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Biomedical subjects

N Takasu

Publications and source records attributed to N Takasu.

At least 19 recordsLinked to original sources
PubMed1992

[Forty-one cases of Cushing's syndrome: a comparison between Cushing's syndrome (adrenal adenoma) and Cushing's disease (adrenal hyperplasia)].

We experienced 41 cases of Cushing's syndrome (12 males and 29 females, 15 years old - 65 years old) during the last 20 years. These included 20 patients with unilateral adrenal adenoma (Cushing's syndrome), 19 patients with bilateral adrenal hyperplasia (Cushing's disease), one patient with adrenal carcinoma and one patient with primary adrenocortical nodular dysplasia (PAND). Moreover, these cases included some special ones, i.e. 5 cases with destructive thyroiditis after treatment, 2 cases with aggravation of arthritis after treatment, a case of Carney's complex with PAND, one case with paradoxical response to dexamethasone, and one case combined with empty sella syndrome. The most specific clinical signs were moon face (95% occurrence), hypertension (95%) and subcutaneous bruising (80%). Other significant signs were eye edema (66%), buffalo hump (68%), subcutaneous purpura (63%) and osteoporosis (49%). Skin striae was not a common sign in our cases (41%). Renal stone was observed in only 20% of our patients but was a significant sign in this syndrome. There was no difference in the occurrence of each clinical sign between Cushing's syndrome and Cushing's disease. The elevation of white blood cell count (WBC) and serum sodium, a decrease of serum potassium, and a decrease of reabsorption of phosphate (%TRP) were observed. Thyroid-stimulating hormone (TSH) and human growth hormone (HGH) were suppressed in patients with Cushing's syndrome and patients with Cushing's disease. These results were consistent with those of previous reports. However, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) were high in those patients with Cushing's syndrome and those with Cushing's disease. Oral glucose tolerance test was carried out in 34 patients before and after treatment. Thirty-one percent of those had diabetes mellitus and 26% had impaired glucose tolerance (IGT). The response of IRI in this test was high in patients with Cushing's syndrome and patients with Cushing's disease, and decreased 4 weeks after treatment in those with Cushing's syndrome but remained high in those with Cushing's disease. Plasma ACTH level and urinary 17-OHCS excretion were significantly higher in Cushing's disease than in Cushing's syndrome. During an 8mg-high-dose dexamethasone suppression test, urinary 17-OHCS excretion in 13 of 14 patients with Cushing's disease (93%) was suppressed by more than 50% of baseline on the second day of testing. However, all of 18 patients with Cushing's syndrome, who had an 8mg-dexamethasone suppression test, failed to suppress urinary 17-OHCS by 50% of baseline.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenoma↗
PubMed1992

Disappearance of thyrotropin-blocking antibodies and spontaneous recovery from hypothyroidism in autoimmune thyroiditis.

BACKGROUND: Hypothyroidism may result from the production of antibodies that block the actions of thyrotropin. How often these thyrotropin-blocking antibodies are a cause of hypothyroidism and whether their production may cease, causing hypothyroidism to disappear, have not been extensively studied. METHODS: We determined the frequency with which thyrotropin-blocking antibodies were present in 172 hypothyroid patients with goitrous autoimmune thyroiditis (Hashimoto's disease) and 64 hypothyroid patients with atrophic autoimmune thyroiditis (idiopathic primary hypothyroidism). For 6 to 11 years we then followed 21 of these patients who were found to have thyrotropin-blocking antibodies. They received levothyroxine therapy for 3.5 to 8 years, after which it was discontinued. At frequent intervals during this time we measured the patients' serum concentrations of thyroxine, triiodothyronine, thyrotropin, and thyrotropin-blocking antibodies (measured as immunoglobulins that inhibit thyrotropin binding and immunoglobulins that inhibit thyrotropin bioactivity). RESULTS: Thyrotropin-blocking antibodies were detected in 9 percent of the patients with goitrous autoimmune thyroiditis and in 25 percent of those with atrophic autoimmune thyroiditis. Among the 21 patients studied serially while receiving levothyroxine, thyrotropin-blocking antibodies disappeared in 15 (group 1), 7 of whom had goiter initially, and persisted in 6 (group 2), none of whom had goiter initially. Levothyroxine therapy was subsequently discontinued in these 21 patients. Six of those in group 1 (four with goiter) remained euthyroid (mean follow-up after discontinuation of therapy, 2.1 years), and nine became hypothyroid again within 3 months. All six patients in group 2 remained hypothyroid. CONCLUSIONS: Hypothyroidism in some patients with autoimmune thyroiditis may be due to thyrotropin-blocking antibodies. The production of thyrotropin-blocking antibodies may subside, producing remissions of hypothyroidism. Chronic autoimmune thyroiditis may therefore cause transient as well as permanent hypothyroidism.

