Search PubMed⌕ Search

Biomedical subjects

W C Yang

Publications and source records attributed to W C Yang.

At least 145 records · Page 8Linked to original sources
PubMed1982

Calcifications of cerebral medullary veins associated with carotid-jugular fistula.

Unusual calcification of the cerebral medullary veins is noted in a 34-year-old mentally retarded female who had a right carotid-jugular anastomosis 30 years earlier. The patient was hospitalized because of a right neck mass, proptosis, and the recent onset of left flaccid hemiplegia. Arch aortography and CT of the head and neck were performed. Surgery to oblate the fistula provided dramatic relief of venous engorgement in the orbits and face. The finding of medullary vein calcification is emphasized because it is a hitherto unreported entity.

Adult↗
PubMed1982

Studies on the effect of deoxyadenosine on deoxycoformycin-treated myeloid and lymphoid stem cells.

Adenosine deaminase (ADA) deficiency has been reported in association with severe combined immunodeficiency disease (SCID). The mechanism by which ADA deficiency causes immune dysfunction has been investigated in model systems to which the ADA inhibitor deoxycoformycin (dCf) had been added. Previously, we demonstrated that dCF did not prevent proliferation and differentiation of myeloid and lymphoid stem cells. We have now shown that addition of deoxyadenosine to dCf-containing cultures inhibited proliferation of hemopoietic stem cells. This inhibition was, however, equally effective for both normal myeloid and lymphoid stem cells. These findings suggest that other differences may exist between SCID myeloid and lymphoid stem cells to account for the relative sparing of myelopoiesis in SCID patients.

Adenosine Deaminase Inhibitors↗
PubMed1981

Effects of chronic emetine treatment on mitochondrial function.

Emetine has long been recognized as a cardiotoxic drug, but its mechanism remains unknown. Since many studies reported an effect of emetine on cardiac metabolism, permanent damage to the heart could result from such treatment. To investigate this action of emetine in relation to the cardiotoxicity seen after a therapeutic regimen, New Zealand albino rabbits were given 2 mg/kg/day ip of emetine for 9 days. Heart and liver mitochondrial metabolism was assessed polarographically using pyruvate, pyruvate plus malate, or succinate as the substrate. Heart mitochondrial metabolism was reduced in emetine-treated rabbits in comparison to the normal controls. However, the metabolic activity of the pair-fed control group was equally reduced. Only the liver mitochondrial metabolism of the pair-fed control group was reduced in relation to the normal controls, while the liver mitochondrial metabolism of emetine-treated rabbits remained unchanged. These data indicated that the reduction in heart mitochondrial metabolism resulted from the inanition induced by the chronic emetine treatment and not from a primary effect of the drug.

Animals↗
PubMed1981

Mechanism of the inhibitory action of phenelzine on microsomal drug metabolism.

Aminopyrine N-demethylase was inhibited by phenelzine in vitro and in microsomes isolated from rats treated with phenelzine in vivo. The inhibition was greater if phenelzine was incubated with the microsomal suspension before the addition of the substrate. In vitro, the addition of phenelzine produced immediate decrease in cytochrome P-450. This initial decrease was found to be due to the direct binding of phenelzine to the ferrous heme of cytochrome P-450. Further decrease in cytochrome P-450 occurred upon incubation of microsomes with phenelzine in the presence of NADPH. This secondary decrease in cytochrome P-450 was found to be paralleled by a loss of the home content in cytochrome P-450. The decrease in cytochrome P-450 with concomitant loss of heme can be partially inhibited by a substrate (aminopyrine) or by an inhibitor (metyrapone) of the microsomal enzymes, indicating the possible involvement of the metabolism of phenelzine to a reactive intermediate. The comparison of the effect of phenelzine to that of phenylhydrazine strengthened the possibility that a reactive metabolic intermediate of phenelzine can cause heme destruction in cytochrome P-450. Thus, phenelzine exerts its inhibitory action on microsomal drug metabolism most likely by decreasing the cytochrome P-450 content largely through heme destruction.

Aminopyrine N-Demethylase↗
PubMed1980

Ventriculo-subgaleal shunt: evaluation by computed tomography.

Ventriculo-subgaleal shunting was used for temporary decompression of hypertensive hydrocephalus. Pre- and post-shunt computed tomography was utilized in five cases as a method for detecting complications and determining shunt function. A clear-cut clinical improvement and stabilization followed the subgaleal diversion, but nevertheless usually only a mild decrease in ventricular size was demonstrated after shunting.

Adolescent↗