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Biomedical subjects

M L Garg

Publications and source records attributed to M L Garg.

87 records · Page 5Linked to original sources
PubMed1976

Quality assurance in undergraduate medical education at the Medical College of Ohio.

This paper reports a four-year experience in teaching evaluation of care at a three-year medical school, the Medical College of Ohio at Toledo. Informal patient care evaluation evolved to more structured medical care evaluation in seminars and by chart audits. The introduction of professional standards review organizations prompted the teaching and evaluation of the quality and cost of primary care, especially as it applies to learning clinical tasks.

Attitude of Health Personnel↗
PubMed1975

Teaching students the relationship between quality and cost of medical care.

The usefulness of hospital charges as a means of teaching medical students the relationship between the quality of the cost of medical care provided by primary care physicians (internists and family physicians) is presented. The comparative role of these two types of primary care physicians as "generators of costs" is described. The cost of hospital care provided by primary care physicians is also compared with the cost of care provided by the cardiologist, a prototype of the highest quality of secondary and tertiary care for cardiovascular diseases. Data indicate that internists generated hospital costs that were consistently higher than family physicians. Moreover, a comparison of costs generated by internists, family physicians, and cardiologists in managing patients with cardiovascular diseases revealed that cardiologists generated lower costs than the other two types of specialists. It is believed that case studies such as this will provide evidence that will enable undergraduate medical students to reflect upon their own attitudes toward their developing role as "generators of cost".

Adolescent↗
PubMedDate not supplied

Alpha-linolenic acid and metabolism of cholesterol and long-chain fatty acids.

Animal studies have demonstrated that dietary 18:3n-3 reduces 20:4n-6 content in plasma and tissue lipids. At megadose levels of 18:3n-3, the reduction in phospholipid 20:4n-6 is brought about by a combination of inhibition of desaturase activities and redistribution of 20:4n-6 from phospholipids to neutral lipid pools. The shifting phenomenon is not apparent when the dietary level of 18:3n-3 is low. Dietary 18:3n-3 reduces cholesterol levels in blood and liver tissue; however, the mechanism by which this effect is mediated is not known. Further studies are warranted to investigate the role of dietary 18:3n-3 on cholesterol biosynthesis, storage, and mobilization into and from the tissues and on the secretion of cholesterol into bile. The effect of the ratio of dietary 18:2n-6 to SFA as a determinant of 20:4n-6 and lipid-lowering effects should be further explored in human subjects. It is important to elucidate whether dietary 18:3n-3 interacts with other nutrients to modulate the parameters implicated in the pathogenic processes. The optimum level of dietary 18:3n-3 required to obtain health beneficial effects needs to be determined. Specific effects of dietary 18:3n-3 on low- and high-density lipoprotein cholesterol levels also deserves further investigation before any recommendation to achieve health benefits can be made.

Animals↗
PubMedDate not supplied

Protective effects of zinc on oxidative stress enzymes in liver of protein deficient rats.

This study was designed to evaluate the protective effects of zinc on the liver activities of antioxidant enzymes in protein-deficient rats. Zinc sulfate at a dose level of 227 mg/l in drinking water was administrated to Sprague Dawley normal control as well as to protein-deficient rats for a total duration of eight weeks. The effects of zinc treatment and protein deficiency alone as well as combined were studied on rat liver antioxidant enzymes which included catalase, glutathione peroxidase (GPX), glutathione reductase (GR), superoxide dismutase (SOD), and glutathione S-transferase (GST). Protein deficiency in normal rats resulted in a significant increase in hepatic lipid peroxidation and in catalase, Gpx, GR and GST activity. A significant inhibition in the levels of SOD activity and reduced glutathione (GSH) was observed following protein deficiency in normal rats. Zn treatment to protein deficient animals lowered lipid peroxidation and catalase, Gpx and GST activities, and also resulted in a significant elevation in the levels of GSH and SOD activity. The concentration of zinc decreased significantly in protein deficient animals but returned to normal levels when zinc was administered.

Animals↗
PubMedDate not supplied

Ineffectiveness of nickel in augmenting the hepatotoxicity in protein deficient rats.

This study was designed to determine the toxic effects of nickel sulfate on the biochemical and elemental profile of liver in protein deficient rats. Nickel sulfate in the dose of 800mg/l in drinking water was administrated to Sprauge Dawley (S.D) normal control as well as protein deficient rats for a total duration of eight weeks. The effects of nickel treatment and protein deficiency when given separately and in combination were studied on rat liver marker enzymes like Alkaline phosphatase (ALP),Glutamate oxaloacetate transaminase (GOT), Glutamate pyruvate transaminase (GPT) and also on the status of essential elements in rat liver. Protein deficient, Ni treated as well as combined protein deficient and nickel treated rats showed significant reductions in the body weight and hepatic protein contents as compared to normal control rats. Hepatic alkaline phosphatase activity and alanine aminotransferase showed a significant elevation in rats subjected to protein deficiency, nickel treatment and combined protein deficiency and nickel treatment. As regards to hepatic levels of aspartate aminotransferase a significant elevation was observed in protein deficient and nickel treated protein deficient animals. Nickel administration to normal and protein deficient rats has resulted in a significant increase in concentrations of nickel, phosphorus and sulfur in liver tissue. The concentration of zinc and copper in liver tissue decreased significantly in protein deficient, nickel treated and nickel treated protein deficient animals. Tissue iron concentrations were found to be decreased in protein deficient animals, but the concentrations of iron got elevated significantly in nickel treated and nickel treated protein deficient animals. It has been observed that selenium got decreased significantly in protein deficient, nickel treated and nickel treated protein deficient animals when compared to normal animals. The elevation of selenium in nickel treated protein deficient animals was also significantly higher when compared to protein deficient animals.

Animals↗