on chronic organic arsenic exposure and its adverse effects on kidney were limited. The purpose of current study was to determine the effects of chronic organic arsenic exposure in rats kidney by light and electron microscopy. Materials and Method: Thirty-six male SpragueDawley rats were divided into six groups (n=6); three control and three treatment group respectively. All the control group was given distilled water via oral gavage. The treatment group was given oral gavage of MSMA at 42.10 mg/kg body weight (BW) which is equivalent 1/30 LD50 of MSMA. The control and treatment groups were sacrificed at two month, four month and six months interval. Both kidneys harvested for light microscopy and electron microscopy study. Results: Showed progressive changes. The changes initially focal and became diffused involving glomerular; such as glomerular hypercellularity, glomerular shrinkage and dilated Bowman's space. Meanwhile, in proximal tubules, showed diminished brush borders, detachment of nucleus and basement membrane thickening. Electron microscopy showed flattened cell bodies of podocytes, effacement and fusion of podocytes foot processes, thickening of glomerular basement membrane, and discontinuity of brush border. The control and two-months treated group appeared to be normal. Conclusion: Chronic organic arsenic (MSMA) exposure induced chronic kidney injury.
Myeloproliferative neoplasm (MPN) is a group of myeloid disorders which leads to erythrocytosis, thrombocytosis and leucocytosis. MPN with BCR-ABL positive is chronic myeloid leukaemia (CML) while BCR-ABL negative MPN includes polycythaemia Vera (PV), essential thrombocytemia (ET) and primary myelofibrosis (PMF). One of the major criteria for diagnosis of BCR-ABL negative MPN is the presence of JAK2-V617F mutation which is positive in 95% of PV and around 60% of ET and MF. Beside peripheral blood specimen, formalin-fixed paraffin-embedded (FFPE) marrow specimen can be used for detection of this mutation. Unfortunately, FFPE produces low quality DNA that put a challenge for successful amplification of DNA. We aimed to evaluate the utility of High Resolution Melting (HRM) analysis for detection of JAK2-V617F mutation in FFPE specimen from MPN cases. Materials andMethods:This study is a descriptive cross-sectional study. Forty FFPE marrow specimens were retrieved from the years 2014-2016. Bio-Rad Precision Melt Analysis software was used for analysis of HRM data. Allele-specific PCR was done for validation of results. Positive samples were subjected to Sanger sequencing. Results:JAK2-V617F mutation was positive in 13 out of 40 MPN cases. Level of agreement between HRM and AS-PCR was 97.5%. Conclusion:HRM is a rapid and powerful diagnostic assay which is suitable for detection of JAK2-V617F mutation in FFPE marrow specimen.
Although there is a growing insight into the causes and mechanisms of
kidney diseases, preventive and therapeutic measures are still few. The aim of this study
was therefore to determine the renoprotective effect of tualang honey against high
cholesterol diet induced acute kidney disease in an animal model. (Copied from article).
Liver perfusion has been the standard method to digest and isolate liver
cells including liver sinusoidal endothelial cells (LSEC). Poor cannulating skills through
portal vein results in a waste of animal resource. Familiarization of both liver perfusion
technique and adhering strictly to aseptic technique during cell handling ensure high
cell yield, minimum morphology disruption and cell contamination. We aimed to present
a method of liver perfusion procedure followed by the isolation of LSEC. (Copied from article).
The epigenetic changes of RELN that are involved in the development of dopaminergic neurons may fit the developmental theory of schizophrenia. However, evidence regarding the association of RELN DNA methylation with schizophrenia is far from sufficient, as studies have only been conducted on a few limited brain samples. As DNA methylation in the peripheral blood may mirror the changes taking place in the brain, the use of peripheral blood for a DNA methylation study in schizophrenia is feasible due to the scarcity of brain samples. Therefore, the aim of our study was to examine the relationship of DNA methylation levels of RELN promoters with schizophrenia using genomic DNA derived from the peripheral blood of patients with the disorder. The case control studies consisted of 110 schizophrenia participants and 122 healthy controls who had been recruited from the same district. After bisufhite conversion, the methylation levels of the DNA samples were calculated based on their differences of the Cq values assayed using the highly sensitive real-time MethyLight TaqMan® procedure. A significantly higher level of methylation of the RELN promoter was found in patients with schizophrenia compared to controls (p = 0.005) and also in males compared with females (p = 0.004). Subsequently, the RELN expression of the methylated group was 25 fold less than that of the non-methylated group. Based upon the assumption of parallel methylation changes in the brain and peripheral blood, we concluded that RELN DNA methylation might contribute to the pathogenesis of schizophrenia. However, the definite effects of methylation on RELN function during development and also in adult life still require further elaboration.