Adult↗
PubMed1992

Role of adrenal androgens in the development of arteriosclerosis as judged by pulse wave velocity and calcification of the aorta.

To evaluate the role of adrenal androgens in the development of arteriosclerosis, serum dehydroepiandrosterone sulfate (DHEAS), dehydroepiandrosterone (DHEA), aortic calcification and pulse wave velocity (PWV) were measured in 69 males and 119 females without overt cardiovascular disease. The steroids decreased with age in both sexes, and the reduction was significantly steeper in younger (< or = 40 years) than in older (> 40 years) subjects only in females. When adjusted for age, the steroids were significantly lower in subjects with aortic calcification than in those without it, and the PWV was significantly slower in the latter. Adrenal androgens appear to retard the development and/or progression of arteriosclerosis.

Adolescent↗
PubMed1992

Studies on the association of NIDDM in Japanese patients with hyperthyroid Graves' disease.

We attempted to analyze the association of hyperthyroid Graves' disease with non-insulin-dependent diabetes mellitus (NIDDM). Forty-nine patients (23 males and 26 females; 7.6%) of a total of 647 patients with hyperthyroid Graves' disease had NIDDM, several years before or after Graves' disease was diagnosed. Only 1 patient had insulin-dependent diabetes mellitus. Compared with the general Japanese population (n = 9,133), the incidence of NIDDM (n = 348; 3.9%) in patients with Graves' disease was higher in all age groups. Only 4 patients (8.2%) of the 49 hyperthyroid patients with NIDDM had a history of being overweight (body mass index > 25). In contrast, 276 (79.9%) of the 348 diabetic patients were currently or previously overweight. Moreover, the incidence of a family history of diabetes (13 of the 49 hyperthyroid Graves' patients with NIDDM; 26.5%) was also lower in the patients with NIDDM in the general Japanese population (50% incidence). The male:female ration in patients with Graves' disease and NIDDM was 1:1.1; much different from that in the total Graves' disease population (1:4.1). Analysis of the HLA loci A, B, C, DR and DQ (35 determinations) in 35 hyperthyroid patients with NIDDM and in 386 subjects from the general population revealed a highly significant difference between them in the incidence of HLA-Cw4, -DR2, -DQw1, -DQw3 and -DQw4. This study suggests that there was an association of Graves' disease with NIDDM. A significant association of HLA-DR and -DQ loci was observed in hyperthyroid Graves' patients with NIDDM.

Adolescent↗
PubMed1992

Differential effects of nifedipine on plasma atrial natriuretic peptide in normal subjects and hypertensive patients.

The physiology of atrial natriuretic peptide (ANP) secretion was studied in normotensive subjects and hypertensive patients both young and old. Basal plasma ANP concentration was least in young normotensives, intermediate in old normotensives and young hypertensives, and highest in old hypertensives. Nifedipine, a known stimulator of ANP secretion, acutely increased plasma ANP in young and old normotensive subjects but not in young hypertensive patients and half of the old hypertensive patients. Increase in serum ANP level in response to nifedipine did not augment its hypotensive effect. However, the increase of aldosterone in response to nifedipine-induced rise in plasma renin activity (PRA) seemed to be suppressed by elevated ANP.

Adult↗
PubMed1992

Mastoparan-induced hormone release from rat pancreatic islets.

