This study investigated the role of systemic inflammation in the development of atrial fibrillation (AF) after coronary artery bypass grafting (CABG). CABG was performed using cardiopulmonary bypass in 77 patients. Pre-operative AF was present in six patients (7.8%) and postoperative AF developed in 13 (18.3%) of the 71 patients with pre-operative sinus rhythm. Post-operative mediastinal drainage was significantly increased in patients with post-operative AF compared with those with sinus rhythm. Plasma E-selectin, P-selectin and vascular cell adhesion molecule levels were not significantly different between patients with pre- and post-operative sinus rhythm, those with pre-operative sinus rhythm and post-operative AF, and those with pre- and post-operative AF. There were significant differences between pre- and post-operative C-reactive protein, interleukin (IL)-6 and IL-10 levels within all three groups, but no differences in these parameters between the groups. Thus, in all groups there were significant alterations in mediators indicative of systemic inflammation following CABG, but comparisons between the groups revealed no differences predictive of AF.
Prostate-specific antigen (PSA) is a 33 kDa serine protease which is produced by many different tissues in the body and has been shown to be present in low concentrations in breast milk and in about 30% of breast cancers. The presence of PSA in breast cancers is associated with the presence of steroid-hormone receptors and may be a favourable prognostic indicator. In this study, PSA immunoreactivity was measured in breast cyst fluid obtained from women with palpable breast cysts which is the most common benign breast disease. PSA was found to be present in very low concentrations in breast cyst fluid. In an attempt to understand the possible role of PSA in the breast, the effect of PSA on growth of the hormone-dependent MCF-7 and hormone-independent MDA-MB-231 human breast cancer cell lines was studied. In addition, the effect of PSA on oestrone sulphatase activity and oestrogen 17-oxidoreductase activity in these cell lines was investigated. PSA, in low concentrations, was found to inhibit MCF-7 cell growth and to stimulate the conversion of oestradiol to the less potent oestrogen oestrone in this cell line. PSA had no effect on the MDA-MB-231 cell line. Our findings suggest that PSA may act as a negative growth regulator in hormone-dependent breast cancers.
Breast cancer remains one of the most common types of cancer. High levels of arginase and ornithine in different carcinomas may indicate their relation to cancer. Carnitine is a cofactor required for the transformation of free long-chain fatty acids into acetyl-carnitines. We have examined the protective effect of carnitine and the possibility that it disturbs arginase-nitric oxide (NO) interaction. Histopathological examination, arginase activity, ornithine and NO levels were determined in tumour tissues. Mitotic cells significantly decreased in the treatment group. Tissue arginase activity and ornithine levels decreased significantly with carnitine. NO levels were significantly higher in the treatment group. One of the possible mechanisms of carnitine's protective role in tumour progression might be its promotion of NO. This mechanism could decrease the production of tumour-promoting agents, polyamines, and increase the production of NO, thereby exerting a protective effect on cancer development.
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