Infective endocarditis--an Indian perspective.
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Biomedical subjects
Publications and source records attributed to S Ramakrishnan.
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In a patient with a debulked müllerian adenocarcinoma involving the ovary, an elevated serum concentration of macrophage-colony stimulating factor (M-CSF) (5.3 ng/ml) was lowered into the range of the age- and gender-matched controls by a 24-hour infusion of 135 mg/m2 of taxol, as was a Ca125 of 1480 U/ml by three such taxol courses given at 3-week intervals (to 14 U/ml). A downward trend of M-CSF in serum with an about-14-hour ultradian modulation during the first chemotherapy course resembles that of the concomitantly assessed Ca125. A decreasing trend modulated by an about-half-weekly component is found in M-CSF of fractionated urines collected at spontaneous voidings around the clock for 5 days. M-CSF may serve as a chronobiologic marker for optimizing, on an individualized basis, 1) the infradian scheduling of chemotherapy courses and 2) the ultradian-circadian within-course time patterns. Timing based on markers of the anticancer effect aims at teh as-yet unattained transfer from rodent to human of cancer cures that were not previously feasible without chronobiologic considerations. This goal can be pursued with M-CSF as well as Ca125 and UGP as possibly complementary chronobiologic markers in a chronotherapy trial with taxol in humans.
The role of vagus and hydrocortisone in the regulation of lung surfactant was studied in adult albino rats. Dynamic surface tension and phospholipid content were measured in the lung wash for estimating surfactant activity. The results indicate that vagotomy significantly decreases the surfactant activity whereas hydrocortisone does not alter it. But when hydrocortisone was administered prior to vagotomy it could prevent the decrease in surfactant activity. Thus it is concluded the regulation of lung surfactant in the adult lung is mainly by vagus nerve and hydrocortisone as such has no role but in the absence of vagal regulation hydrocortisone could maintain normal lung surfactant activity.
Systematic study of producing graded lesions of myocardium with the use of Isoproterenol (IPT) reveals that mild to severe degree of infarction can be induced by administering the compound for one to four consecutive days in the dose of 85 mg/kg body weight in rats. These findings differ slightly from those of Rona et al. where they have not attempted to produce the lesions in a graded fashion. The experimental period can be reduced to two days by using high dose (170 mg/kg), but such procedure increases significantly the mortality in these animals and lesions are not produced in graded fashion.
The hemodynamic effects of intravenous administration of acetaldehyde were determined in anesthetized control (group I), propranolol pretreated (group II) and phentolamine pretreated (group III) guinea pigs. Acetaldehyde produced an immediate and significant increase in mean arterial pressure followed by its progressive decrease resulting in hypotension. Heart rate increased significantly. In propranolol treated animals, acetaldehyde-induced tachycardia was not produced whereas in phentolamine treated animals, the initial pressor response was converted into a depressor one. Hence the increase in mean arterial pressure and heart rate produced by acetaldehyde are likely to be due to catecholamine release from adrenergic nerve endings.
Telomerase, a ribonucleoprotein complex, adds hexameric repeats of 5' T T A G G G 3' to the ends of chromosomes called telomeres. Telomerase activity is present in germ cells but not in most somatic cells. An overwhelming majority of cancer cells show elevated levels of telomerase activity. Once thought to be cancer-cell specific, it is becoming apparent that many proliferating normal cells express telomerase activity. In this study, we demonstrate that normal human endothelial cells express telomerase activity: the activity is growth related. In quiescent, confluent cultures, the telomerase activity is repressed. Furthermore, the activity is lost upon subculturing of the endothelial cells in vitro. Finally, G2/M arrest induced by nocodazole treatment of endothelial cells abolished telomerase activity. Primary cultures of endothelial cells offer a powerful model to study the role, if any, of telomerase in normal cells.
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