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Biomedical subjects

Yuzuru Kato

Publications and source records attributed to Yuzuru Kato.

At least 37 records · Page 2Linked to original sources
PubMed2003

Echocardiographic investigation of pericardial effusion in a case of anorexia nervosa.

OBJECTIVE: Pericardial effusion has recently been reported as a complication of anorexia nervosa. A distinct pathophysiological cause of it could not be revealed. In some reports, there was a probable correlation between weight gain and reduction of pericardial effusion in anorexia nervosa cases. We encountered a case in which pericardial effusion remitted completely along with body weight increase and normalization of low T3 syndrome. These findings suggest that the reduction of pericardial effusion may correlate with both weight gain and low T3 normalization. Plasma brain natriuretic peptide (BNP) levels were increased in this case despite heart failure, and plasma BNP decreased as pericardial effusion remitted. The measurement of serum BNP level may be a clinical parameter in such a case of pericardial effusion.

Adult↗
PubMed2003

Effect of high concentration of glucose on dopamine release from pheochromocytoma-12 cells.

To investigate the mechanism of the action of high concentration of glucose on transmitter release from neuronal cells, we examined the effect of high concentration of glucose on dopamine release from pheochromocytoma-12 (PC12) cells. When the cells were incubated with 9.0 or 13.5 mg/mL glucose (2- or 3-fold of the optimum glucose concentration for PC12 cells), dopamine release was increased in a dose-related manner. Glucose-induced increase in dopamine release was blunted by nicardipine, a Ca2+ channel blocker. Following addition of 13.5 mg/mL glucose, intracellular Ca2+ concentration was increased, which was eliminated by nicardipine. Administration of 9.0 or 13.5 mg/mL glucose induced membrane depolarization in a dose-related manner. Glucose-induced dopamine release was inhibited by pinacidil or diazoxide, adenosine triphosphate (ATP)-sensitive K+ channel (KATP channel) openers. These results suggest that a high concentration of glucose induced ATP production, which blocked the KATP channel to induce membrane depolarization, and increased intracellular Ca2+ concentration and dopamine release. When the cells were cultured with 9.0 or 13.5 mg/mL glucose for 7 days, high potassium chloride (KCl)-induced dopamine release and 45Ca2+ uptake were increased. These results suggest that long-term incubation with a high concentration of glucose increased the capacity of Ca2+ uptake to enhance depolarization-induced dopamine release from PC12 cells. These data taken together suggest that a high concentration of glucose induced activation of the Ca2+ channel to stimulate dopamine release from PC12 cells.

Adenosine Triphosphate↗
PubMed2003

Frequent appearance of autoantibodies against prohormone convertase 1/3 and neuroendocrine protein 7B2 in patients with nonfunctioning pituitary macroadenoma.

Among pituitary disorders having mass effect of the pituitary gland, nonfunctioning pituitary macroadenoma and lymphocytic hypophysitis are difficult to differentiate without histological examination. In order to efficiently distinguish lymphocytic hypophysitis and pituitary tumors, we studied the presence of autoantibodies against prohormone-processing enzymes, prohormone convertase (PC) 1/3, PC2, carboxypeptidase E (CPE), and PC2 regulatory protein, 7B2, by radioligand assay using recombinant human 35S-labeled protein in patients with clinically nonfunctioning pituitary macroadenoma, lymphocytic hypophysitis, and other pituitary diseases. The indexes for anti-PC1/3 antibodies (Ab) were significantly higher in patients with nonfunctioning pituitary macroadenoma than in patients with lymphocytic hypophysitis. Patients positive for either anti-PC1/3 or anti-7B2 Ab were significantly frequent among patients with nonfunctioning pituitary macroadenoma than in other pituitary diseases and healthy controls. None of the patients was positive for anti-PC2 Ab or anti-CPE Ab. These results suggest that autoantibodies against PC1/3 and 7B2 are novel tumor-associated autoantibodies and can be helpful in the diagnosis of clinically nonfunctioning pituitary macroadenoma.

Adenoma↗
PubMed2003

Anti-alpha-enolase antibodies in pituitary disease.

