Preparation and standardisation of platelet rich plasma and platelet concentrates in a developing blood bank.
Explore the source record for details and available documents.
Blood Banks↗
Biomedical subjects
N Taneja
Publications and source records attributed to N Taneja.
Indomethacin-induced apoptosis in esophageal adenocarcinoma cells involves upregulation of Bax and translocation of mitochondrial cytochrome C independent of COX-2 expression.
The prolonged use of nonsteroidal anti-inflammatory drugs (NSAIDs) has been shown to exert a chemopreventive effect in esophageal and other gastrointestinal tumors. The precise mechanism by which this occurs, however, is unknown. While the inhibition of COX-2 as a potential explanation for this chemopreventive effect has gained a great deal of support, there also exists evidence supporting the presence of cyclooxygenase-independent pathways through which NSAIDs may exert their effects. In this study, immunohistochemical analysis of 29 Barrett's epithelial samples and 60 esophageal adenocarcinomas demonstrated abundant expression of the COX-2 protein in Barrett's epithelium, but marked heterogeneity of expression in esophageal adenocarcinomas. The three esophageal adenocarcinoma cell lines, Flo-1, Bic-1, and Seg-1, also demonstrated varying expression patterns for COX-1 and COX-2. Indomethacin induced apoptosis in all three cell lines, however, in both a time- and dose-dependent manner. In Flo-1 cells, which expressed almost undetectable levels of COX-1 and COX-2, and in Seg-1, which expressed significant levels of COX-1 and COX-2, indomethacin caused upregulation of the pro-apoptotic protein Bax. The upregulation of Bax was accompanied by the translocation of mitochondrial cytochrome c to the cytoplasm, and activation of caspase 9. Pre-treatment of both cell lines with the specific caspase 9 inhibitor, z-LEHD-FMK, as well as the broad-spectrum caspase inhibitor, z-VAD-FMK, blocked the effect of indomethacin-induced apoptosis. These data demonstrate that induction of apoptosis by indomethacin in esophageal adenocarcinoma cells is associated with the upregulation of Bax expression and mitochondrial cytochrome c translocation, and does not correlate with the expression of COX-2. This may have important implications for identifying new therapeutic targets in this deadly disease.
Adenocarcinoma↗
Effect of phenytoin on semen.
Male patients receiving antiepileptic drugs (AEDs) have often complained of hyposexuality. Few studies have been done on semen analysis, which is relevant for assessment of potential and possible reproductive outcome in such cases. We evaluated the effect of epilepsy itself and/or phenytoin (PHT) on the male reproductive system. Fifty-five patients with epilepsy (42 with PHT and 13 untreated) and 28 healthy normal controls were studied by semen analysis. Serum samples from 21 of the 55 patients were also analyzed for testosterone, luteinizing hormone (LH), and follicle-stimulating hormone. Results showed lower volume of seminal fluid, spermatozoa concentration, and total sperm count in untreated and PHT-treated patients as compared with controls, although no difference was evident between the patient groups. Morphologically abnormal sperm were more increased in untreated patients than in PHT treated and control subjects. Hormonal analysis showed lower levels of testosterone in 9 patients. LH levels were increased in one third of the patients. Our results suggests an effect of seizures on the male reproductive system, and PHT may have a slight additive (if any) influence.
Adult↗