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Biomedical subjects

M David

Publications and source records attributed to M David.

At least 685 records · Page 38Linked to original sources
PubMed1977

Studies of glutamate dehydrogenase. Methionine-169: the preferentially carboxymethylated residue.

In phosphate buffer at pH 7.0, 5,5'-dithio-bis(2-nitrobenzoic acid), N-ethylmaleimide or iodoacetamide do not alter the activity of beef liver glutamate dehydrogenase. Iodoacetate, however, inactivities the enzyme irreversibility by alkylation. Combined addition of the coenzyme NADH and the substrate 2-oxoglutarate or the effector GTP protects against this inactivation. The alkylation reaction is independent of pH between pH 6-9 indicating that amino, imidazole or phenolic groups are probably not involved in this reaction. Titration of the thiol groups, after denaturation of the enzyme, revealed the loss of approximately one group per polypeptide chain. However, this is not due to the exclusive alkylation of a cysteine residue, since alkylation with iodo-[2-14C]acetic acid also labels a methionine residue. 50% of the label is incorporated into methionine-169 and only 7% into cysteine-115, the remaining radioactivity is distributed in minor quantities (4%) in several unidentified residues. A probable cause of the erroneous thiol groups titration is discussed.

Amino Acid Sequence↗
PubMed1977

Linear growth and pubertal development in treated congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

21 years experience with management of seventeen cases of congenital adrenal hyperplasia due to 21-hydroxylase deficiency has been analysed with respect to growth, bone maturation and related events at puberty: age at menarche and the occurrence of menstrual irregularities, this study showed that growth retardation is still a problem; that irregular treatment and prolonged exposure to adrenal androgens or oestrogens, may lead to disturbance in hypothalamo-pituitary-gonadal function and may be the cause fo delayed menarche, or menstrual irregularities in the case of the female. In males the start of puberty and its completion was within the normal range.

17-Ketosteroids↗
PubMed1977

[Albright's type II osteodystrophy and hypothyroidism due to TSH deficiency. Apropos of a case in a child].

The report is dealing with a 10 year-old girl. The diagnosis of Albright's type II osteodystrophy relied on clinical, radiological and biological symptoms: evocative dysmorphic syndrome and absence of disturbances in the phosphocalcic metabolism. Hypothyroidism was secondary to an isolated defect in TSH, and a TRH stimulation test did not induce an increase in plasma TSH.

Calcinosis↗
PubMed1977

Midgut volvulus with secondary thrombosis of superior mesenteric vessels in a pregnant woman.

An anomaly of the position of the midgut in a pregnant woman predisposes to volvulus. Vascular repair, despite the abdominal catastrophe, sometimes allows parts of the intestine to be saved. A case of volvulus in a pregnant woman is described. At operation, 18 hours after onset, two anomalies were found: reverse rotation of the midgut and an anomaly of the collecting system of the superior mesenteric vein. Most of the midgut was infarcted. Thrombi were removed from the superior mesenteric vessels, and a portion of the anamalous superior mesenteric vein was reconstructed. All but 3 M. of the small bowel and the entire right colon were resected. Prolonged treatment with parenteral hyperalimentation enabled us to control the appearance of a moderate degree of malabsorption. To our knowledge, no similar case has been reported previously in the literature.

Adult↗
PubMed1976

Effect of sodium restriction and angiotensin II infusion in Bartter's syndrome.

Five patients with Bartter's syndrome were investigated. Sodium restriction (less than 10 mEq/day for at least 5 days) showed a renal sodium wastage in only two patients (I and II) in spite of increased aldosterone secretion rate (from 151-427 to 680-842 mug/day). The effect of angiotensin II (A II) 80ng/kg/min for 30-180 min, on plasma renin activity (PRA), plasma aldosterone, and urinary sodium excretion was compared with the effect of a previous infusion of 5% dextrose given at the same rate, 0.5 ml/min for 1 hr. A II infusion resulted in increased plasma aldosterone levels: from 236-330 pg/ml to 800-881 pg/ml in 30 min. This increase was also observed in patient II (from 139 to 600 pg/ml). PRA was decreased by A II infusion (from 1,142-2,462 to 121-1,625 ng/liter/min). In patient IV, this decrease in PRA was also observed when he was on a salt-restricted diet (from 1,934 to 370 ng/liter/min); but the minimal PRA was still higher (370 ng/liter/min) than with a normal diet (121 ng/liter/min). In no case could normal PRA level be obtained. A II infusion induced an increase in urinary sodium excretion only in the two patients with renal sodium wastage (from 80-90 to 265-230 muEq/min in 30 min). Urinary sodium excretion decreased in the other patients from (37.5-213 to 4.30-46 muEq/min) and fractional sodium excretion was reduced in patient V (from 0.56% to 0.45% at 30 min and to 0.29% at 120 min). No significant change with A II infusion was observed in patient IV when he was on a sodium-restricted diet (from 1 to 2.5 muEq/min in 30 min). Urinary potassium excretion was similar to sodium excretion. No change was observed in plasma potassium and sodium.

Aldosterone↗