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Biomedical subjects

N Amino

Publications and source records attributed to N Amino.

At least 145 records · Page 8Linked to original sources
PubMed1994

A case of hyperthyroidism due to pituitary resistance to thyroid hormone.

A fifteen-year-old male was admitted to our hospital because his thyroid function showed a lack of TSH suppression in the face of elevated thyroid hormone. This patient complained of heat intolerance, palpitation and hand tremor. Peripheral indices of thyroid hormone action indicated a hypermetabolic state. Serum TSH did not respond sufficiently to TRH stimulation, suggesting TSH-secreting pituitary adenoma. However, sellar CT scan and MRI images did not demonstrate any pituitary adenoma. Moreover, the serum TSH alpha-subunit concentration was not high and serum TSH was partially suppressed by the administration of T3. Furthermore, the results of single stranded conformation polymorphism (SSCP) suggested the existence of mutation(s) in the exon 7 of T3 receptor beta (TR beta) gene of this patient. These findings support the diagnosis of pituitary resistance to thyroid hormone.

Adenoma↗
PubMed1994

Change in serum concentration of insulin-like growth factor II (IGF-II) in patients with thyroid disease.

We investigated the serum concentration of IGF-II in patients with thyroid diseases (25 with untreated Graves' patients, 30 with hypothyroidism, 23 with thyroid adenoma) and in 72 healthy adults as normal controls, by a sensitive radioimmunoassay of serum IGF-II. Thyroid hormones are known to increase IGF-I production in the liver through the enhancement of GH secretion. In case of IGF-II, however, knowledge has been rather limited. The mean +/- SD concentration in healthy subjects was 556 +/- 94 micrograms/L with neither sex nor age dependence. In untreated Graves' patients, serum IGF-II levels (675 +/- 129 micrograms/L) were significantly (P < 0.01) higher than in normal controls, and significantly lower in patients with hypothyroidism (460 +/- 106 micrograms/L; P < 0.01). Thyroid hormones revealed positive correlation with the IGF-II concentration.

Adult↗
PubMed1994

Reducing effect of nadolol on serum levels of free thyroid hormones in hyperthyroidism.

We evaluated the effect of the beta-adrenergic receptor blocking agent nadolol on serum levels of free thyroid hormones in 20 untreated patients with Graves' disease, aged between 17 and 57 years (mean +/- SD, 32.9 +/- 10.5). All the patients were treated with 30 mg of nadolol alone once-daily for 2 weeks, and clinical and laboratory parameters before and after the treatment were compared. Systolic blood pressure was depressed significantly (P < 0.001) from 132.7 +/- 11.1 mmHg to 122.8 +/- 10.9 mmHg. The resting pulse rate was also reduced significantly (from 110.3 +/- 9.2/min to 86.0 +/- 13.2/min, P < 0.001). Serum free thyroxine levels were reduced significantly from 7.1 +/- 3.1 ng/dl to 5.7 +/- 3.6 ng/dl (P < 0.05) and serum free triiodothyronine levels were reduced from 21.9 +/- 5.6 pg/ml to 17.2 +/- 6.9 pg/ml (P < 0.01). In the present study, the beta-adrenergic receptor blocking agent nadolol was newly found to have a reducing effect on serum free thyroxine, as well as free triiodothyronine concentrations.

Adolescent↗
PubMed1994

Genistein but not staurosporine can inhibit the mitogenic signal evoked by lithium in rat thyroid cells (FRTL-5).

Long-term administration of lithium is one of the well-known causes of goiter. It can stimulate DNA synthesis in rat thyroid cells (FRTL-5) treated with thyroid-stimulating hormone (TSH). To investigate the mitogenic signal transduction system activated by lithium, lithium-induced DNA synthesis and Ca2+ influx were studied using two protein kinase inhibitors, genistein as a specific tyrosine kinase inhibitor and staurosporine as a potent inhibitor of protein kinase C. Genistein but not staurosporine blocked the DNA synthesis induced by lithium in TSH-primed cells but neither compound had any effect on the Ca2+ entry stimulated by lithium. Genistein clearly attenuated the phosphotyrosine content of the 175 kDa substrate in the presence of lithium but staurosporine failed to do so. Moreover, lithium could also stimulate DNA synthesis in protein kinase C down-regulated cells. These data demonstrate that lithium may require the activation of a particular genistein-sensitive kinase, possibly a tyrosine kinase, to induce cell proliferation. It is suggested that the phorbol ester-sensitive protein kinase C family might not participate in the mitogenic signal transduction pathway activated by lithium.

Alkaloids↗
PubMed1994

Abundant existence of 40kD-cdc2-related protein in rat thyroid cells.

