Search PubMed⌕ Search

Biomedical subjects

M Wang

Publications and source records attributed to M Wang.

At least 1,063 records · Page 59Linked to original sources
PubMed1981

The effect of copper and protein on iron metabolism in rats fed a cereal diet.

Weanling male white rats were fed a diet containing a commercially available breakfast cereal. In 28 days they developed a mild anemia coupled with an increased amount of iron in the liver. In parallel work, this same diet was supplemented in a factorial fashion with casein, iron, copper and zinc. The zinc had no effect. Copper supplementation increased the hemoglobin level. Casein decreased liver iron. The copper and casein, when fed together, produced results approaching normal control levels. Supplementation of the diet with additional iron did not increase the hemoglobin or hematocrit but it did further increase iron storage in the liver. It is suggested that cereal enrichment programs might do well to consider copper and protein rather than focus total attention to additional iron and zinc.

Animals↗
PubMed1981

Dietary aluminum and Alzheimer's disease--a review.

Current evidence suggests that dietary aluminum is neither an essential nutrient nor a toxic element causing neurological damage. The phosphate and fluoride salts of aluminum are very insoluble. When fed in excess, aluminum increases the dietary needs for these anions. Aluminum hydroxide is used as an antacid that can prevent the phosphatemia seen in severe kidney damage. In Alzheimer's disease there is progressive decrease in brain mass with the accumulation of phospholipid-rich cell debris. These membrane tangles tend to accumulate aluminum and are easily stainable with silver.

Aluminum↗
PubMed1981

Influence of protein intake on S-adenosyl methionine decarboxylase activity in normal and chronically uremic rats.

The activity of S-adenosyl methionine decarboxylase (SAM decarboxylase), an enzyme mediating polyamine biosynthesis, was measured in liver and kidney of chronically uremic rats and their pair-fed controls. Effects of protein intake were assessed in groups of rats fed either 8 or 18% casein or switched from 18 to 70% casein for 14 hours. In control rats, both hepatic and renal SAM decarboxylase activities increased with the higher levels of dietary casein. In uremic rats, SAM decarboxylase activity was not responsive to alterations in protein intake. Hepatic and renal SAM decarboxylase activity was significantly higher in control rats than in uremic rats, but this was due to increases in activity that occurred with diets containing higher amounts of protein (18 and 70% casein versus 8% casein).

Adenosylmethionine Decarboxylase↗
PubMed1980

Metabolism of 1-14C-ornithine and 1,4-14C-putrescine in chronically uremic and control rats.

The metabolism of ornithine and putrescine was studied in vivo in chronically uremic and control rats. Rats were injected intraperitoneally with 1,4-14C-ornithine or 1,4-14C-putrescine and expired 14CO2 was collected for 4 hr. After injection of 1-14C-ornithine. 14CO2 expiration was decreased in uremic rats as compared to controls. Conversely, after 1,4-14C-putrescine injection, expiration of 14CO2 was increased in uremic rats as compared to controls. Four hours after the injection of 1-14C-ornithine, there was more radioactivity in liver and muscle and less radioactivity in kidney of uremic rats as compared to the respective sources in control rats. In uremic rats, 4 hr after 1,4-14C-putrescine injection, the radioactivity retained in the muscle and plasma was greater than in corresponding sources in control rats; whereas the radioactivity retained in uremic liver and kidney was similar to that of control rats. The greater putrescine-derived radioactivity retained in uremic tissues reflects either the retention of injection racer compounds, or retention or decreased catabolism of putrescine metabolites. From 14CO2 expiration data obtained, it appears that ornithine catabolism is reduced while putrescine catabolism is increased in uremia.

Animals↗
PubMed1979

Diamine oxidase activity in plasma and urine in uremia.

Diamine oxidase activity was measured in plasma or urine in 12 normal men, 4 men with chronic liver or heart disease, 13 men with chronic renal failure, and 12 men undergoing maintenance hemodialysis. Also in five studies in 4 patients, plasma diamine oxidase activity and total amine levels were measured at hourly intervals during a hemodialysis treatment. Plasma diamine oxidase activity was normal in patients with liver or heart disease and was at least three times normal in chronically uremic patients and in patients undergoing maintenance hemodialysis. Plasma diamine oxidase activities before and after a hemodialysis therapy were similar and did not change during dialysis until the 4th hour when they fell transiently; plasma total amine levels, which were elevated initially, tended to rise during the 4th hour of dialysis. Urinary diamine oxidase activity was reduced in the chronically uremic patients as compared to normal subjects. These observations are consistent with three alterations in diamine oxidase in patients with renal failure: activity (a) is increased in plasma of chronically uremic patients and those undergoing maintenance hemodialysis, (b) does not increase normally in response to heparin administration during dialysis therapy, and (c) is reduced in urine of chronically uremic patients.

Amine Oxidase (Copper-Containing)↗
PubMed1979

Formation of carcinogenic N-nitroso compounds in corn-bread inoculated with fungi.

DMNA, DENA and MBNA are formed in corn-bread which has been inoculated with the most common species of fungi found in foodstuffs of Lin Xian County, Henan Province, such as F. moniliforme, A. flavus and others, and then, added with small amount of NaNO2 after a few days of incubation. These carcinogenic N-nitroso compounds can induce cancer of the liver or/and esophagus in experimental animals. Results of the present study show the capability of some fungi to produce chemical carcinogens as well as mycotoxins in contaminated food, and thus, open a new field of research in cancer etiology.

Aspergillus flavus↗
PubMed1979

Modulation of transmission at a glutamate synapse.

The amino acid L-aspartate markedly potentiates the responses elicited by L-glutamate at excitatory neuromuscular synapses in lobster walking limbs. Results are consistent with the idea that aspartate increases the affinity between glutamate and its binding sites in the postsynaptic receptor. Although complications due to release from other amino acid sources are a serious qualification, studies of neurally induced release of glutamate and aspartate suggest that both amino acids are released from excitatory nerve terminals. Experiments comparing the potentiating action of a variety of amino acids with their ability to inhibit glutamate uptake are not supportive of the notion that inhibition of agonist removal is the primary mode of action in the potentiation process. However, this idea, as well as the suggestion that aspartate may induce release of glutamate from extrajunctional entrapment sites, are not ruled out. Indeed, it is likely that the modulatory process embodies a multiplicity of reactions with given ones dominating from preparation to preparation.

Animals↗
PubMed1978

Diamine oxidase in renal failure.

The enzyme, diamine oxidase, is present in many tissues and plays a role in the metabolism of certain amines, some of which may be toxic. In renal failure, plasma diamine oxidase activity was found to be increased in chronically uremic patients and before and after dialysis therapy in patients undergoing maintenance hemodialysis. Diamine oxidase activity was decreased in urine of the chronically uremic patients as compared to normal subjects. In chronically uremic rats, diamine oxidase activity was observed to be increased in plasma and reduced in urine as compared to sham-operated, pair-fed control rats. In the uremic rats diamine oxidase activity was also decreased in kidney and unchanged in liver and muscle. Total amine levels were elevated in plasma and reduced in urine of patients and rats with chronic renal failure. Although the clinical significance of abnormal diamine oxidase activity in renal failure is not clear, it is possible that this enzyme may have a pathophysiologic role in uremia.

Adult↗