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Biomedical subjects

K Ramachandran

Publications and source records attributed to K Ramachandran.

At least 109 records · Page 6Linked to original sources
PubMed1967

Effect of pyridoxine on vitamin B6 concentrations and glutamic-oxaloacetic transaminase activity in whole blood of tuberculous patients receiving high-dosage isoniazid.

An earlier report from the Tuberculosis Chemotherapy Centre, Madras, showed that, in tuberculous patients receiving high-dosage isoniazid (12.5-15.6 mg/kg body-weight), the concomitant administration of 6 mg of pyridoxine prevented peripheral neuropathy. In that study, biochemical determinations of B(6) concentrations and GOT activity in whole blood had been routinely undertaken on all patients on admission to treatment, and at 6, 12, 24 and 52 weeks thereafter; in addition, extra determinations were undertaken for patients who developed peripheral neuropathy. The present paper reports the findings of these investigations, which are: (a) peripheral neuropathy developed predominantly among slow inactivators of isoniazid, and was associated with a substantial reduction in GOT activity but no apparent change in B(6) concentration; (b) the reduction in GOT activity appeared to be due to deficiency of both the coenzyme (pyridoxal phosphate) and the apoenzyme; (c) the concomitant administration of pyridoxine (6 mg or 48 mg) with high-dosage isoniazid to 3 patients with peripheral neuropathy, 1 of whom had convulsions also, resulted in increased B(6) concentrations and GOT activity, and no further convulsions; and (d) the concomitant administration of pyridoxine 6 mg daily, as a prophylactic, resulted in a significant increase in B(6) concentrations and GOT activity and prevention of the neuropathy.These findings establish the existence of a definite association between the occurrence of isoniazid-induced toxicity and diminished pyridoxine function.

Aspartate Aminotransferases↗
PubMedDate not supplied

Supplementary iron dose in pregnancy anemia prophylaxis.

This study was conducted to determine the optimum dose of supplemental iron for prophylaxis against pregnancy anemia. One hundred and ten pregnant women were randomly allocated to three groups: Group A receiving equivalent of 60 mg, group B 120 mg and Group C 240 mg, elemental iron as ferrous sulphate daily; the content of folic acid was constant in all the three groups (0.5 mg). These women had at least consumed 90 tablets in 100 +/- 10 days. Blood was drawn at the beginning and at the end of the treatment. Fifty percent were anemic (less than 11 g/100 ml). The hemoglobin levels rose similarly in all groups and the differences were statistically not significant. Fifty-six percent had depleted iron stores (serum ferritin value less than 12 micrograms/l) at the beginning of the study. Following therapy a statistically significant increase in iron stores was observed in group B and C as compared to group A. The difference between group B and C was not significant. The side effects increased with increasing doses of iron; 32.4%, 40.3% and 72% in group A, B and C respectively. Based on these findings, the authors advocate that optimum dose of iron should be 120 mg instead of 60 mg as is currently being used in the National Nutritional Anemia Prophylaxis Programme.

Anemia, Hypochromic↗
PubMedDate not supplied

A potential donor gene for the bm1 gene conversion event in the C57BL mouse.

The mammalian major histocompatibility complex (MHC; H-2 complex in mouse) is a large multigene complex which encodes cell-surface antigens involved in the cellular immune response to foreign antigens. Class I polypeptides expressed at the H-2K and H-2D loci of numerous mouse strains exhibit an unusually high degree of genetic polymorphism, which is assumed to be related to their function as primary recognition elements in the immune response. We suggested that this H-2 polymorphism may arise by gene conversion-like events between non-allelic class I genes. This is supported by our recent comparison of the DNA sequences of the normal H-2Kb gene sequence, from the C57BL/10 mouse, and a mutant form of this gene called H-2Kbm1: the mutant allele differs from the H-2Kb gene in seven bases out of a region of 13 bases in exon 3 of the class I gene (which encodes alpha 2 (C1) the second highly polymorphic protein domain), suggesting that this region of new sequence had been introduced into the H-2Kb sequence following unequal pairing of two class I genes in the genome of the C57BL mouse. Schulze et al. have obtained similar results. Here we report work identifying a potential donor gene in our library of 26 class I genes cloned from the C57BL/10 mouse.

Animals↗
PubMedDate not supplied

Avascular necrosis of the femoral head in neuroblastoma: a case report.

Avascular necrosis of bone is a well-described complication of cancer chemotherapy containing corticosteroids, and has been observed in lymphomas and acute lymphoblastic leukemia. Avascular necrosis occurring in association with neuroblastoma has never been reported before. This study reports on a 7-year-old boy with stage IV neuroblastoma developing avascular necrosis of the femoral head of both hips during treatment with combination chemotherapy using cyclophosphamide, cisplatin, etoposide, and doxorubicin. He was given conservative treatment in view of the progressive disease.

Antineoplastic Combined Chemotherapy Protocols↗