The cdc2 kinase family is known to be one of the important factors for cell proliferation in both yeast and mammalian cells. By using polyclonal antibodies against PSTAIRE region of cdc2HS, we studied the amount of cdc2-related kinases in the rat thyroid cell line, FRTL-5, during the cell cycle. The immunoreactive protein with molecular weight 34kD was hardly detectable, instead, 40kD protein exists constantly in amount through G0 phase to S phase. Further, it did not decrease when the cells were cultured in serum- and hormone-free medium. Moreover, we observed an increase of this protein in the nuclear fraction as the cells enter S phase. On the contrary, we could not detect any immunoreactive 40kD protein in primary cultures of rat thyroid cells. These results may indicate abundant existence of this protein might concern cell cycle regulation of FRTL-5 or its immortal feature.

Animals↗
PubMed1994

Phorbol ester inhibits DNA synthesis induced by interleukin-6 in TSH-pretreated FRTL-5 cells.

Combination of TSH and Interleukin-6 (IL-6) can stimulate DNA synthesis in FRTL-5 cells. Phorbol 12-myristate 13-acetate (PMA) stimulates G0 to G1 transition but inhibits G1 to S transition in these cells. We studied the effect of IL-6 on DNA synthesis in TSH-pretreated FRTL-5 cells in the presence or absence of PMA. IL-6 induced DNA synthesis when it was added to TSH-pretreated cells. Further, PMA inhibited the DNA synthesis induced by IL-6. These data might suggest that in FRTL-5 cells IL-6 can show its mitogenic effect in G1 phase of their cell cycle progression.

Animals↗
PubMed1994

Serum concentrations of apolipoproteins in patients with thyroid dysfunction.

We measured serum concentrations of apolipoproteins (apo A-I, A-II, B, C-II, C-III and E) in patients with thyroid disease (hyperthyroidism; n = 44, hypothyroidism; n = 15) and in normal subjects (n = 89). We found that apoA-II, B and C-III concentrations revealed significant difference among three groups of the normal (apoA-II; 31.4 +/- 4.9 mg/dl, apoB; 85.8 +/- 16.3 mg/dl, apoCIII; 7.45 +/- 2.99 mg/dl), hyperthyroidism (apoA-II; 29.8 +/- 5.4, apoB; 63.4 +/- 18.9, apoC-III; 6.28 +/- 2.45) and hypothyroidism (apoA-II; 27.5 +/- 5.3, apoB; 108.0 +/- 30.9, apoC-III; 9.43 +/- 2.74). Thyroid hormones showed clear negative correlation to apoB (r = 0.70, p < 0.001). Furthermore, apoC-III was also found to be negatively correlated with thyroid hormone concentrations (r = 0.47, p < 0.001).

Adult↗
PubMed1993

Effect of interleukin-6 on cell proliferation of FRTL-5 cells.

We studied the effects of interleukin-6(IL-6) on DNA synthesis and cyclic AMP production in rat thyroid FRTL-5 cells. When cells were incubated with IL-6 in the presence or absence of IGF-I, cell proliferation was not observed. By contrast, IL-6 stimulated DNA synthesis in a dose dependent manner when TSH was added concomitantly. On the other hand, IL-6 did not modulate the cAMP accumulation in the presence or absence of TSH. These data demonstrate that, like IGF-I, IL-6 may be able to act as a growth factor through activation of a mitogenic signal transduction pathway different from A-kinase in FRTL-5 cells.

Animals↗
PubMed1993

Functional regulation of GTP-binding protein coupled to insulin-like growth factor-I receptor by lithium during G1 phase of the rat thyroid cell cycle.

The regulatory effects of lithium on the function of pertussis toxin-sensitive GTP-binding (G(i))-proteins located on the mitogenic pathway activated by insulin-like growth factor-I (IGF-I) in FRTL-5 cells were studied. Addition of GTP-gamma-S to the thyroid stimulating hormone-primed cell membranes resulted in a decreased affinity of IGF-I receptor binding, and the dissociation constant (Kd) increased from 0.46 nM to 3.1 nM. Moreover, IGF-I stimulated GTP-gamma-S binding to a 40-kDa protein, and pertussis toxin (PT) attenuated the stimulatory effect of IGF-I on the same protein. Lithium lowered the affinity of IGF-I receptor binding and the Kd (3.4 nM) was in the same range as that in the presence of GTP-gamma-S. The inhibitory effect of lithium was markedly abolished by pretreatment with PT. Lithium attenuated the amounts of ADP-rebosylation of the 40-kDa protein by PT. In addition, lithium stimulated Ca2+ entry, similar to that by IGF-I, and induced cell proliferation via a PT-sensitive step. These findings suggest that lithium may be capable of modulating the function of G(i)-proteins coupled to IGF-I receptors during the G1 phase of the FRTL-5 cell cycle.

Adenosine Diphosphate Ribose↗
PubMed1993

Genistein, a tyrosine kinase inhibitor, blocks the cell cycle progression but not Ca2+ influx induced by BAY K8644 in FRTL-5 cells.