Mastoparan, a tetradecapeptide purified from wasp venom, stimulates insulin and glucagon release by rat pancreatic islets in a dose-related manner. In perifusion experiments, mastoparan produces monophasic hormone release, which ceases within 10 min of removal of the peptide. After exposure of the isles to mastoparan, glucose-induced insulin release is clearly retained. In incubation experiments, mastoparan-induced insulin release is greatly blocked by pretreatment of the islets with pertussis toxin or neomycin (inhibitor of phosphoinositide turnover) or by lowering the ambient temperature to 17 C. Pretreatment of the islets with nifedipine (calcium channel blocker), H-7 (inhibitor of A- and C-kinase), somatostatin, or divalent cation-free medium does not affect the response to mastoparan. Pretreatment with parabromophenacylbromide (phospholipase-A2 inhibitor) does not block the response induced by a high concentration of (58 microM) mastoparan. The peptide does not stimulate insulin synthesis during 30 min of incubation. Mastoparan raises the cytosolic free Ca2+ concentration, measured by fura-2, in isolated islet cells at normal (1.9 mM) and very low (6.5 microM) extracellular Ca2+ concentrations. Intravenous administration of mastoparan in rats causes a significant elevation of both insulin and glucagon. Together with the previous data, we conclude that mastoparan stimulates islet hormone release through a temperature-dependent process mediated by pertussis toxin-sensitive GTP-binding protein(s). Activation of phospholipase-C and liberation of intracellular Ca2+ are likely to be coupled to exocytosis. Ca2+ influx through the Ca2+ channel and protein kinase-A and -C appear not to be involved in mastoparan's hormone-releasing action. Phospholipase-A2 may be involved in the hormone release induced by low, but not high, concentrations of the peptide.

Animals↗
PubMed1992

Requirements of follicle structure for thyroid hormone synthesis; cytoskeletons and iodine metabolism in polarized monolayer cells on collagen gel and in double layered, follicle-forming cells.

Thyroid cells take up iodine and synthesize thyroid hormones. Thyroid cell polarity plays an important role in the uptake of iodine. However, we do not know whether polarity itself is enough for thyroid hormone synthesis or whether follicle structure is required for it. Using polarized monolayer porcine thyroid cells, cultured on collagen-coated filters, and double layered, follicle-forming cells, we analyzed the relationships of iodine metabolism and cell polarity (and follicle formation). We demonstrated that follicle structure was required for thyroid hormone synthesis. A quick-freezing and deep-etching method revealed the three-dimensional ultrastructures of cytoskeletons in the thyroid cells. On the collagen gel, the thyroid cells are reorganized into polarized monolayer cells; the basal cell membranes are in contact with the collagen gel and the apical ones face the culture medium. Actin microfilaments predominate under the apical cell membranes and intermediate filaments in the basal cytoplasm. The arrangement of these cytoskeletons determines the polarity of the cells. When the cells are cultured as double layers, follicle structures are reconstructed between the two monolayers. When apical cell membranes are in contact with other apical ones or when the cells are cultured as double layers, the cells are reorganized into follicles; the basal cell membranes are in contact with the collagen gel, and the apical ones face the follicle cavities. Actin microfilaments predominate at the apical cell membranes and intermediate filaments in the basal cytoplasm. Polarized thyroid cells transport iodine from the basal compartments to the apical ones, but cannot organify iodine into thyroid hormones. However, follicle-forming cells, cultured as double layers, take up iodine and organify it into thyroid hormones. Polarity is important for iodine uptake, and follicle structure is required for thyroid hormone synthesis.

Animals↗
PubMed1992

Ten-year follow-up of Japanese overweight subjects with impaired glucose tolerance: identification of a diabetes-prone subpopulation.

