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Biomedical subjects

T Takai

Publications and source records attributed to T Takai.

At least 145 records · Page 8Linked to original sources
PubMed1981

Goitrous hypothyroidism due to iodide-trapping defect.

A 32-yr-old man with goitrous hypothyroidism due to an iodide-trapping defect is described. He was admitted because of goiter which had been increasing in size. His parents were unrelated, and no cases of goiter were found in his family. On admission, serum T3 was 39 ng/dl, serum T4 was 1.0 micro g/dl, and serum TSH was 217 micro U/ml. His 24-h thyroidal 131 I uptake was 0.05%. Antithyroid antibodies were negative. In a tracer study, the thyroidal 131 I uptakes were 6.3% at 2 h, 4.0% at 6 h, and 0.9% at 24 h after iv injection of the radioiodide. The decline in the neck counts was linear and parallel to that in the serum 131 I. The 24-h urinary excretion of 131 I was 92%. The saliva to serum and gastric juice to serum ratios of 131 I concentrations at 2 h were very low (0.95 and 0.97, respectively). After the administration of iodine (14 mg in Lugol's solution/day for 10 days), serum T3 was 228 ng/dl, serum T4 was 6.8 micro g/dl, and serum TSH was 24 micro U/ml. Some biochemical studies were carried out using the patient's thyroid tissue. In a kinetic study on iodide trapping by thyroid slices, the thyroid to medium ratio of iodide concentration in the patient's tissue was constantly about 0.1, in contrast to 1.5-4.0 in a control subject. The microsomal peroxidase activity in the patient's thyroid, assessed by iodination of bovine serum albumin, was about 3-fold that in a control subject on the basis of DNA content. Both ouabain-sensitive and -insensitive thyroidal Na+ -K+ -ATPase activities were present. These results suggest that the iodide-trapping defect in this patient was due to an impairment in the specific iodide carrier system rather than in the Na+ -K+ -ATPase itself.

Adult↗
PubMed1980

Thyroxine 5'-monodeiodinase activity in regenerating liver of triiodothyronine-treated rats.

The effect of triiodothyronine (T3) on hepatic thyroxine (T4) 5'-monodeiodinase and the subcellular localization of the enzyme were examined in regenerating rat liver, because it seemed likely that the effect of T3 might be accentuated during liver regeneration. Five days after T3 treatment, the specific activity of the monodeiodinase in the microsomal fraction (105,000 X g pellet) of regenerating liver was increased to 207% of the control value. Lineweaver-Burk plots showed that the Vmax for T4 5'-monodeiodination was about 3 times greater in T3-treated rats than in controls, but that there was no difference between the two groups in the apparent Km value for T4. About 55% of the total enzyme activity was found in the endoplasmic reticulum (ER) of the liver of both controls and T3-treated rats. The subcellular distribution of the enzyme was similar to that of NADPH-cytochrome c reductase (NADPH-cyt c reductase), a marker of the ER, but different from that of Na+,K+-ATPase, a marker of plasma membranes (PM).

Animals↗
PubMed1977

Serum creatine kinase isoenzymes in Duchenne muscular dystrophy.

Creatine kinase isoenzymes in sera of 51 patients with Duchenne muscular dystrophy were separated on a micro-column of DEAE Sephadex A-50. MB isoenzyme was detected in the sera of 32 cases (63%). MB percentage of total creatine kinase activity correlated significantly with urinary creatine/creatinine ratio in the early stages of the disease. No close relationship between MB levels and ECG findings was observed. The origin of serum MB in Duchenne dystrophy is discussed.

Adolescent↗