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Biomedical subjects

W A Neal

Publications and source records attributed to W A Neal.

At least 19 recordsLinked to original sources

Partial characterization of an erythropoiesis inhibitory factor.

An inhibitory factor of erythropoiesis, obtained from normal human urine, is indicated to be a complex of a fragment of alpha 1-acid glycoprotein and prostaglandin F2 alpha. Immunoelectrophoresis reveals two protein components in the EIF complex which separate during acrylamide gel electrophoresis. A gamma-globulin (MW 185,000) is a carrier of the complex. A fragment of alpha 1-acid glycoprotein (MW 9300) retains the inhibitory factor, PGF2 alpha. Noncovalent forces bind the PGF2 alpha to the protein, and PGF2 alpha can be extracted with benzene.

Blood Proteins

An alternative method for repair of partial anomalous pulmonary venous connection to the superior vena cava.

The surgical management of 15 patients with partial anomalous pulmonary venous connection (PAPVC) to the high superior vena cava (SVC) is described. This new technique redirects the anomalous pulmonary venous flow into the left atrium through the cardiac end of the SVC, transected and oversewn above the anomalous pulmonary vein or veins, by coaptation of the atrial septal defect (or of the surgically created septal defect in patients with an intact atrial septum) to the intracardiac orifice of the SVC. Normal SVC-right atrial flow is reconstituted by atriocavoplasty to the cephalad portion of the transected SVC. A 31-year-old woman with severe pulmonary hypertension died early in the series; this was the only death. Surviving patients enjoy full activity. Except for one symptomatic SVC obstruction due to technical error (since relieved), this technique has achieved total correction of these congenital defects with marked reduction in the undesirable postoperative sequelae often associated with other methods of repair.

Adolescent

Lysosomal glycogen storage disease without acid maltase deficiency.

We studied two brothers with lysosomal glycogen storage disease without acid maltase deficiency in skeletal muscle. Although no specific biochemical defect was identified, a characteristic clinical picture emerged from evaluation of these siblings and two other previously reported patients. The syndrome is manifested by proximal muscle weakness, hypertrophic cardiomyopathy, probable intellectual impairment, and possible liver involvement.

Adolescent

Patent ductus arteriosus in premature infants: a review of current management.

Problems related to the ductus arteriosus confront the pediatrician more than any other isolated cardiac defect. Due to increased awareness of the problems of prematurity, the reported frequency of patent ductus arteriosus increased threefold between 1970 and 1975. Aggressive therapy directed toward closure of the ductus is indicated within the first week of life in the very immature infant. Pharmacologic closure of the PDA with indomethacin is effective about half the time.

Ductus Arteriosus, Patent

Indomethacin for closure of patent ductus arteriosus in prematures.

A controlled, double blind trial of indomethacin versus placebo was conducted in prematures of birth weight less than 1750 g, with a murmur of patent ductus arteriosus (PDA). The dose of indomethacin was 0.2 mg/kg for 2 doses, orally, 24 hours apart. Forty-seven patients entered the trial. Twenty-four received indomethacin and 12 of these met the criteria for response; 23 received the placebo and two met the criteria for response (p less than 0.01). Subsequent surgical ligation for symptomatic PDA was required in 13 of 23 in the placebo group and 4 of 24 in the indomethacin group (p less than 0.01). When administered early, indomethacin is moderately effective in closing PDA in premature infants.

Clinical Trials as Topic

Inhibition of Friend virus (FVP)-induced murine erythropoiesis with prostaglandin (PGF2 alpha): potentiation and inhibition of erythropoietin and prevention of both with PGD2.

An erythropoietin-independent virus-induced murine erythroleukemia (FVP) is used to compare the effects of an erythropoiesis inhibitory factor (EIF) isolated from human urine with the effects of prostaglandin F2 alpha. The consequent inhibition of FVP-induced erythropoiesis suggests that EIF and PGF2 alpha have similar effects on the FVP-induced erythropoiesis in mice, and the effect of PGF2 alpha is indirect. The similarity of the actions of EIF and PGF2 alpha may indicate a potential role for prostaglandins in the physiological control of some types of erythrocytosis.

Animals

Inhibition of erythropoiesis by plasma component(s) from sheep, goats, and rabbits.

Plasma from hypertransfused and normal sheep and experimentally induced anemic and normal goats was fractionated by ultrafiltration. Fractions obtained were assayed for erythropoiesis stimulatory factor (ESF) or erythropoiesis inhibitory factor (EIF) activity (or both) in the posthypoxic polycythemic mouse assay. The most potent sheep plasma-inhibitor fraction was found in the retentate on a membrane with a cutoff at mol wt 50,000. The most potent EIF fraction from anemic goats passed into the ultrafiltrate, but the comparable EIF from normal goats remained in the retentate on a membrane with a cutoff at mol wt 500. The yield of the most potent EIF fraction was higher from anemic goats than was the yield from normal goats. During thin-layer chromatography, EIF extracted from goat plasma fractions had the same mobility as did prostaglandin F2 alpha. Cohn rabbit plasma fraction IV-4 had an inhibitory factor, and a benzene extract of the fraction contained a component that had the same mobility as did prostaglandin F2 alpha. Cohn rabbit plasma fraction V contained a component that potentiated an erythropoietin-generating factor.

Animals