Biomedical subjects
Publications and source records attributed to S Varma.
Various glomerular lesions are described in association with malignancy. We report a rare case of crescentic glomerulonephritis occurring in association with renal cell carcinoma. A granular deposition of immune complexes and complement strongly suggests a tumor associated immune complex glomerulonephritis.
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OBJECTIVE: Hypoglycemia occurring during management in patients of severe malaria is often overlooked, which can be associated with higher morbidity and mortality rates. METHOD: Capillary glucose was estimated in 32 patients of malaria before, at one hour and at six hours of quinine administration. Quinine was given in saline solution intravenously. RESULTS: Pretreatment capillary glucose was found to be lower (71-80 mg/dl) in 12.5% cases. After one hour of intravenous quinine administration, capillary glucose levels fell by 11.84% in all the cases. A further fall of 20.50% was observed in 75% of cases after six hour. Two patients died and both were suffering from cerebral malaria. Statistically, fall in capillary glucose was highly significant at one hour (t=9.4, p < 0.001) and at six hours. (t=3.87, p < 0.001) CONCLUSION: Statistically significant fall in capillary glucose levels has been observed in patients of malaria with quinine administration.
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AIMS: Moxonidine, a new imidazoline II receptor agonist was evaluated in patients with essential hypertension. METHODOLOGY: After an informed consent, 16 patients with essential hypertension were recruited. After a wash out period, the patients received increasing doses of Moxonidine (maximum dose 0.6 mg) for four weeks to control the blood pressure. RESULTS: The mean reduction in blood pressure (systolic/diastolic) was 17.6/14.5 mm Hg in supine position and 18.2/12.6 mm Hg in standing position. The significant side effect was observed only in one patient. CONCLUSIONS: Moxonidine thus appears to be safe and effective antihypertensive drug in patients with essential hypertension.
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We have recently shown that Receptor-Ck regulated genes, involved in cellular growth and death through a transcriptional factor (SREBP) which has affinity for sterol regulatory element (SRE) present in the promoter region of these genes. The present study revealed that blasts, derived from both ALL and AML patients, were unable to express SREBP gene product although they had the capacity to express Receptor-Ck gene product. These results which depict defective Receptor-Ck-dependent signalling are in conformity with our previous results which showed that lymphocytes from CML patients as well as other human leukemic cell lines are unable to express gene coding for Receptor-Ck leading again to a state of impaired Receptor-Ck-dependent signalling. On the basis of these results, we propose that deregulated Receptor-Ck-dependent signalling may have an important role in leukemogenesis.
Thyroid function tests (serum levels of thyroxine-T4, triiodothyronine-T3 and thyroid stimulating hormone-TSH) were performed in fifty-eight men (mean age: 31.7 +/- 10.6 years; mean duration of lead exposure: 156.9 +/- 122.7 months). These subjects were exposed to lead either as petrol pump workers or automobile mechanics. The mean whole blood lead (Pb-B) levels were 2.49 +/- 0.45 micromole/l (51.90 +/- 9.40 microg/dl) in the lead exposed workers and were approximately 5 times higher than in the control (n = 35) subjects. No significant alteration was seen in their mean T3 and T4 levels as compared with the controls. Interestingly, T3 was significantly lower with the longer (210 months) exposure time in comparison with the group having shorter (29 months) exposure duration. The mean TSH levels were significantly (p < 0.01) higher in workers exposed in comparison with the control group. This rise in TSH was independent of exposure time, but it was definitely associated with the Pb-B levels. The increase being more pronounced with mean Pb-B levels of 2.66 +/- 0.2 micromole/l (55.4 +/- 4.25 microg/dl) when compared with the group having mean levels of 1.51 +/- 0.30 micromole/l (31.5 +/- 6.20 microg/dl). The rise is TSH associated with Pb-B levels was only statistical valid, however, the levels fall within the normal laboratory range. We thus conclude that the Pb-B levels of > or = 2.4 micromole/l (50 microg/dl) could enhance the pituitary release of TSH without having any significant alterations in the circulating levels of T3 and T4.
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