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Biomedical subjects

M K Bhatnagar

Publications and source records attributed to M K Bhatnagar.

At least 19 recordsLinked to original sources
PubMed1994

Hypoparathyroidism with extensive intracranial calcification: a case report.

We present a case of hypoparathyroidism, demonstrating extensive intracranial calcification, not only in basal ganglia, but also outside the extrapyramidal system. The patient presented with an unexplained epileptifors disorder, accompanied by extrapyramidal dysfunction in the form of choreoathetosis and hemiballismus. Hemiballismus is reported for the first time to our knowledge in association with hypoparathyroidism.

Adolescent↗
PubMed1994

A study of hyperinsulinaemia in Indian hypertensive subjects.

Fasting and 2 hours post-prandial serum insulin levels were estimated in 100 hypertensive subjects and 25 matched, healthy controls, by radio-immuno assay (RIA). Seventy four of the 100 hypertensives exhibited fasting hyperinsulinaemia. Post-prandial hyperinsulinaemia was present in 85 hypertensives. None of the healthy individuals demonstrated hyperinsulinaemia. Although, most hyperinsulinaemic patients exhibited an abnormal lipo-protein profile, there was no statistical correlation between absolute values of lipo-protein and insulin.

Chronic Disease↗
PubMed1994

Microalbuminuria in non insulin dependent diabetes and essential hypertension: a marker of severe disease.

Sixty five (65) hypertensive, 91 non-insulin dependent diabetes and 50 matched, healthy controls were examined for the presence of microalbuminuria, using the Micral strip test. Microalbuminuria was observed in 25 per cent of diabetics and 21.54 per cent of hypertensive subjects. None of the controls demonstrated microalbuminuria. Diabetics with microalbuminuria were poorly controlled and demonstrated significantly higher systolic pressure. In hypertensive subjects, microalbuminuria was seen more in patients with severe disease. In both diabetics and hypertensives, presence of microalbuminuria was significantly influenced by the disease duration.

Albuminuria↗
PubMed1992

Musculoskeletal injuries in the Afghan war.

Among the 1274 patients admitted to a Pakistan border hospital from 1985 to 1987, the distribution and outcome of musculoskeletal war injuries differed from those seen in other conflicts. Serious complications from injuries were found in approximately 50 per cent of patients, of which most were wound infections, chronic osteomyelitis, and restriction of joint motion. Guerrillas in the Afghan war had no access to acute medical treatment in the field. Many patients died before reaching the hospital, as reflected in the low proportion of paraxial injuries; very high complication rates were noted for all injuries. Although some complications, such as soft tissue infection and foreign body retention are not site specific, other complications such as contracture, non-union, loss of range of motion, and chronic osteomyelitis are highly related to the region injured. Early surgical management and evacuation of those with musculoskeletal war injuries can greatly improve the outcome from war trauma and reduce the subsequent disability. However, the increasing use of hand-held anti-aircraft missiles may prevent the rapid evacuation of the wounded in future conflicts, and may make the situation seen in Afghanistan more common.

Adolescent↗
PubMed1992

The effects of administering methylmercury in combination with ethanol in the rat.

Methylmercury (MeHg) is a potent neurotoxicant and nephrotoxicant in several animal species including humans. Although the in vivo toxicity of MeHg per se is well known, the interaction between MeHg and other pollutants and with nutritional factors is not well understood. Since ethanol (EtOH) is a widely consumed toxicant which has been shown to enhance the histopathologic effects of MeHg on renal tissues, a study was undertaken to examine the effects of the combined administration to rats of MeHg and EtOH on renal function and on mercury distribution in body tissues. Forty-eight rats were divided into 6 treatment groups of 8 rats each. Rats in groups 1, 2 and 3 were given feed ad libitum, a restricted liquid diet of 70 mL/d or distilled water orally, respectively. Rats in groups 4, 5 and 6 were given 1.5 mg MeHg/kg bw, 2.0 g EtOH/kg bw, or 1.5 mg MeHg + 2.0 g EtOH/kg bw, respectively, by oral gavage daily for 45 d. All rats except those in group 1 (ad libitum) were fed 70 mL of liquid diet/d for the entire study period. The ingestion of MeHg + EtOH in combination induced a greater increase in renal weight compared to treatment with either MeHg + EtOH alone. Only those rats given MeHg in combination with EtOH exhibited oliguria and elevated blood urea nitrogen levels. Despite this antidiuresis, urinary concentrating ability was impaired in those rats given both MeHg and EtOH. In contrast, the ingestion of MeHg by itself caused the most rapid loss of glucose in urine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Combined effects of methylmercury and ethanol on renal metallothionein and mercury residues in rats fed restricted amounts of a liquid diet.

