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Biomedical subjects

R Ramanathan

Publications and source records attributed to R Ramanathan.

98 records · Page 6Linked to original sources

Radioprotection of lipogenesis from glucose (U-14C) and activities of pyridine nucleotide dehydrogenases in liver of gamma-irradiated female rats by cystamine.

Whole-body gamma-irradiation (1200 R) of female rats significantly increased liver glycogen and incorporation of glucose (U-14C) into liver fatty acids. Administration of cystamine before irradiation protected the enhanced lipogenesis from glucose (U-14C), but afforded only a partial protection of liver glycogen levels. Irradiation significantly decreased the activities of liver pyruvate kinase and isocitrate dehydrogenase, and this decrease was not prevented by the administration of cystamine before irradiation. A significant increase in the activity of liver malate dehydrogenase (dehydrogenating) was noted in irradiated rats, which was not prevented by the administration of cystamine before irradiation. Irradiation did not affect the activities of combined hexose monophosphate pathway dehydrogenases and of malate dehydrogenase (decarboxylating).

Animals↗

Radioprotection of whole-body gamma irradiation induced alterations in lipid metabolism of liver and plasma by AET (S-2, aminoethyl isothiuronium Br. H. Br.) and serotonin in rats.

Radioprotective effect of AET, serotonin and their mixture has been studied on liver and plasma lipid metabolism 24 hrs and 48 hrs after irradiation in fasted male rats. AET and serotonin both gave significant radioprotection to certain liver and plasma lipid components, but the mixture of the two afforded a better protection. The non-radioprotection of plasma NEFA, phospholipids and phosphatidyl choline levels by serotonin observed in irradiated rats was because serotonin itself raised the levels of these lipids in control rats. Serotonin alone or in mixture effectively protected the radiation-induced increased incorporation of NaH2(32)PO4 into liver phospholipids. Mixture of AET and serotonin failed to protect the increased incorporation of aceae-1-14-C into liver total fatty acids and cholesterol, but it prevented this increased incorporation into liver triglycerides and phospholipids.

Acetates↗

Low serum cortisol in term newborns with refractory hypotension.

OBJECTIVES: The aim of this study is to measure baseline serum cortisol levels and clinical response to glucocorticoid therapy in a group of term infants with refractory hypotension. STUDY DESIGN: Seven term newborns with refractory hypotension were included. Serum cortisol levels were drawn before initiation of glucocorticoid therapy and measured by either fluorescence polarization immunoassay or radioimmunoassay. Baseline blood pressures, heart rate, and inotropes doses were recorded at baseline, then 4, 8, 12, 24, 48, 72, and 96 hours after glucocorticoid therapy. Urine output and volume expanders the infants received were recorded 24 hours before and after glucocorticoid therapy. Dexamethasone was used at a starting dose of 0.2 mg/kg per day divided every 12 hours. The statistical analysis was done using analysis of variance with repeated measures and paired t-test. RESULTS: Serum cortisol levels of the infants ranged from 2.0 to 15.4 micrograms/dl. After initiation of glucocorticoid therapy, there was significant improvement of blood pressure. Vasopressors were rapidly weaned and discontinued within 72 hours. In three of seven infants, no volume expanders were required after initiation of steroids, and none needed volume expanders after 2 days. Urine output increased significantly within 24 hours. All infants survived. CONCLUSIONS: Glucocorticoids improved pressure and stabilized clinical conditions of a group of term newborns with refractory hypotension. Serum cortisol levels of these infants were relatively low. We speculate that a subset of critically ill term infants has relative adrenal insufficiency and glucocorticoid therapy may be essential.

Blood Pressure↗

Diagnostic value of cytology of voided urine.

Cytologic examination of the sediment of voided urine is the only noninvasive method of detection, diagnosis and follow-up of tumors of the bladder and other anatomic components of the lower urinary tract. In order to assess the value of cytology of voided urine, we analyzed the diagnostic yield in 203 episodes, each composed of three sediments of voided urine obtained on consecutive days. For each one of these episodes, histologic material was available and was reviewed. Of special interest were 181 instances of primary or recurrent bladder tumors; in 37 of these patients, random biopsies of the bladder were also available for review. The concept of intraurothelial neoplasia (IUN), graded I, II or III, was introduced to describe degrees of atypia in flat urothelium, with IUN grade III corresponding to nonpapillary carcinoma in situ. The results documented that cytology of voided urine is highly reliable in the diagnosis of high-grade tumors, with a sensitivity of 94.2%. In primary flat carcinoma in situ (IUN III), the sensitivity was 100%. The method failed in the recognition of grade I papillary tumors and in about one-third of grade II tumors. There were no false-positive results in this study. In the 151 positive cases, the cytologic diagnosis was established on the first specimen in 79%, on the second specimen in an additional 14% and on the third specimen in 7% of cases. These results justify the use of three consecutive daily urine specimens for optimal diagnostic results. There is a remarkable similarity between the presence of cancer cells in voided urine and the DNA ploidy of bladder tumors, as established by Tribukait. The observations reported herein suggest that positive urine cytologies may correspond to aneuploid tumors and hence be not only of diagnostic but also of prognostic value. A direct proof of this hypothesis is under investigation; the results of this study justify the need for a field trial of an automated image analysis diagnostic system that was developed in this department.

Carcinoma↗

Severe retinopathy of prematurity in extremely low birth weight infants after short-term dexamethasone therapy.

With advances in neonatal intensive care survival of extremely low birth weight (< 1 kg) infants has increased significantly over the past decade. Dexamethasone is used increasingly for the prevention and treatment of chronic lung disease in these infants. The impact of dexamethasone therapy on the incidence or severity of retinopathy of prematurity (ROP) remains controversial. We conducted a retrospective study to evaluate the association between short-term dexamethasone treatment and severe ROP in extremely low birth weight infants. From October 1989 to December 1992, 309 very low birth weight infants were admitted to the neonatal intensive care unit. A total of 266 infants (86%) survived until hospital discharge. Of these, 90 weighed less than 1 kg. Thirty-eight of 90 infants received short-term dexamethasone therapy for chronic lung disease and the remaining 52 infants did not. Infants treated with dexamethasone and those not treated with dexamethasone were comparable in birth weight (820 vs 828 gm), gestational age (26.5 vs 26.9 weeks), inborn (11 vs 14), and occurrence of sepsis (13/38 vs 21/52). Infants treated with dexamethasone required longer periods of mechanical ventilation (44 +/- 23 vs 26 +/- 15 days, p < 0.001), had longer duration of supplemental oxygen (57 +/- 28 vs 29 +/- 23 days, p < 0.001), had higher incidence of patent ductus arteriosus (28/38 vs 18/52, p < 0.0003), and required surfactant therapy more often for respiratory distress syndrome (17/38 vs 11/52, p < 0.01), when compared with infants who did not receive dexamethasone. Severe ROP developed in 16 infants (stage III or higher); 12 of these were in the dexamethasone-treated group (p < 0.003). Thirteen infants required cryotherapy; nine were from the dexamethasone-treated group (p < 0.13). This study demonstrates an apparent association between the incidence of severe ROP and dexamethasone therapy. Prospective, randomized, controlled studies are needed to correct for differences in severity of cardiorespiratory illness to establish whether a causal role exists for steroid therapy in ROP. Until such studies are available, careful consideration must be given to indications, dosage, time of initiation, and duration of treatment with dexamethasone in extremely low birth weight infants.

Case-Control Studies↗