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Biomedical subjects

P M Das

Publications and source records attributed to P M Das.

9 recordsLinked to original sources
PubMed2004

Reversion of molecularly engineered, partially attenuated, very virulent infectious bursal disease virus during infection of commercial chickens.

A molecularly cloned, tissue culture-adapted infectious bursal disease virus (BD-3tc) was generated from a very virulent strain by the reverse genetics approach following site-directed mutagenesis (Q253H and A284T in VP2). The pathogenicity of BD-3tc was tested in commercial chickens. The wild-type strain (BD-3wt) and the molecularly cloned parental strain (BD-3mc) were included for comparison. The subclinical course of the disease, with delayed and milder pathological lesions followed by quick follicular regeneration in the bursa of Fabricius in BD-3tc-inoculated birds, suggested that these amino acid substitutions made BD-3tc partially attenuated. However, severe bursa atrophy was observed at 14 days after inoculation. Reverse transcription-polymerase chain reaction coupled with restriction enzyme analysis revealed that both point mutations in BD-3tc had reverted 14 days after inoculation. Further investigations demonstrated that the codon for amino acid at position 284 had already reverted to the wild-type phenotype (T284A) 3 days after inoculation.

Animals↗
PubMed1999

FNAC of papillary and solid epithelial neoplasm of pancreas--a case report.

A case of solid papillary epithelial neoplasm (PSEN) of pancreas in a young woman is reported in which the nature of tumour was recognised pre-operatively by ultrasound guided Fine needle aspiration. The pre-operative cytologic diagnosis enabled prompt and appropriate surgical treatment. FNAC revealed large cell clumps in the aspirate showing branching papillary appearance in which multiple layers of tumour cells surrounded central vascular stalks. The above was confirmed on histopathological examination of the excised tumour tissue.

Adolescent↗
PubMed1989

Experimental selenium toxicity in guinea pigs: biochemical studies.

Biochemical studies were conducted in experimentally induced selenium toxicity in recently weaned guinea pigs. A significant drop in blood glucose level, in comparison to controls, was observed in animals fed selenium-enriched barley (organic form) as well as those fed ordinary barley mixed with sodium selenite (inorganic form). Estimation of total serum proteins also revealed a significant drop in both these groups. SGOT (EC 2.6.1.1) activity was comparatively lower but no significant alteration was noticed in SGPT (EC 2.6.1.2). The erythrocytic glutathione peroxidase activity was significantly increased in inorganic selenosis followed by that in organic one, in comparison to controls. All these alterations were of mild degree in guinea pigs which were given sodium arsenite (10 ppm) along with sodium selenite (30 ppm) in the feed.

Animals↗
PubMed1989

Experimental selenium toxicity in guinea pigs: haematological studies.

Haematological studies were conducted in recently weaned guinea pigs fed selenium-enriched barley (organic selenium) and barley mixed with sodium selenite (inorganic selenium). An attempt was made to study the effect of sodium arsenite supplementation in sodium selenite toxicity. A significant (p less than 0.01) decrease was noticed in the mean values of haemoglobin, haematocrit, mean corpuscular haemoglobin and mean corpuscular volume thereby indicating a microcytic hypochromic anaemia. The anaemia was comparatively more marked in guinea pigs fed selenium-enriched barley than in those kept on barley mixed with sodium selenite. There was a significant decrease in total leucocyte count which was the result of lymphocytopenia in organic toxicity and a decrease in both neutrophils and lymphocytes in inorganic toxicity. Dietary supplementation with sodium arsenite resulted in less reduction in the mean values of different erythrocytic indices thereby indicating that addition of sodium arsenite has some protective effect against toxicity with sodium selenite.

Anemia, Hypochromic↗
PubMed1981

Hypertension in childhood.

Hypertension is seen in 1-2% of children. It is multifactorial in origin. An analysis of 245 children with hypertension seen in 3 years in the Southern Railway Hospital, Madras is presented. In this series, all cases are secondary to some underlying causes. The so called "Benign Essential Hypertension" is not so uncommon in children but the authors have not had a case til now. In more than 80% of the cases, it is due to acute glomerulonephritis where hypertension is temporary. 8% of all the cases can be cured by surgery (If acute glomerulonephritis is excluded, this forms 50%). In another 8%, hypertension is permanent. Routine measurement of blood pressure in all children during physical examination is essential to detect the cases early. Extensive investigations are necessary to diagnose the cause in some cases. Three typical case histories are presented. Hypertensive crisis is an emergency and should be managed by intensive medical care. Today, even in India, various sophisticated investigations can be done for the detection of the cause, and surgical treatment including cardiac surgery can be done, aggressive medical treatment can be given with the availability of all anti-hypertensive drugs, and so the paediatricians and paediatric surgeons must diagnose the cases early and institute appropriate treatment.

Abdominal Neoplasms↗
PubMed1978

Massive proteinuria in light chain disease.

A 33-year-old man with overall renal function in the lower normal range had daily excretion in the urine of between 31 and 70 gm of protein composed entirely of free monoclonal K light chains. K light chains were also present in the serum. Serum protein electrophoresis and findings on bone marrow and lymph node biopsy were diagnostic of light chain disease. Amyloid was absent from renal tissue. General clinical improvement and almost total disappearance of protein from the urine followed treatment with phenylalanine mustard.

Adult↗