Simultaneous treatment of rats with ethanol (EtOH) and methylmercury (MeHg) increases the frequency of lesions in the rat kidney. Therefore, it was of interest to us to study the effects of simultaneous treatment of rats with MeHg and EtOH on kidney metallothionein (MT) and mercury residues levels in kidneys of rats maintained on 70% of ad libitum diet. Treatment with MeHg alone induced kidney MT the most (twice) compared to its pair-fed control. Simultaneous treatment with MeHg and EtOH also induced kidney MT but to a lesser degree than treatment with MeHg alone (by about 30%). Ethanol by itself caused a slight increase in kidney MT although starvation resulting from pair-feeding with mercury-treated animals may have contributed to this observation. Simultaneous treatment with MeHg and 2 g/kg EtOH caused a significant reduction in inorganic mercury levels in the kidney (P less than 0.05) compared to treatment with MeHg alone or in combination with 1 g/kg EtOH. Corresponding with the decrease in kidney inorganic mercury levels was a significant increase in urine inorganic mercury levels in this group compared to treatment with 1 g/kg ethanol + MeHg.

Animals↗
PubMed1991

The renal histology and ultrastructure in rats given methylmercury and ethanol in combination.

The effects of combined administration of methylmercury (MeHg) and ethanol (EtOH) on renal morphology were examined in the rat. Forty-eight male Wistar rats were divided into 6 groups of 8 rats each as follows: group 1 was given feed ad libitum with no treatment; group 2 was restricted to 70 mL of feed daily with no treatment; groups 3-6 were restricted to 70 mL of feed daily and gavaged with distilled water, MeHg alone, EtOH alone, or MeHg in combination with EtOH, respectively, daily for 45 days. The ingestion of MeHg and EtOH in combination caused severe structural renal lesions which involved the glomerulus and all segments of the uriniferous tubule. Only with this combination treatment (group 6) was glomerular pathology observed; accumulations of platelets and inflammatory cells, fibrosis and thickening of the mesangium were observed in the glomerulus. There was also severe tubulointerstitial nephritis characterized by tubular atrophy, accumulation of inflammatory cells especially neutrophils, and increased collagen deposition in the same group. In contrast, the ingestion of either MeHg or EtOH produced less severe lesions mainly in the proximal tubular epithelium. This study suggests that EtOH enhanced the nephrotoxicity of MeHg.

Alcoholic Intoxication↗
PubMed1990

Effect of subchronic administration of ethanol and methylmercury in combination on the tissue distribution of mercury in rats.

The effect of oral administration for 14 weeks of 8 g.kg-1.day-1 ethanol and 0.5 mg.kg-1.day-1 methylmercuric chloride in combination to rats fed isocaloric diets has been investigated. Ethanol, in contrast to published studies, failed to influence the tissue distribution of methylmercury and its inorganic mercury metabolite in brain and kidney, and did not inhibit the increase in kidney weight induced by methylmercury. Ethanol and methylmercury, in combination and individually, reduced the renal but not the hepatic activity of gamma-glutamyltransferase, but did not affect the renal and biliary concentration of reduced glutathione. Further study is required to determine the circumstances under which ethanol can influence the tissue distribution of methylmercury and its inorganic mercury metabolite.

Animals↗
PubMed1989

Combined nephrotoxicity of methylmercury, lead, and cadmium in Pekin ducks: metallothionein, metal interactions, and histopathology.

This report describes the metallothionein (MT) levels and accumulation of mercury, lead, and cadmium, as well as their interaction with tissue zinc, copper, and iron, and the histopathological changes in kidneys of ducks exposed to methylmercury chloride (MeHgCl), lead acetate (PbAc), and cadmium chloride (CdCl2), singly or in combination for 13 wk. Forty-eight female Pekin ducks, divided into 8 groups of 6 birds each, were fed diets containing no added metals (control), 8 mg MeHgCl/kg feed, 80 mg PbAc/kg feed, 80 mg CdCl2/kg feed, 8 mg MeHgCl + 80 mg PbAc/kg feed, 8 mg MeHgCl + 80 mg CdCL2/kg feed, 80 mg PbAc + 80 mg CdCl2/kg feed, and 8 mg MeHgCl + 80 mg PbAc + 80 mg CdCL2/kg feed. Cadmium (Cd) when administered alone or in combination caused a 60-fold increase in kidney MT levels, while methylmercury (MeHg) or lead (Pb) administration caused a threefold increase in kidney MT levels. No significant changes in kidney MT levels were observed when metals were administered concurrently when compared with single-treatment groups. Residue analysis revealed accumulation of administered metals in kidney tissue. However, lead administration resulted in accumulation of small amounts of this element in kidney tissue. Simultaneous administration of MeHgCl and PbAc significantly increased the accumulation of lead in kidney when compared with PbAc-treated group. Cadmium when administered alone or in combination caused an increase in the levels of zinc and copper in kidney. Administration of MeHgCl or PbAc either alone or in combination caused increased iron levels in kidney, while cadmium administration either alone or in combination caused decreased iron levels. Administration of cadmium either alone or in combination caused degenerative changes in kidney proximal tubules. The severity of degenerative lesions increased when cadmium was simultaneously administered with other metals. These results indicate that combined administration of MeHg, Pb, and Cd has no significant effect on kidney MT levels or on essential elements in kidney tissue when compared with single metal groups. However, there appears to be an increase in the severity of histopathologic changes.

Animals↗