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Articles by P.M. Thani
Total Records ( 2 ) for P.M. Thani
  Srikumar Chakravarthi , Linda Tjoa Husin , P.M. Thani and Nadeem Irfan Bukhari
  Benign Prostatic Hyperplasia (BPH) is an enlargement of the prostate gland caused by an increase in the number of glandular units. Apoptosis is a programmed cell death necessary for the regulation of the size of organs in adult life. Disruption of apoptotic pathways has been suggested as an important regulatory mechanism in BPH. A high level of the BCL-2 protein suppresses apoptosis by preventing the activation of the enzymes that carry out the process. In this study, an attempt was made to observe the abnormal expression of BCL-2 protein in BPH tissues in paraffin sections and to demonstrate the disruption of apoptotic pathways in BPH. Prostatic tissue from 30 patients with BPH and no prior prostatic carcinoma were obtained by transurethral resection of prostate procedure. Apoptotic index was compared in the H and E sections. Expression of BCL-2 was analyzed by immunohistochemistry and evaluated. Apoptotic index in BPH tissues was found to be twice lower than that of normal tissues. Wilcoxon signed rank test was employed and the p-value proved that the results were highly significant (p<0.01). This data supported the research hypothesis that apoptotic index is decreased in benign prostatic hyperplasia. Out of 30 tissue samples, 20 (67%) shown positivity for BCL-2 expression. Kendall’s Tau-B test was applied and the result showed negative correlation between the intensity of BCL-2 expression and apoptosis, however not significantly. This proves, the theory that BCL-2 regulates individual cell death up to a certain extent.
  Srikumar Chakravarthi , Nagaraja Haleagrahara , Chong Fu Wen , Nagaraja Lee and P.M. Thani
  Cyclosporine-A (CsA) is an immunosuppressant prescribed in organ transplants to prevent rejection. It is a calcineurin inhibitor produced by the fungi Trichoderma polysporum and Cylindrocarpon lucidum, its adverse effect of renal dysfunction has limited its use in a clinical setting. Apigenin (4', 5',7'-Trihydroxyflavone), a herbal extract, with anti-inflammatory and anti-tumour properties has shown to reverse this adverse effect. This research was conducted to study the effects of apigenin on reversal of Cyclosporine-A induced damage and this was assessed by immunohistochemical estimation of expression of c-myc and estimation of apoptosis in histopathological sections. Rats were divided into groups and administered with CsA with Apigenin in different doses. The kidneys from the rats were harvested, weighed and observed for gross pathology changes. The renal tissue was processed and stained for haemotoxylin and eosin staining, to assess the apoptotic index and stained by immunohistochemistry, for the analysis of the apoptosis regulatory gene c-myc. The apoptotic index was then compared with the c-myc intensity to observe for any correlation. It was found that there was a high apoptotic index and c-myc intensity in the Cyclosporine-A group. Apigenin managed to reduce the values of both parameters. The apoptotic index correlated with the c-myc intensity, especially in the glomeruli. The study proved that Cyclosporine-A enhanced the expression of c-myc in the rat kidney, which signifies accelerated apoptosis. Therefore, c-myc and apoptotic index may be used to assess apigenin and its effect on Cyclosporine-A induced renal damage.
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