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Biomedical subjects

H Nishitani

Publications and source records attributed to H Nishitani.

At least 235 records · Page 13Linked to original sources

Defective iodide transport and normal organification of iodide in cold nodules of the thyroid.

Eleven thyroid follicular adenomas, cold on scintigram were analysed to determine whether defect in iodide organification or iodide transport causes low iodide uptake in cold nodules of the thyroid. The results were compared with perinodular tissue samples used as controls. In eight of eleven adenomas incubated in medium with 0.1 microM of iodide, newly organified iodide was 85.6 +/- 8.6% of total trapped iodide, which was significantly higher than 52.3 +/- 12.8% in controls. The remaining three adenomas showed a value as low as 4.0 +/- 2.7%. These data suggest that follicular adenomas are of two different groups; one with high organic iodinating activity and the other with none. These two groups were defined as FA-1 and FA-2. Thyroid:medium ratios of iodide of both groups were significantly depressed, indicating that the essential alteration in the thyroid follicular adenoma is a disturbance of iodide transport. In contrast to controls of organification of iodide was not inhibited by the addition of 100 microM iodide to the medium in FA-1 adenomas. In both FA-1 and FA-2, the degree of iodination of thyroglobulin (Tg) in equilibrium was significantly lower than that in controls. Therefore, in most cases with the follicular adenoma, the principal cause of decreased iodination of Tg was considered to be a depressed iodide transport, but not an impairment of organic iodination.

Adenoma↗

1-year controlled trial of 1 alpha-hydroxycholecalciferol in patients on maintenance hemodialysis.

A 1-year controlled trial was performed to confirm the effects of 1 alpha-hydroxycholecalciferol (1 alpha-OH-D3) in chronic hemodialysis patients. Initially, a daily dose of 2 micrograms of 1 alpha-OH-D3 was given orally to 24 patients and its placebo to another 24 patients during the first 3 months. For the following 9 months the dose of 1 alpha-OH-D3 or its placebo was reduced to 1 microgram per day in the individual groups. Serum calcium was significantly increased to the normal level after 1 month of treatment and sustained at this level for 1 year. Serum parathyroid hormone was significantly decreased at 3 months. Serum alkaline phosphatase was decreased to the normal level at the 5th month and thereafter. At 2 months serum phosphorus was significantly increased in the 1 alpha-OH-D3 group. None of the patients on 1 alpha-OH-D3 showed increased subperiosteal resorption on X-rays, whereas 8 out of 20 patients on placebo did (p less than 0.002). No adverse effects were seen apart from 3 patients with the 'red eye' of scleral calcification.

Alkaline Phosphatase↗

Myasthenia gravis: relation between jitter in single-fiber EMG and antibody to acetylcholine receptor.

In 39 patients with myasthenia gravis, we measured jitter in the extensor digitorum communis muscle, using single-fiber electrode (SFEMG) and the serum titer of antiacetylcholine receptor antibody. Clinical severity was correlated more closely with jitter, especially the percentage of abnormal jitter pairs with blocking than with antibody titer. In patients who responded fairly well clinically after certain treatments, both the SFEMG abnormalities and antibody titer tended to improve in parallel with clinical improvement. After the plasma exchange, there was a time lag between the recovery from the defective neuromuscular transmission and the rapid decrease in antibody titer. The percentage of abnormal jitter pairs with blocking and the mean jitter value reflect defective neuromuscular transmission in generalized myasthenia gravis.

Adolescent↗