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Biomedical subjects

D Mukherjee

Publications and source records attributed to D Mukherjee.

At least 181 records · Page 10Linked to original sources
PubMed1979

Steroids and related products. XLVI. The regiospecific alpha-hydroxymethylation of saturated carbonyl compounds via preformed enolate ions. An improved synthesis of 17-hdyroxymethyl 20-keto steroids.

As demonstrated for pregnenolone, saturated ketones are conveniently alpha-hydroxymethylated by their transformation into a lithium enolate and by the reaction of the latter with formaldehydr. The 17-hydroxymethylpregnenolone prepared by this method in very good yield was readily converted to 17-hydroxymethylprogesterone; either by selective acetylation in position 17(1) and subsequent Jones oxidation, followed by hydrolysis, or by conversion to the 4,5-dibromo 3-ketone - by bis(tri-n-butyltin)oxide-bromine oxidation or by dibromination and oxidation with N-bromoacetamde - and debromination with zinc and acetic acid.

Chemical Phenomena↗
PubMed1977

Keto acids and free amino acids during leaf growth in Bauhinia purpurea L.

The biosynthesis of keto acids and free amino acids was studied during the growth of Bauhinia purpurea leaves. Alpha-KGA, OAA, pyruvic acid and PEP are the important keto acids observed at various stages. The first 2 metabolites show a progressive increase and PEP leads to OAA pathway is very active during the process of growth.

Amino Acids↗
PubMed1977

Steroids and related products. XLIII. The synthesis of 17-hydroxymethylprogesterone.

The synthesis of the first 17-hydroxymethyl analogue of a steroid hormone of the progesterone-corticoid group, 17-hydroxymethylprogesterone, is described. The starting material for its preparation was 3alpha,12alpha-diacetoxy-5beta-pregnan-20-one and the 17-hydroxymethyl structure was developed by functionalization of the 17-methyl group of a 17alpha-methyl etio ester by a Barton reaction. Neither 17-hydroxymethylprogesterone nor its acetate shows appreciable progestational activity in the Clauberg-McPhail assay.

Methods↗
PubMed1976

Nitroprusside therapy. Treatment of hypertensive patients with recurrent resting chest pain, ST-segment elevation, and ventricular arrhythmias.

Five hypertensive patients with acute myocardial infarction and persistent postinfarction hypertension who experienced severe and recurrent resting chest pain, ST elevations, and severe ventricular arrhythmias refractory to conventional treatment with bed rest, sedation, oxygen inhalation, nitrates, and antiarrhythmic agents received sodium nitroprusside by continuous intravenous infusion, titrated to reduce systolic blood pressure to 100 to 110 mm Hg. Treatment resulted in noticeable improvement in symptoms, reduction in ST elevations, and abolition of ventricular arrhythmias in all five patients. In four patients, cessation of nitroprusside infusion after 48 hours resulted in prompt recurrence of hypertension, chest pain, ST-segment elevations, and ventricular arrhythmias. These were all rapidly reversed following reinstitution of the nitroprusside therapy for seven to eight days, strongly suggesting a cause-and-effect relationship. Nitroprusside infusion in these patients suggests a potentially important use for such therapy in this clinical setting.

Acute Disease↗
PubMed1976

Steroids and related products. XLII. (1) The synthesis of 11-oxa steroids. IV. (2) The synthesis of 17,21-dihydroxy-11-oxa-4-pregene-3,20-dione, an 11-oxa analogue of the 17-hydroxylated glucocorticoids.

The synthesis, from 11-oxa-5alpha-pregnane-3,20-dione, available from hecogenin, of 17,21-dihydroxy-11-oxa-4-pregnene-3,20-dione, the first 11-oxa analogue of corticoid hormones, is described. The acetate of its 1-dehydro derivative, 17-hydroxy-21-acetoxy-1,4-pregnadiene-3,20-dione, analogous in structure to the acetates of prednisone and prednisolone, is an intermediate in the synthesis.

Magnetic Resonance Spectroscopy↗
PubMed1968

The influence of dietary protein on ascorbic acid metabolism in rats.