A previous study reported a high prevalence of autoantibodies to alpha-enolase in lymphocytic hypophysitis and these antibodies efficiently distinguished lymphocytic hypophysitis from pituitary tumors. To confirm this, we examined autoantibodies to alpha-enolase in patients with lymphocytic hypophysitis (n = 17), pituitary non-functioning adenoma (n = 13), other pituitary diseases (n = 17) and other autoimmune diseases (n = 30), and compared to healthy controls (n = 46). Autoantibodies were found in 41.2%, 46.2%, 23.5%, 20.0% and 4.3%, respectively. Our findings indicate that detection of anti-alpha-enolase antibodies is not suitable for specific diagnosis of lymphocytic hypophysitis.

Adenoma↗
PubMed2003

Hypercholesterolemia and obesity in adult patients with hypopituitarism: a report of a nation-wide survey in Japan.

Dyslipidemia and obesity are common in adult patients with hypopituitarism. Possible contributions of age, sex and hormone deficiencies to hypercholesterolemia and obesity in adult hypopituitary patients were analyzed in 1, 272 Japanese cases based on a database of a national survey on adult hypopituitarism. In patients on routine hormone replacement therapy, 30.5% of male and 40.7% of female subjects were considered hypercholesterolemic. In univariate analysis, hypercholesterolemia was more prevalent in female, aged, untreated Gn-deficient and TSH-deficient groups. In multivariate analysis, sex of female, age older than 40 yr and TSH deficiency were the independent contributing factors to hypercholesterolemia. Obesity (body mass index (BMI) > or = 25 kg/m2) was more prevalent in male, TSH-deficient and ADH-deficient groups. Severe obesity (BMI > or = 30) was observed in high prevalence in the youngest group. These findings suggest that hypercholesterolemia and obesity were prevalent in different age and gender groups in Japanese adult patients with hypopituitarism. Insufficient replacement of thyroid hormone and possibly gonadotropin deficiency might contribute to hypercholesterolemia. In contrast, hypothalamic dysfunction as well as hormone deficiencies might play roles in obesity in these patients.

Adult↗
PubMed2003

A survey of pituitary incidentaloma in Japan.

OBJECTIVE: The development of computed tomography (CT) and magnetic resonance imaging (MRI) has resulted in the discovery of unsuspected endocrinologically silent pituitary masses (pituitary incidentalomas). The aim of this study was to perform a national survey on pituitary incidentalomas in order to establish an appropriate approach to them. DESIGN AND METHODS: Five hundred and six patients with pituitary incidentalomas were obtained by questionnaire from March 1999 to May 2000 under the auspices of the Ministry of Health, Labor and Welfare in Japan. Two hundred and fifty-eight patients underwent surgery (surgical group), while 248 patients were followed up conservatively for a mean period of 26.9 Months (range 6-173 Months) (non-surgical group). Clinical and biochemical assessment, CT or MRI of the pituitary, and visual field testing by Goldman perimetry were assessed at baseline and 6 Months and Yearly thereafter. RESULTS: Thirty-three patients with pituitary incidentalomas (13.3%) developed tumor enlargement during the mean follow-up period of 45.5 Months. Of 115 estimated non-functioning adenomas, 23 tumors (20.0%) increased during a mean follow-up period of 50.7 Months (range 10-173 Months), while 5 of 94 (5.3%) estimated Rathke's cysts increased in size during follow-up. Pituitary apoplexy occurred in one of 248 patients (0.4%). CONCLUSIONS: Pituitary incidentalomas usually follow a benign course. We recommend transsphenoidal adenectomy for a solid mass attached to the optic chiasma estimated to be a pituitary adenoma by MRI. Other patients should be followed up by MRI every 6 Months for the first 2 Years, and then Yearly.

Adenoma↗
PubMed2002

Possible involvement of tetrahydrobiopterin in the trophic effect of insulin-like growth factor-1 on rat pheochromocytoma-12 (PC12) cells.

