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Biomedical subjects

M T Wang

Publications and source records attributed to M T Wang.

8 recordsLinked to original sources
PubMed1992

The screening diagnosis of tetrahydrobiopterin deficient phenylketonuria.

Since 1990, 20 diagnostically confirmed phenylketonuria (PKU) patients have been screened with a tetrahydrobiopterin (BH4) loading test, in which plasma phenylalanine and urinary pterin metabolites were investigated, ind activity of dihydropteridine reductase (DHPR) was determined as well. The results showed that there was no statistical difference between the concentrations of plasma phenylalanine before and after BH4 (20mg/kg) administration in all patients, and values of urinary neopterin and biopterin were within the range of classic PKU. All patients but one had normal activity of DHPR in red cells. This suggests that incidence of BH4 deficiency in PKU patients amounts to five percent (1/20) which is almost the same as reported abroad.

Biopterins↗
PubMed1992

Hypothalamic-pituitary function assessment in children by a combined stimulation test.

We utilized a combined stimulation test using insulin, thyrotropin-releasing hormone, gonadotropin-releasing hormone and levodopa to assess multiple pituitary hormones including growth hormone, thyrotropin, prolactin and gonadotropins in 32 children of short stature and 18 girls with early appearance of puberty. It was found that this combined stimulation test can assess multiple hormone responses with satisfactory results in a single 90-min test. Compared with any of those laborious classic stimulation tests alone, it is easier to be carried out and willingly accepted by children.

Child↗
PubMed1992

Hemorrhagic shock inhibits lipopolysaccharide-induced myelopoiesis in both germ-free and conventional rats.

BACKGROUND: Bacterial translocation has been implicated in the alteration of the immune response after shock and trauma. This study examined the effect of bacterial translocation on myelopoiesis after hemorrhagic shock in germ-free and conventional rats. METHODS: Awake, unrestrained germ-free and conventional rats were bled to a mean arterial pressure of 30 mm Hg until the animal required infusion of 10% of the shed blood. Rats were resuscitated with shed blood and crystalloid. Sham rats were catheterized but not bled. Twenty-four hours after shock or sham, rats were administered lipopolysaccharide 100 micrograms or saline intraperitoneally. Twenty-four hours later, bone marrow cells were cultured for growth of granulocyte-macrophage colony-stimulating factor (CFU-GM). RESULTS: Lipopolysaccharide increased the number of CFU-GM/femur in sham germ-free rats (801 +/- 129 versus 455 +/- 110; p less than 0.05) and conventional rats (1458 +/- 200 versus 492 +/- 59; p less than 0.05) compared with saline-treated rats. In contrast, hemorrhagic shock inhibited lipopolysaccharide-induced CFU-GM growth in both germ-free and conventional rats. Shock, itself, was a stimulus for CFU-GM growth in germ-free but not conventional rats. Bone marrow white blood cell counts were unaffected by shock, lipopolysaccharide administration, or the germ-free state. CONCLUSIONS: Hemorrhagic shock inhibited lipopolysaccharide-induced CFU-GM proliferation independent of the germ-bearing status of the rat, and bacterial translocation exerted no influence on myelopoietic dysfunction after hemorrhagic shock.

Animals↗
PubMed1979

Quantitative N-terminal analysis of fibrinogen-fibrin-related antigen [FR antigen] from human plasma.

Fibrinogen-fibrin-related antigen (FR antigen) was isolated from as little as 1 ml of human plasma by immuno-affinity chromatography with agarose-bound antibody to human fibrinogen. N-terminal analysis was performed to determine the nature and extent of proteolytic degradation of the FR antigen in patients with disseminated intravascular coagulation and in normal subjects. Thrombin cleavage of the A- and B-peptides from fibrinogen in vitro was monitored by the appearance of N-terminal glycine, and an increase in glycine was shown in the FR antigen of patients with disseminated intravascular coagulation. As plasmin progressively degraded fibrinogen, increases in N-terminal alanine, aspartic acid and lysine were observed, corresponding to the known plasmin-cleavage points of fibrinogen; increases in these N-terminal amino acids were also found in the patients' FR antigen. Thrombin treatment in vitro was used to remove fibrinopeptide A (N-terminal alanine) from the samples and to reflect specifically the N-terminal alanine at the plasmin-cleavage point (Arg-42-Ala-43) of the B beta-chain on assay; this alanine was increased progressively in the FR antigen of a patient during urokinase therapy, and was high in other patients when the FR antigen was examined by this procedure.

Alanine↗
PubMed1975

Gas-liquid chromatographic and mass fragmentographic determination of 3-O-methylated catecholamines in human plasma.

Plasma 3-O-methylated catecholamines, i.e. 3-methoxytyramine, normetanephrine and metanephrine, were separated from catecholamines by passing through alumina and further purified by adsorbing on weakly acidic resin and Amberlite XAD-4. The amines were trifluoroacetylated and determined by gas chromatography or mass fragmentography. Tracer quantities of tritiated 3-MT, NMN or MN were used as internal standards for total recovery estimations. The contents of 3-O-methylated catecholamines in the plasma of normal persons and patients with hyperthyroidism, hypertension, neuroblastoma and pheochromocytoma were measured.

Adult↗