Search PubMed⌕ Search

Biomedical subjects

T Usa

Publications and source records attributed to T Usa.

At least 19 recordsLinked to original sources
PubMed1994

Effect of transforming growth factor-beta on the insulin-like growth factor-I autocrine/paracrine axis in cultured rat articular chondrocytes.

Transforming growth factor-beta (TGF-beta) and insulin-like growth factor-I (IGF-I) are essential anabolic factors in articular cartilage. In this study, we concentrated on the elucidation of TGF-beta interaction with IGF-I on cell growth and differentiation in monolayer articular chondrocytes obtained from 5-week-old rats. TGF-beta (1 ng/ml) and IGF-I (25 ng/ml) stimulated DNA synthesis about 6.5- and 2.1-fold over control values, respectively. When TGF-beta and IGF-I were added in combination, DNA synthesis was enhanced about 10.4-fold, indicating that the two peptides act in synergism. This synergistic action was also present in the expression of aggrecan mRNA. To study the mechanism of synergistic action, the effect of TGF-beta on the IGF-I autocrine/paracrine axis was investigated. Administration of increasing concentrations of TGF-beta (0.1-10 ng/ml) resulted in a dose-dependent decrease in medium IGF-I concentration that was reflected by decreased levels of IGF-I mRNA. TGF-beta also inhibited the production of a 41-kDa IGF-binding protein into the culture medium. Pretreatment with TGF-beta (1 ng/ml) for 12 h increased the binding of [125I]IGF-I to 140% of control by increasing the number of receptors without changes of affinity. Immunoprecipitation against phosphorylated tyrosine indicated that IGF-I-dependent autophosphorylation of IGF-I receptor beta-subunit was inhibited by simultaneous TGF-beta stimulation. These observations demonstrate that TGF-beta acts synergistically with IGF-I and regulates the IGF-I autocrine/paracrine axis via a complex regulatory mechanism with decreased production of IGF-I and IGFBPs and dephosphorylation of IGF-I receptor, whereas there is an apparent up-regulation of the binding of [125I]IGF-I.

Aggrecans↗
PubMed1992

Impairment of the TSH signal transduction system in human thyroid carcinoma cells.

In order to further evaluate the role of TSH in the proliferation and the differentiation of human thyroid carcinoma cells, we have analyzed the function of the TSH receptor in the established thyroid carcinoma cell lines NPA and WRO. The TSH signal transduction system in the carcinoma cells was also compared with that in normal thyroid cells. Although unresponsiveness to bovine and human TSH was demonstrated by measurement of cAMP production and [3H]thymidine incorporation after treatment of TSH, cAMP production was induced after stimulation of these cells by forskolin, cholera toxin, and isoproterenol. Specific binding to 125I-TSH was demonstrated in both NPA and WRO cells in addition to the existence of a TSH receptor mRNA and thyroglobulin mRNA species, although thyroid-specific gene expression in these cells was not regulated by TSH. These findings suggest that the unresponsiveness to TSH in these cells may be due to an abnormality of TSH receptor-G protein coupling rather than to a decreased level of TSH-receptor expression or a Gs protein abnormality.

Base Sequence↗
PubMed1991

[A case of dural arteriovenous malformation in the region of the cavernous sinus improved by Matas procedure].

A 55-year-old woman developed the sudden onset of headache and diplopia. The neurological findings showed the left 3rd and 4th cranial nerve palsies, loss of pain and temperature sensation in the region innervated by the ophthalmic nerve, and bruit on the left orbit. The mixed type of dural arteriovenous malformation (AVM) in the region of the cavernous sinus was diagnosed by MRI and cerebral angiography. The Matas procedure in which the patient was guided to compress the cervical carotid artery herself for 10 minutes three times a day was performed. Neurological signs and symptoms disappeared completely 3 months after starting the Matas procedure, and MRI revealed the regression of AVM. These results suggest that Matas procedure may promote its spontaneous regression of dural AVM occurred in the region of the cavernous sinus.

Carotid Arteries↗
PubMed1990

[A case of hypothyroidism associated with hypokalemic periodic paralysis].

A case of hypothyroidism associated with hypokalemic periodic paralysis was reported. The patient, a 50 year-old female was admitted because of recurrent paralytic attacks. She had not presented any symptoms of hypothyroidism. Physical examination on admission revealed muscle weakness of limbs, but not enlargement of thyroid glands. Paralytic attack was induced by oral intake of 100 g of glucose, and during attacks, serum K levels ranged from 3.4 to 3.0 mEq/l. She was diagnosed chronic thyroiditis by the high level of TSH and thyroid related anti-antibodies in the serum. Muscle biopsy showed type II atrophy. After the improvement of thyroid function, her paralytic attack disappeared. Present study suggested that hypothyroidism could be a cause of hypokalemic periodic paralysis. This case was very rare and seemed important in etiology of periodic paralysis.

Chronic Disease↗
PubMed1986

[Pharmacological studies on Y-8894. (III). Its effect on the abnormal electrocorticogram induced by destruction of the internal capsule].