1. d-Glucuronolactone reductase, l-gulonolactone oxidase, uronolactonase, dehydroascorbatase, l-gulonate dehydrogenase and l-gulonate decarboxylase have been measured in the tissues of rats fed on diets containing variable amounts of protein. Rats fed on a protein-free or a 2% casein diet for 15 days showed a marked decline in the activities of d-glucuronolactone reductase, l-gulonolactone oxidase, uronolactonase and dehydroascorbatase in the liver, and no change in l-gulonate dehydrogenase and l-gulonate decarboxylase activities in the kidney when compared with rats fed on diets containing 9%, 18% or 25% casein. Giving diets containing 60% or 88% casein to rats did not appreciably alter the activities of uronolactonase, dehydroascorbatase, l-gulonate dehydrogenase and l-gulonate decarboxylase, but inhibited considerably the activities of d-glucuronolactone reductase and l-gulonolactone oxidase in the liver, resulting in decreased synthesis of ascorbic acid. 2. Rats fed on a 25% casein diet showed maximal weight gain, higher tissue reserve of ascorbic acid and higher urinary excretion of both ascorbic acid and glucuronic acid when compared with rats fed on diets containing lower or higher amounts of protein.

Alcohol Oxidoreductases↗
PubMed1968

The effect of molybdenum on ascorbic acid metabolism in rats.

1. The effect of dietary molybdenum on the growth rate and also on ascorbic acid metabolism in rats was studied. An excess of dietary molybdenum resulted in growth retardation and loss of weight. Tolerance to molybdenum was affected by the nature of the molybdenum salt administered. 2. Molybdenum ingestion altered certain aspects of ascorbic acid metabolism in rats. The conversion of d-glucuronolactone into l-ascorbic acid in vitro and the oxidative breakdown of l-ascorbic acid by liver enzymes decreased with high molybdenum intakes. The activity of liver uronolactonase was slightly inhibited. The activities of l-gulonate dehydrogenase and l-gulonate decarboxylase were not affected appreciably. 3. Molybdenum supplementation of the control diet resulted in an increase in ascorbic acid content of spleen and adrenal gland, and in a marked decrease in the urinary excretion of ascorbic acid and glucuronic acid. The implications of these findings are discussed.

Adrenal Glands↗
PubMedDate not supplied

Risk of cardiovascular events associated with selective COX-2 inhibitors.

Atherosclerosis is a process with inflammatory features and selective cyclooxygenase 2 (COX-2) inhibitors may potentially have antiatherogenic effects by virtue of inhibiting inflammation. However, by decreasing vasodilatory and antiaggregatory prostacyclin production, COX-2 antagonists may lead to increased prothrombotic activity. To define the cardiovascular effects of COX-2 inhibitors when used for arthritis and musculoskeletal pain in patients without coronary artery disease, we performed a MEDLINE search to identify all English-language articles on use of COX-2 inhibitors published between 1998 and February 2001. We also reviewed relevant submissions to the US Food and Drug Administration by pharmaceutical companies. Our search yielded 2 major randomized trials, the Vioxx Gastrointestinal Outcomes Research Study (VIGOR; 8076 patients) and the Celecoxib Long-term Arthritis Safety Study (CLASS; 8059 patients), as well as 2 smaller trials with approximately 1000 patients each. The results from VIGOR showed that the relative risk of developing a confirmed adjudicated thrombotic cardiovascular event (myocardial infarction, unstable angina, cardiac thrombus, resuscitated cardiac arrest, sudden or unexplained death, ischemic stroke, and transient ischemic attacks) with rofecoxib treatment compared with naproxen was 2.38 (95% confidence interval, 1.39-4.00; P =.002). There was no significant difference in cardiovascular event (myocardial infarction, stroke, and death) rates between celecoxib and nonsteroidal anti-inflammatory agents in CLASS. The annualized myocardial infarction rates for COX-2 inhibitors in both VIGOR and CLASS were significantly higher than that in the placebo group of a recent meta-analysis of 23 407 patients in primary prevention trials (0.52%): 0.74% with rofecoxib (P =.04 compared with the placebo group of the meta-analysis) and 0.80% with celecoxib (P =.02 compared with the placebo group of the meta-analysis). The available data raise a cautionary flag about the risk of cardiovascular events with COX-2 inhibitors. Further prospective trial evaluation may characterize and determine the magnitude of the risk.

Anti-Inflammatory Agents, Non-Steroidal↗