IGF-I, when added to TSH-primed FRTL-5 cells, induces a long lasting Ca2+ influx and then DNA synthesis. Ca2+ channel agonist, BAYK 8644, is capable to mimic these effects on cell proliferation. We studied the effect of genistein, a specific tyrosine kinase inhibitor, on BAY K8644- or IGF-I- induced cell cycle progression in FRTL-5 cells. Genistein inhibited DNA synthesis induced by BAY K8644 and by IGF-I. In contrast, Ca2+ influx stimulated by BAY K8644 was not inhibited. These data demonstrate that the signal transduction pathway induced by BAY K8644 or IGF-I may possibly involve genistein-sensitive process at the downstream step of Ca2+ entry.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1993

Portal vein calcification: a clinical review of the last 50 years and report of a case associated with dysplasminogenemia.

We report herein a case of a 68-year-old Japanese woman in whom calcification of the portal vein was recognized by plain abdominal X-ray radiograph and computed tomography (CT) scan when she presented with repeated thrombosis of the portal system. Following emergency small bowel resection for intestinal necrosis caused by superior mesenteric vein thrombosis, hematological studies revealed the association of dysplasminogenemia. A review of 21 cases of portal vein calcification reported between 1940 and 1990 revealed the average age to be 53.7 +/- 10.2 years and the male/female ratio 17:4. Although the majority of cases suffered from portal hypertension (81%), only 38% had any evidence of liver cirrhosis, while 52% had normal liver function, being comparable to idiopathic portal hypertension. The calcified lesions were located in the portal vein in 100% of cases, the splenic vein in 62%, the superior mesenteric vein in 33%, and the inferior mesenteric vein in 0%. The precise etiology of the calcification was not elucidated in any of the reviewed cases. The patient reported herein is the first reported case of portal vein calcification due to repeated thrombosis of the portal system caused by dysplasminogenemia, which could be accounted as a cause of idiopathic portal hypertension.

Aged↗
PubMed1993

Crucial role of serum human chorionic gonadotropin for the aggravation of thyrotoxicosis in early pregnancy in Graves' disease.

Thyrotoxicosis in Graves' disease is often aggravated in early pregnancy and is closely associated with postpartum recurrence of stimulative thyrotoxicosis. To examine whether thyroid-stimulating TSH receptor antibody (TSAb) or human chorionic gonadotropin (hCG), which also has thyroid-stimulating activity (TSA), was responsible for this early aggravation, the respective TSA due to TSAb or hCG was evaluated by a highly sensitive cAMP accumulation assay using FRTL-5 cells. TSA was detectable in all of 11 women in normal early pregnancy, correlated positively with serum hCG concentration, and was abolished completely by the pretreatment of serum sample with the solid-phase hCG antibody coupled with Sepharose 4B. The model serum samples of Graves' disease with pregnancy were made by the mixture of normal pregnant and Graves' sera, and their TSA were reduced by the pretreatment with the solid-phase hCG antibody, just corresponding with the reduction in hCG-induced TSA. TSA of early pregnant sera in 20 patients with Graves' disease decreased significantly but were still positive even after the pretreatment with the hCG antibody. Serial changes in TSAb and hCG-induced TSA were measured in 5 of these 20 pregnant patients. hCG-induced TSA increased associated with the increase in free thyroxine, while TSAb did not show striking change in early pregnancy. These data indicate that (1) respective TSA due to TSAb or hCG can be measured distinctively by using the solid-phase hCG antibody and (2) hCG plays a crucial role in the aggravation of Graves' thyrotoxicosis in early pregnancy.

Autoantibodies↗
PubMed1993

A new classification for human autoimmune thyroid disease.

We propose a new classification for the human autoimmune thyroid diseases including Graves' disease and Hashimoto's disease. The system proposed involves redefining the term "thyroiditis" and recognition that all clinicians need to speak the same language of medicine whatever their specialty and whatever their nationality. Major advances in our understanding of autoimmune mechanisms suggest that a new classification can add considerable clarity to clinical definitions.

Autoimmune Diseases↗
PubMed1993

Intrathyroidal lymphocyte subsets, including unusual CD4+ CD8+ cells and CD3loTCR alpha beta lo/-CD4-CD8- cells, in autoimmune thyroid disease.

