Introduction: Over the decades, organic arsenic has been thought to be less toxic than inorganic arsenic.
Monosodium methylarsonate (MSMA) is a potent organoarsenical herbicide that is still being used in most
Asian countries. Reported studies on the effects of organic arsenic are mainly to the gastrointestinal system,
however there are limited research on its impacts to the liver. Therefore, this study aimed to investigate the
effect of MSMA exposure on hepatocytes and liver sinusoidal endothelial cells (LSEC). Materials and Methods:
Fourteen Sprague Dawley rats (n=14) were divided equally into arsenic-exposed (n=7) and control (n=7)
groups. The rats in arsenic-exposed group were given MSMA at 63.20 mg/kg daily for 6 months through oral
gavage. While the rats in control group were given distilled water ad libitum. At the end of the duration,
they were euthanized and underwent liver perfusion for tissue preservation. Liver tissues were harvested and
processed for light microscopy, scanning and transmission electron microscopy. The findings were analysed
descriptively. Results: MSMA had caused necrotic and apoptotic changes to the liver. Normal organelles
morphology were loss in the hepatocytes while LSEC revealed defenestration. Conclusion: In this study,
chronic low dose organic arsenic exposure showed evidence of toxicity to hepatocytes. Interestingly, LSEC
demonstrated capillarization changes.
Over the decades, organic arsenic has been thought to be less toxic than inorganic arsenic. Monosodium methylarsonate (MSMA) is a potent organoarsenical herbicide that is still being used in most Asian countries. Reported studies on the effects of organic arsenic are mainly to the gastrointestinal system, however there are limited research on its impacts to the liver. Therefore, this study aimed to investigate the effect of MSMA exposure on hepatocytes and liver sinusoidal endothelial cells (LSEC). Materials and Methods: Fourteen Sprague Dawley rats (n=14) were divided equally into arsenic-exposed (n=7) and control (n=7) groups. The rats in arsenic-exposed group were given MSMA at 63.20 mg/kg daily for 6 months through oral gavage. While the rats in control group were given distilled water ad libitum. At the end of the duration, they were euthanized and underwent liver perfusion for tissue preservation. Liver tissues were harvested and processed for light microscopy, scanning and transmission electron microscopy. The findings were analysed descriptively. Results:MSMA had caused necrotic and apoptotic changes to the liver. Normal organelles morphology were loss in the hepatocytes while LSEC revealed defenestration. Conclusion:In this study, chronic low dose organic arsenic exposure showed evidence of toxicity to hepatocytes. Interestingly, LSEC demonstrated capillarization changes
In the management of chronic pain, stepwise oral analgesics of graded strength are
considered as first-line therapy. Minimally invasive interventional procedures remain an
option for its treatment when pharmacological therapy fails to control the pain. We
reported three classical cases of chronic trigeminal neuralgia that were managed with
two types of pain intervention approaches after failing conservative management. (Copied from article).
Synovial sarcoma (SS) is a rare cancer and accounts for 5-10% of adult soft tissue sarcomas. Making an accurate diagnosis is difficult due to the overlapping histological features of SS with other types of sarcomas and the non-specific immunohistochemistry profile findings. Molecular testing is thus considered necessary to confirm the diagnosis since more than 90% of SS cases carry the transcript of t(X;18)(p11.2;q11.2). The purpose of this study is to diagnose SS at molecular level by testing for t(X;18) fusion-transcript expression through One-step reverse transcriptase real-time Polymerase Chain Reaction (PCR).
Polymorphisms within the beta2-adrenergic receptor (ADRB2) gene have been repeatedly linked to hypertension. Among the ADRB2 polymorphisms detected, Arg16Gly and Gln27Glu codons are considered the two most important variations. The amino acid substitution at these codons may lead to abnormal regulation of ADRB2 activity. The aim of the present study was to assess the association between ADRB2 polymorphisms and hypertension. This case-control study consisted of 100 unrelated subjects (50 hypertensive and 50 matched normal controls). Arg16Gly and the Gln27Glu polymorphisms were analyzed by polymerase chain reaction-restriction fragment length polymorphism assay. There were no significant evidence of association in allelic and genotypes distribution of Arg16Gly and Glu27Gln with blood pressure and hypertension. These findings suggest that the variation within codon 16 and 27 of ADRB2 gene were unlikely to confer genetic susceptibility for hypertension in our population samples.
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.