Ninety-four overweight subjects with normal glucose tolerance (NGT) or impaired glucose tolerance (IGT) were followed for 10 years. No one from the NGT group developed diabetes, however 32% of the IGT subjects did develop diabetes. Initial data of the IGT subjects who developed diabetes were significantly different from those who did not develop diabetes. Fasting, peak and/or sigma plasma glucose (PG), IRI and CPR at 180 minutes and CPR/IRI at 0 and 180 minutes were increased, and the peak time of PG was delayed; also the prevalence of a positive family history was higher, and the body weight heavier. Seventy-nine percent of IGT subjects with the initial sigma PG of greater than or equal to 40 mM or a positive family history developed diabetes whereas only 3% of those with sigma PG of less than 40 mM and a negative family history developed diabetes. Therefore, it might be considered that among the overweight adults with IGT, those with sigma PG of greater than or equal to 40 mM or a positive family history are diabetes prone and those with sigma PG of less than 40 mM and a negative family history are diabetes resistant.

Adult↗
PubMed1992

[Experimental study on the effect of forced running on occurrence of osteoarthritis in the knee of C 57 BL mice].

We investigated the effects of running load on the development of osteoarthritis (OA) in C 57 black male mice (Silberberg), a strain which spontaneously develops OA of the knee joint, and in Std:ddy male mice, a strain which does not develop OA. Six-week-old mice of both strains were randomly assigned to a non-forced running (control) group or forced running groups, which ran on treadmill 1 or 2 hours per day of 5 day/week program. Six, 18, and 30 weeks after the running period, the mice were sacrificed and the knee joints examined histologically and bone morphometrically. In the control C 57 black mice, OA occurred at 6 months of age, while in the forced running C 57 black mice, OA occurred at 3 months of age (6 weeks after the end forced running). In 6 and 9 months old C 57 black mice the incidence of OA in the forced running group was higher than that in corresponding control group. These data suggest that forced running load accelerates the process of OA in the knee joint in young mice of a strain which spontaneously develops OA.

Animals↗
PubMed1992

Primary hypothyroidism and multiple endocrine failure in association with hemochromatosis in a long-term hemodialysis patient.

A 56-year-old male patient on chronic hemodialysis developed liver cirrhosis. He received a total of 20 liters of blood transfusion. Bronze pigmentation of the skin and iron deposition to the liver, spleen, pancreas and thyroid gland, which was demonstrated by computed tomography and magnetic resonance imaging studies, and histological demonstration of iron deposition to the thyroid gland, bone marrow and gastric mucosa established a diagnosis of secondary hemochromatosis. Endocrine work-up revealed the presence of diabetes mellitus with minimum insulin secretory response, primary (or thyroprivic) hypothyroidism, hypoparathyroidism and hypogonadotropic hypogonadism. A wide-spread endocrine involvement as seen in this patient is a rare clinical feature of hemochromatosis secondary to massive blood transfusion in hemodialysis patients. Particularly, primary hypothyroidism due to iron deposition to the thyroid gland was quite a rare feature of hemochromatosis.

Diabetes Mellitus↗
PubMed1991

Interrelationship between insulin-like growth factor I-induced activation of the Na+/H(+)-antiporter and intracellular Ca(2+)-mobilization in thyroid cells.

Insulin-like growth factor I (IGF-I) increased cytoplamic pH (pHi) and cytoplasmic Ca2+ [( Ca2+]i) in cultured porcine thyroid cells. Inhibition of the Na+/H(+)-antiporter by dimethylamiloride or a reduction of external Na(+)-concentrations attenuates the increases in pHi and [Ca2+]i. The [Ca2+]i response to IGF-I is a pHi-dependent process. IGF-I activates Na+/H(+)-antiporter and alkalinizes thyroid cells. The resulting increase in pHi facilitates the [Ca2+]i response by adjusting the pHi closer to the pHi-optimum of the intracellular Ca(2+)-mobilizing system. One of the biological functions of IGF-I-induced activation of the Na+/H(+)-antiporter is to shift the pHi to an optimal value for the [Ca2+]i response.

Amiloride↗
PubMed1991

Intracellular localization of group II phospholipase A2 in rat vascular smooth muscle cells and its possible relationship to eicosanoid formation.