Intrathyroidal lymphocyte subsets were analysed in 13 euthyroid patients with autoimmune thyroid disease by two-colour flow cytometry and compared with subsets in peripheral blood. In both Graves' and Hashimoto's diseases, proportions of intrathyroidal CD5- B cells were higher than in peripheral blood. The numbers of such cells were correlated with serum levels of anti-thyroid microsomal antibodies. Proportions of T cells bearing alpha beta chains of T cell receptors (TCR alpha beta+ T; T alpha beta) and CD16+CD57+ natural killer (NK) cells were lower in the thyroid, but proportions of CD3hiTCR alpha beta-TCR gamma delta+ (T gamma delta) cells were not different. Proportions of CD4+Leu-8- helper T cells and CD4+CD57+ germinal centre T cells were higher and proportions of CD4+Leu-8+ suppressor-inducer T cells and CD8+CD57+ or CD8+CD11b+ suppressor T cells were lower than in the blood in both diseases. Proportions of CD5+ B cells were high in Graves' disease, and proportions of CD8+CD11b- cytotoxic T cells were high in Hashimoto's disease. Unexpectedly, CD4+CD8+ cells and CD3loTCR alpha beta lo/-CD4-CD8- cells were present in thyroid tissues of both diseases. These findings suggest that: (i) an imbalance in the numbers of regulatory T cells and of NK cells that had appeared in the thyroid resulted in the proliferation of CD5- B cells, which were related to thyroid autoantibody production; (ii) CD5+ B cells and cytotoxic T cells are important for the different pathological features in Graves' and Hashimoto's diseases, respectively; and (iii) intrathyroidal CD4+CD8+ cells and CD3loTCR alpha beta lo/-CD4-CD8- cells may be related to the pathogenesis of autoimmune thyroid disease.

Adolescent↗
PubMed1993

Gestational thyrotoxicosis and hyperemesis gravidarum: possible role of hCG with higher stimulating activity.

OBJECTIVE: The thyroid gland is physiologically stimulated in normal early pregnancy. However, clinical thyrotoxicosis in normal pregnancy has not been well described. In order to clarify this we examined thyroid function and thyrotoxic symptoms in relation to emesis in normal pregnancy. We also investigated the possible mechanism of gestational thyrotoxicosis. DESIGN: Thyroid function was evaluated in view of the clinical thyrotoxic symptoms and the severity of gestational emesis in early pregnancy of 51 normal women. Two pregnant women who showed clinical thyrotoxicosis were followed serially during and after pregnancy. MEASUREMENTS: Serum free T4, free T3 and TSH were measured by radioimmunoassay and hCG by fluoroimmunoassay. Thyroid-stimulating activity of pregnancy sera was measured by cAMP increase in cultured FRTL-5 cells. RESULTS: Fifty-one pregnant women were divided into three groups: those without emesis (n = 24), with emesis (n = 19) and with hyperemesis (n = 8). Serum free T4 and free T3 were higher in the hyperemesis group (P < 0.01) and the emesis group (P < 0.01), and serum TSH was suppressed to less than 0.1 mU/l in both groups, while serum hCG was not significantly different among these three groups. However, serum thyroid-stimulating activity was remarkably high in the hyperemesis group (P < 0.01). Thus the ratio of thyroid-stimulating activity to hCG was higher in the hyperemesis group (P < 0.05) and the emesis group (P < 0.05) compared with that in the group without emesis. These thyroid-stimulating activities were abolished by treatment of the serum with anti-hCG antibody. Two of eight women with hyperemesis, who had the highest free T4 and thyroid-stimulating activity/hCG ratio, showed overt clinical symptoms of thyrotoxicosis; all the symptoms disappeared in association with a fall in thyroid-stimulating activity and free T4. CONCLUSION: Clinical thyrotoxicosis is caused by circulating hCG with higher biological activity in pregnant women with hyperemesis. A new clinical entity of 'gestational thyrotoxicosis' is proposed and tentative characteristics are discussed.

Chorionic Gonadotropin↗
PubMed1993

Recurrence of thyrotoxicosis after attack of allergic rhinitis in patients with Graves' disease.

Graves' disease is frequently aggravated during antithyroid drug therapy; however, little is known of its aggravating factors. We studied 83 patients with Graves' disease who were euthyroid for at least 6 months under antithyroid maintenance therapy, and we examined the relationship between thyrotoxicosis relapse, attack of allergic rhinitis, and peripheral eosinophil increase. Forty-one patients showed thyrotoxicosis relapse; of these, 22 (54%) showed peripheral eosinophil increase, and 14 (34%) had attacks of allergic rhinitis. In the remaining 42 patients without thyrotoxicosis relapse, only 4 (10%, P < 0.001) showed an increase in peripheral eosinophils, and only 3 (7%, P < 0.01) had allergic rhinitis. Recurrence of thyrotoxicosis was observed with the increase in serum levels of TSH-receptor antibodies and increase in eosinophils 2 months after the attack of allergic rhinitis. Three patients with seasonal allergic rhinitis showed thyrotoxicosis relapse at the same time of year within 2 consecutive years. Our findings indicate that allergic rhinitis can be an aggravating factor of Graves' disease and suggest that the preceding increase in peripheral eosinophils can be a predictive indicator of recurrence of thyrotoxicosis during antithyroid drug therapy.

Adolescent↗