Tetrahydrobiopterin (BH(4)) has a trophic effect on pheochromocytoma-12 (PC12) cells such as insulin-like growth factor-1 (IGF-1). We investigated involvement of BH(4) in the trophic effect of IGF-1 on PC12 cells. IGF-1 (10-300 ng/ml) increased cellular BH(4) content in a dose-related manner. Cellular BH(4) content increased after 6-36 h incubation with IGF-1. IGF-1-induced increase in the cellular BH(4) content was blunted by 0.3 mM 2,4-diamino-6-hydroxypyrimidine (DAHP), an inhibitor for BH(4) synthesis. IGF-1 protected PC12 cells from the cell death induced by depletion of serum and nerve growth factor, which was attenuated by DAHP. The effects of IGF-1 on the cellular BH(4) content and cell viability were eliminated by 0.2 microM wortmannin. These results suggest that BH(4) is involved in the trophic effect of IGF-1 on PC12 cells and that the effect of IGF-1 on BH(4) synthesis is mediated by phosphatidylinositol 3-kinase.

Androstadienes↗
PubMed2002

Effect of continuous subcutaneous administration of a low dose of G-CSF on stem cell mobilization in healthy donors: a feasibility study.

We investigated the effects of low-dose granulocyte colony-stimulating factor (G-CSF) on the mobilization of stem cells in 6 healthy subjects. When G-CSF was administered by continuous subcutaneous infusion at a rate of 72 microg/day for 5 days, the numbers of white blood cells and granulocytes rapidly increased to maximal levels. CD34+ cells were mobilized to the peripheral blood in 3 days, and the maximal level was reached 4 or 5 days after the start of treatment. We attempted to determine whether the levels of mobilized stem cells that we could obtain using this method would be sufficient for peripheral blood stem cell transplantation. Two of the 6 subjects complained of mild bone pain 4 or 5 days after the start of treatment, but the pain did not affect their daily activities. Only 1 abnormal result (for serum alkaline phosphatase) was found in the laboratory data. The present preliminary results have provided us with a framework for a prospective study comparing low-dose continuous infusion with conventional mobilization procedures.

Adult↗
PubMed2002

Involvement of nitric oxide in glucose toxicity on differentiated PC12 cells: prevention of glucose toxicity by tetrahydrobiopterin, a cofactor for nitric oxide synthase.

Effects of high concentrations of glucose on cell survival of differentiated PC12 cells were examined. Seven day-culture with D-glucose (9.0-27.0 mg/ml as 2-6-fold of the optimal level) induced cell death in a dose-related manner but 3-day culture with high concentrations of glucose had no effect on cell viability. L-glucose had no effect on viability of PC12 cells, suggesting that D-glucose toxicity was independent of its osmolarity effect. Seven-day culture with D-glucose (13.5 mg/ml as 3-fold of the optimal level) increased nitric oxide metabolites (NOx) in the culture medium. Glucose-induced increase in NOx was eliminated by 0.1 mM L-nitro-arginine methylester (L-NAME), a nitric oxide synthase (NOS) inhibitor. Intracellular Ca(2+) concentration was increased by D-glucose in a dose-related manner, suggesting that D-glucose activated NOS by increasing intracellular Ca(2+) concentration in PC12 cells. Glucose-induced cell death was blunted by 0.1 mM L-NAME, showing that nitric oxide (NO) was involved in the glucose toxicity to PC12 cells. Tetrahydrobiopterin (BH(4)), a cofactor for NOS, attenuated both glucose-induced cell death and NOx production at 1 microM but not at 10 microM. The effects of BH(4) on glucose-induced cell death and NOx production were not mimicked by reducing agents such as ascorbate and cysteine. These results taken together suggest that high concentrations of glucose induced cell death via NO production and that low concentration of BH(4) had a protective effect against glucose neurotoxicity in differentiated PC12 cells.

Animals↗
PubMed2002

Twenty-six-week repeat-dose toxicity study of a recombinant human granulocyte colony-stimulating factor derivative (nartograstim) in cynomolgus monkeys.