We investigated the localization of group II phospholipase A2 (PLA2-II) in rat vascular smooth muscle cells (VSMCs) by applying immunofluorescence and immunoelectron microscopy with its polyclonal antibody. In unstimulated cells, no immunolabelling was detected in the cells. On the other hand, in the cells stimulated with tumor necrosis factor (TNF) and/or forskolin (FK), intense fluorescence was detected in the cytoplasm. The immunoperoxidase reactions were detected in the cisternae of rough endoplasmic reticulum (rER), trans-cisternae of Golgi apparatus, and small vesicles beneath the plasma membrane. Western blot analysis showed VSMCs secrete PLA2-II after stimulation. Secreted PLA2-II was associated with the plasma membrane and extracellular matrix. Colchicine inhibited PLA2-II synthesis and its secretion to the extracellular space. These observations indicate that in VSMCs PLA2-II is synthesized at rER. transported to Golgi apparatus, discharged into extracellular space via the small vesicles, and microtubules may concern with its process. Furthermore, in VSMCs treated with TNF or TNF + FK, prostaglandin E2 formation was also increased. Actinomycin D and cycloheximide inhibited the potentiation of the prostaglandin E2 formation induced by TNF or TNF + FK, indicating that both RNA and protein synthesis are required for the potentiation. These results suggest an involvement of PLA2-II in the prostaglandin formation.

Animals↗
PubMed1991

Alloxan-induced DNA strand breaks in pancreatic islets. Evidence for H2O2 as an intermediate.

Alloxan exhibits the most potent diabetogenicity and has been used for induction of experimental diabetes mellitus. Understanding the mechanisms of action of the typical diabetogenic agent is important for elucidating the causes of diabetes. Okamoto (Okamoto, H. (1985) BioEssays 2, 15-21) proposed a model in which DNA fragmentation plays an important role for the development of diabetes. This DNA fragmentation is supposed to result from the accumulation of superoxide or hydroxyl radicals. However, direct evidence for this accumulation is lacking. Using rat pancreatic islets, we demonstrated that alloxan stimulated H2O2 generation, which induced DNA strand breaks. These findings support Okamoto's proposal that alloxan induces diabetes through the following biochemical events: alloxan----H2O2 generation----DNA strand breaks----diabetes mellitus. Perhaps this report constitutes the first demonstration of alloxan-stimulated H2O2 generation which could conceivably act as an intermediate for alloxan-induced DNA strand breaks.

Alloxan↗
PubMed1991

Gradual delay in glucose-induced first phase insulin secretion by the pancreatic islets of 7 week-, 6 month-, and 1 year-old rats.

The temporal profiles of insulin secretion by isolated pancreatic islets of male Wistar rats with various ages up to 1-year-old were studied using high glucose, potassium (K+) depolarization, and arginine as secretagogues. In the islets of 6-month-old rats, the onset and peak of glucose-induced first phase of insulin release were delayed for 1 min compared to those of 7--week-old rats. The onset and peak were further delayed for 1 min in the islets of 1-year-old rats. The onset of glucose-induced second phase of insulin secretion, and the onset and peak of K+ depolarization- and arginine-induced insulin release were not delayed in the islets of 6-month and 1-year-old rats. Glucose-stimulated increase in cytosolic free calcium ([Ca2+]i) seemed not delayed in the islets of 1-year-old rats. We conclude that the first phase of glucose-induced insulin release by the islets is selectively delayed as rat ages. It was suggested that the defect lies distal to the elevation of [Ca2+]i.

Aging↗
PubMed1991

Necrotizing fasciitis rapidly diagnosed by aspiration cytology.

A case of necrotizing fasciitis caused by beta-hemolytic streptococci is reported. A 66-year-old man was admitted because of pain and swelling in the right buttock. Rapid application of aspiration cytology made it possible to diagnose necrotizing fasciitis with bacterial infection. Unfortunately, however, the patient died of cardiac arrest due to hyperpotassemia 11 h after admission. Mortality from this disease is most often related to failure in recognizing it early. Rapid diagnosis and early treatment is mandatory in order to save the patients' life. We emphasize the usefulness of rapid aspiration cytology, despite the unfortunate outcome in the present case.

Aged↗