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Biomedical subjects

C Nath

Publications and source records attributed to C Nath.

61 records · Page 4Linked to original sources
PubMed1980

Search for potential anticonvulsant agents. Synthesis of 2-phenyl/methyl-3-[o-, m- or p-(benzimidazol-2'-yl)phenyl]-6 or 6,8-substituted/unsubstituted quinazolin(3H)-4-ones.

Sixteen new quinazolones were synthesized by the condensation of substituted 4-oxo-3,1-benzoxazines and 2-(o-, m- or p-aminophenyl)benzimidazoles. All the sixteen compounds were tested for anticonvulsant activity in mice against pentylenetetrazole induced convulsions. Except for five compounds in which there was no protection, the others showed protection ranging from 20 to 80%.

Animals↗
PubMedDate not supplied

Interferon-inducer polyriboinosinic-polyribocytidylic acid: a potent anti-gastric ulcer agent and inhibitor of the gastric proton pump in rats.

1. Polyriboinosinic-polyribocytidylic acid (Poly I:Poly C), an interferon inducer was studied for its effect on gastric ulceration in rats. Polyriboinosinic-polyribocytidylic acid (1, 2 and 4 mg/kg, i.m.) showed a dose-dependent inhibition of gastric ulcers induced by aspirin, cold restraint stress and pylorus ligation (Shay's model). Protective dose (PD50) +/- SEM values of Poly I:Poly C on these models of ulcers were 1.9 +/- 0.2, 2.3 +/- 0.4 and 2.8 +/- 0.4 (mg/kg, i.m.) respectively. 2. Polyriboinosinic-polyribocytidylic acid (10-60 micrograms) produced dose-dependent inhibition of gastric proton pump (H+/K(+)-ATPase) activity in the gastric parietal microsomal fraction. The concentration of Poly I:Poly C causing a 50% inhibition (IC50) +/- SEM was found to be 17.6 +/- 1.2 micrograms. 3. Polyriboinosinic-polyribocytidylic acid caused a significant decrease in free and total acid and pepsin and an increase in mucin content in Shay (pylorus-ligated) rat. 4. Polyriboinosinic-polyribocytidylic acid did not exert a significant influence on isolated tissue preparations for anti-cholinergic (acetylcholine-induced contraction of guinea-pig ileum) and H2-anti-histaminic (histamine-induced contraction of rat uterus and guinea-pig auricle) activities. 5. Thus, the present study indicates that Poly I:Poly C may possess anti-gastric ulcer activity as a result of inhibition of the gastric proton pump.

Animals↗
PubMedDate not supplied

Infant nutrition and supplements.

Today, American consumers believe they need more and better nutrients than their diets provide. Consequently, consumers spend approximately three billion dollars each year on vitamin and nutrition products. Vitamin and/or mineral supplements are relatively inexpensive and available without a prescription; therefore, it is understandable that they are used by a substantial portion of the population. However, the last 50 years have witnessed a steadily increasing understanding of vitamins and trace mineral biochemistry and its role in human nutrition and intermediary metabolism. It has not been shown conclusively that normal breastfed infants of well nourished mothers need any specific vitamin and mineral supplements, with the exception of iron and fluoride. The use of vitamin D supplements remains controversial. Preterm infants may require supplements of vitamin E, iron, and folic acid because of their rapid rate of growth and less complete, intestinal absorption.

Breast Feeding↗
PubMedDate not supplied

Cardiac hypertrophy in experimental hypertension: interaction of the sodium ion, blood pressure and lisinopril.

The interaction of blood pressure, salt intake and the inhibition of angiotensin converting enzyme activity with cardiac hypertrophy were examined in the Dahl rat model. Eight-week-old salt sensitive and salt resistant rats were each separated into two colonies, one of which was maintained on a low salt and the other on a high salt diet for three weeks, at the end of which time both salt sensitive colonies were hypertensive. Each colony was then separated into two groups, one received no medication the other was given lisinopril until normotension was achieved. After 11 weeks of therapy, intra-arterial blood pressures and heart rates were recorded. The rats were sacrificed and heart weight to body weight ratios were determined. Both untreated salt sensitive groups displayed marked cardiac hypertrophy which correlated well with diastolic blood pressure irrespective of salt intake. Lisinopril therapy lowered blood pressures to normotensive levels in all groups except for salt sensitive rats ingesting a high salt diet where, despite a 10-fold increase in drug dose, normotension was not achieved. Significant cardiac regression accompanied lisinopril therapy in rats receiving low salt diets but high salt intake severely attenuated regression in both strains. There was no significant correlation between heart weight and blood pressure in the treated groups. The results suggest that cardiac regression appears to be mediated by other factors besides ventricular afterload pressure and that high salt intake adversely affects blood pressure and heart weight response to lisinopril therapy.

Angiotensin-Converting Enzyme Inhibitors↗