An rhG-CSF derivative, nartograstim (NTG), at dose levels of 0 (saline), 0.1, 1, 10, and 100 microg/kg, was administered subcutaneously to groups of 3 male and 3 female cynomolgus monkeys once daily for 26 weeks to investigate its toxicity. In Week 4 or later, an increase in leukocyte counts consisting mainly of neutrophils was noted in all NTG dose groups, and was considered to be attributable to the pharmacological action of NTG. The degree of this increase was reduced with repetition of dosing. Increases in granulocytic cells and granulocytic cells/erythrocytic cells (G/E) ratio in the bone marrow, increase in serum ALP activity, and enlarged spleens with increase of neutrophils in the red pulp were observed at 10 microg/kg and higher. Anemia was noted at 10 microg/kg and higher in Week 4 and was accompanied by an increase in reticulocytes and a decrease in total cholesterol level at 100 microg/kg. Anti-NTG antibody was detected in 1 female at 100 microg/kg, but neutralizing antibodies were not detected at any dose levels in Week 4. In Weeks 13 and 26, these antibodies were detected sporadically at all dose levels. However, there were considerable individual variations in antibody titer, and no definite correlation could be found between the dose levels and the antibody titer. Seven NTG-dosed animals including 3 high dose-group animals showed obvious increases in leukocyte counts until Week 26 but no obvious elevation of anti-NTG or neutralizing antibody. In these animals, changes including anemia became slighter but were still observed in Week 26. Under the conditions in this study, 1 microg/kg was concluded to be the no-observed-adverse-effect level (NOAEL) in cynomolgus monkeys.

Alkaline Phosphatase↗
PubMed2002

Growth hormone-releasing hormone and gonadotropin-releasing hormone stimulate nitric oxide production in 17beta-estradiol-primed rat anterior pituitary cells.

It was reported that neuronal nitric oxide synthase (nNOS) was expressed only in gonadotrophs and folliculo-stellate cells in the anterior lobe of the pituitary gland. However, recent studies have demonstrated the occurrence of nNOS in the somatotrophs and lactotrophs. In the present study, we investigated effects of growth hormone-releasing hormone (GHRH), gonadotropin-releasing hormone (GnRH), and 17beta-estradiol on nitric oxide (NO) release in cultured rat anterior pituitary cells in vitro. The NO2- level in the incubation medium of the rat anterior pituitary cells was dependent on the cell density. Pretreatment with 10 microM 17beta-estradiol resulted in an increase in medium NO2- level. GHRH and GnRH failed to change medium NO2- levels, but they elicited increases in medium NO2- levels in estrogen-treated cells. The GHRH-induced increase in NO2- level was inhibited by Nomega-nitro-L-arginine methyl ester, a NOS inhibitor. These findings suggest that GnRH and GHRH could activate nNOS in the gonadotrophs and the somatotrophs, respectively.

Animals↗
PubMed2002

Relationship between visceral fat accumulation and anti-lipolytic action of insulin in patients with type 2 diabetes mellitus.

Insulin resistance is closely related to developing type 2 diabetes mellitus. Visceral fat accumulation is associated with insulin resistance, which affects the free fatty acid (FFA) metabolism. We investigated the interactions among visceral fat accumulation, FFA metabolism and insulin resistance in 20 patients with type 2 diabetes mellitus, including 11 obese and 9 non-obese subjects. Body fat distribution was estimated by measuring the areas of both subcutaneous and visceral fat mass on abdominal computed tomography at the umbilical level. Glucose infusion rate (GIR) and plasma FFA responses to insulin were determined as an index of insulin resistance and anti-lipolytic action, respectively, in a euglycemic hyperinsulinemic clamp study. There was an inverse correlation between GIR and insulin-induced decrease in plasma FFA in all diabetic patients (r = -0.652, P < 0.01). Visceral fat mass area was well correlated with GIR (r = -0.583, P < 0.01) and insulin-induced decrease in plasma FFA (r = 0.724, P < 0.001), whereas subcutaneous fat mass area was not correlated either with GIR or plasma FFA decrease. These findings suggest that visceral fat accumulation results in increasing the resistance against the anti-lipolytic action of insulin, and that FFA metabolism is closely related with glucose utilization in patients with type 2 diabetes mellitus.