The effect of Y-8894 on the abnormal electrocorticogram (ECoG) of alcuronium-immobilized rats, induced by destruction of the internal capsule with heat, was compared with that produced by imipramine, amantadine and Ca-hopantenate. ECoG power in the delta + theta (1-7 Hz), alpha (7.5-12.5 Hz) and beta (13-30 Hz) bands was used as an index. Delta + theta power increased following destruction of the internal capsule with heat. The increased delta + theta power (abnormal ECoG) lasted for 60 min following the injection of saline at 60 degrees C for 3 min. Y-8894 (0.1-1 mg/kg, i.v.) apparently improved the abnormal ECoG dose-dependently by significantly reducing the increased delta + theta power. Similar results were obtained with amantadine (10 mg/kg, i.v.), but its potency was weaker than that of Y-8894. Imipramine (1 mg/kg, i.v.) and Ca-hopantenate (30 mg/kg, i.v.), however, both failed to modify the abnormal ECoG. All drugs, except Ca-hopantenate, decreased the magnitudes of the alpha and beta bands. The above results suggest that Y-8894 may be effective in ameliorating cerebral dysfunction induced experimentally by the lesion of the internal capsule.

Amantadine↗
PubMed1982

[Antibody to 1-24 ACTH and hypofunction of the adrenal cortex in a patient who was unilaterally adrenalectomized for Cushing's syndrome (author's transl)].

We report here on a patient who was unilaterally adrenalectomized for Cushing's syndrome, and who developed antibodies to 1-24 ACTH. A 49-year-old nurse had undergone right adrenalectomy for adrenal adenoma. After surgery, she was treated with 0.5 mg of 1-24 ACTH-Z together with glucocorticoid replacement therapy for 40 days. Thereafter she was given 0.25-0.5 mg of ACTH-Z every other day for 4 months. ACTH-Z was then stopped for a year but glucocorticoid therapy was continued. About one year prior to this admission, 1 mg of ACTH-Z was again initiated 1 to 2 times a week. Glucocorticoid therapy was not withdrawn during the four years after adrenalectomy. She was admitted for the purpose of withdrawal of glucocorticoids. Her serum was found to bind labeled ACTH. This labeled ACTH was competitively displaced from binding by unlabeled hormones. Finally, reaction with specific antihuman Ig demonstrated an antibody of the IgG class. The titer of the antibodies gradually decreased after the discontinuation of ACTH-Z, but it is still present in measurable quantity in her serum. The clinical significance of the circulating anti-ACTH antibody in her serum is discussed.

Adrenal Insufficiency↗
PubMed1980

Differences between adrenal adenoma causing primary aldosteronism and other adrenal tissues in the incorporation of labeled steroid precursors into their products.

The incorporation and conversion of several labeled steroid precursors into their products were examined in slices of adrenal tissue from two patients with primary aldosteronism and compared with that in "normal" adrenal tissue and adrenal tissues from a patient with Cushing's syndrome. The products of the incorporation were separated by Sephadex LH-20 column chromatography. The major products of conversion in the adenomatous tissue of primary aldosteronism were 18-hydroxycorticosterone and lesser amounts of aldosterone. Smaller amounts of 18-hydroxycorticosterone were isolated from all other adrenal tissues studied. No aldosterone could be recovered after incubating any of the adrenal tissue studied with labeled 18-hydroxy-11-deoxycorticosterone or 18-hydroxycorticosterone as precursor steroid. These in vitro results seem to suggest that there is increased 18-hydroxylation in the adenoma of primary aldosteronism compared with other tissues and that relatively more 18-hydroxycorticosterone is produced in such tissue than aldosterone.

Adenoma↗
PubMed1977

An extrarenal source of "renin-like" activity in anephric man.

To examine extrarenal sources of "renin-like" activity plasma was obtained from 19 anephric males. Plasma renin activity (PRA), concentration (PRC) (obtained after addition of exogenous renin substrate) and total renin concentration (TRC) (obtained after acid-activation of plasma and subsequent incubation with exogenous renin substrate) demonstrated values for several anephric patients comparable or above those seen in plasma from 10 normal subjects. Incubation of untreated plasma (PRA and PRC) and acid-dialyzed plasma (TRC) for angiotensin I generation was performed at pH 7.5, at 37 degrees C with EDTA, dimercaprol, and 8-OH-quinoline as angiotensinase and converting enzyme inhibitors. The pH optimum for acid-activation of TRC in anephric plasma was the same as that in normal plasma (pH 3.3). Molecular weight determinations following Sephadex gel chromatography demonstrated that the renin-like enzyme in normal plasma had a molecular weight of about 42,000 before and after acid-activation, while that in anephric plasma had a molecular weight of approximately 61,000. A saliva sample from one anephric subject with the highest levels of PRA, PRC, and TRC in plasma also demonstrated measurable amounts of PRA, PRC, and TRC. The molecular weight of this salivary "renin-like" activity also was 61,000. These observations suggest a possible extrarenal source of "renin-like" activity in anephric man. The physiological significance of these studies remains to be clarified.

Adolescent↗