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Biomedical subjects

K Saida

Publications and source records attributed to K Saida.

138 records · Page 8Linked to original sources
PubMed1976

Placento-thyroidal relationship in normal pregnancy.

Estimations of serum HCT, HTSH, T4, T3, PBI, ETR, Triosorb, TBG-binding capacity, BMR and urinary total estrogen were made simultaneously in 160 women in normal pregnancy. TRH stimulation tests were made in 20 cases in each trimester of pregnancy. HCT was detectable even in early pregnancy, tending to increase gradually toward the terminal stage of pregnancy as serum thyrotrophin bioactivity showed. On the other hand, serum TSH level measured by radio-immunoassay remained essentially the same throughout the course of pregnancy as in the nonpregnant state, moreover, it was suggested by the TRH stimulation test that pituitary TSH secreting function of pregnant women was similar to that of the non-pregnant. These findings suggest that thyroid hyperfunction during pregnancy which is shown by progressively increased T3, T4, and PBI may not be due to high estrogen-high TBG binding capacity-low free thyroxinenegative feed back-high TSH secretion but to HCT originating from placenta. In spite of thyroid hormone increase, it is true that the clinical picture of hyperthyroidism is not manifest among normal pregnant women, and ETR remained within the non-pregnant range throughout the course of pregnancy. We have also demonstrated that Triosorb decreased progressively. This may be interpreted to be due to the increase of TBG binding capacity which is increased progressively and binds more of free thyroxine during pregnancy. Such a change in TBG binding capacity is well known to be caused by the effect of estrogen which is progressively increased during pregnancy. In a word, it is possible to say that there is a placento-thyroidal system in pregnancy; HCT elevates thyroid function and TBG increased by estrogen carries thyroid hormone to target organ.

Estrogens↗
PubMed1976

HCT and thyroid function in molar pregnancy.

HCT, TSH, T3, T4, PBI, T3-RSU, TBG binding capacity, BMR and thyroid uptake of radioiodine were measured simultaneously on the volunteers with hydatidiform mole and normal pregnancy. TRH stimulation tests were performed on the two groups. The serum HCT levels were higher in association with molar pregnancy than in normal pregnancy. TSH levels were within the nonpregnant range in the two groups. T3, T4, PBI, ETR, BMR and thyroid uptake of radioiodine suggested thyroid hyperfunction in molar pregnancy with a greater degree than that in normal pregnancy. TBG binding capacity and T3-RSU were similar in two groups. The peak TSH levels of TRH stimulation tests ranged widely in patients with molar pregnancies but were within the nonpregnant range in the subjects with normal pregnancies. These findings suggest thyroid hyperfunction in the molar pregnancy is due to a larger amount of HCT than in normal pregnancy.

Female↗
PubMed1974

Toxic polyneuropathy produced by methyl N-butyl ketone.

A polyneuropathy affecting a large number of workers was recently observed at a plant producing plastic-coated and color-printed fabrics. Epidemiological data suggested strongly that methyl N-butyl ketone (MBK) was responsible for the outbreak. This hypothesis is now supported by the development of a peripheral neuropathy in chickens, rats, and cats exposed to MBK at atmospheric concentrations of 200 to 600 parts per million, 24 hours per day, 7 days per week. Although the animals were exposed continuously and the affected workers were exposed intermittently, the averages of the total number of hours of exposure for development of the peripheral neutropathy in the animals and workers were remarkably close.

Animals↗
PubMedDate not supplied

Contraction and intracellular calcium-ion elevation of cultured human aortic smooth muscle cells by endothelin-1, vasoactive intestinal contractor (VIC) and the derivatives.

Effects of endothelin (ET) family peptides and their derivatives on cellular contraction and calcium-ion level were examined by using cultured human vascular smooth muscle cells (VSM). Contraction of cultured human VSM, isolated from human fetal aortic segments, was induced within 1 min after the treatment with ET-1 (100 nM) as seen in the changes of cytosolic calcium-ion localization. In parallel with the cell contraction, cytosolic calcium-ion level in the human VSM increased very rapidly and then dropped with some oscillation as determined by Anchorage Cell Analyzing System. It was noted that transient calcium-ion mobilization rather than sustained calcium-ion influx was significant in the contraction of cultured human VSM. Vasoactive intestinal contractor (VIC), three amino acids different from ET-1, had less activity in increase of intracellular calcium-ion level and in percent of response cells than ET-1, ET-2, and VIC-S4L6 (one amino acid different from ET-1). EC50 of ET-1, VIC-S4L6, ET-2, and VIC were 0.5 nM, 0.6 nM, 2.0 nM, and 20 nM, respectively. VIC-like peptide (VIC-LP), 16 amino acids fragment of VIC precursor protein, had no effect with a single administration of up to 10 microM. However, the increase in calcium-ion level by VIC was suppressed with a prior treatment of cells with high concentration (10 microM) of VIC-LP. The establishment of cultured human VSM for the simultaneous examination of the contraction and calcium-ion level will provide a new system to study signal transduction of vasocontractor peptides.

Amino Acid Sequence↗
PubMedDate not supplied

MRI in infantile neuroaxonal dystrophy.

A 6-year-old boy with the typical clinical features of infantile neuroaxonal dystrophy was examined with magnetic resonance imaging. The findings suggested increased metal deposition in the globus pallidus. Magnetic resonance imaging findings of Hallervorden-Spatz syndrome and infantile neuroaxonal dystrophy are similar, suggesting that these two disease entities overlap. Magnetic resonance imaging findings, as well as relevant clinical features, may be useful in the diagnosis and classification of infantile neuroaxonal dystrophy.

Basal Ganglia Diseases↗