Adipose Tissue↗
PubMed2002

A case of autoimmune hypophysitis associated with Graves' disease.

In a 76-year-old woman with hyperthyroidism, hyperprolactinemia and thickening of the pituitary stalk on magnetic resonance imaging (MRI) was presented. Thyroid stimulating antibody (TSAb) was positive and anti-pituitary antibodies against 49 and 68 kD human anterior pituitary membrane antigens were detected immunologically. Secretion of pituitary hormones was almost normal except for suppressed TSH and hyperprolactinemia. As autoimmune etiologies were likely involved in the disorders, autoimmune hypophysitis associated with Graves' disease was arrived at as the plausible diagnosis.

Aged↗
PubMed2002

Detection of autoantibodies against the pituitary-specific proteins in patients with lymphocytic hypophysitis.

OBJECTIVE: Several reports have described antipituitary antibodies by immunofluorescent or immunoblotting methods in patients with lymphocytic hypophysitis. However, with the exception of the pituitary hormones, individual antigens specific for the pituitary gland have not been studied. To understand the pathogenesis of lymphocytic hypophysitis and to diagnose this disease efficiently, we studied the presence of autoantibodies against three pituitary-specific proteins, GH and two novel pituitary-specific proteins, namely, pituitary gland specific factor 1a (PGSF1a) and PGSF2. DESIGN: Seventeen patients with lymphocytic hypophysitis, all of whom had pituitary enlargement (5 with lymphocytic adenohypophysitis and 12 with lymphocytic infundibuloneurohypophysitis, including 3 of the latter group proven by biopsy), and 14 patients with hypopituitarism without pituitary enlargement (10 with isolated ACTH deficiency and 4 with idiopathic TSH deficiency) were studied, and compared with 11 patients with non-functioning pituitary macroadenoma, 31 patients with other autoimmune diseases, and 36 healthy controls. METHODS: The presence of each antibody was studied by radioligand assay using recombinant human (35)S-labeled protein. RESULTS: Three (18%) patients with lymphocytic hypophysitis having pituitary enlargement, five (36%) patients with hypopituitarism without pituitary enlargement and three (9.7%) patients with other autoimmune diseases were positive for one or more of the antibodies studied. CONCLUSIONS: Anti-human GH, anti-PGSF1a, and anti-PGSF2 antibodies were detected in patients with lymphocytic hypophysitis and other hypopituitarism, but were not detected in patients with non-functioning pituitary macroadenoma. Detection of these antibodies may be useful for the diagnosis of lymphocytic hypophysitis.

Adolescent↗
PubMed2002

Regulation of human growth hormone secretion and its disorders.

Growth hormone (GH) secretion from anterior pituitary is regulated by the hypothalamus and the mediators of GH actions. Major regulatory factors include GH releasing hormone (GHRH), somatostatin (SRIF), GH releasing peptide (ghrerin) and insulin-like growth factor (IGF-I). The principal physiological regulation mechanisms of GH secretion are neural endogenous rhythm, sleep, stress, exercise, and nutritional and metabolic signals. GH deficiency results from various hereditary or acquired causes, which may be isolated or combined with other pituitary hormone deficiencies. GH deficiency can be treated with recombinant human GH, which results in accelerating growth in children and normalization of intermediary metabolism in adults. GH hypersecretion mostly results from a pituitary tumor and causes acromegaly or gigantism. Hypersecretion of GH can be treated by transshenoidal surgery. Medical treatment with octreotide and analogs is also effective to reduce GH secretion in combination with or without the surgery.

Growth Disorders↗
PubMed2002

[A case of large-cell lung cancer successfully treated with docetaxel in combination with carboplatin and radiotherapy].

A 64-year-old male was referred to our hospital in September, 2000 for further examination of an abnormal chest shadow discovered in a regular health check-up. Chest X-P and CT revealed a large tumor in the left upper lobe, in association with hilar lymphadenopathy and costal invasion. Serum CEA was increased, and lung biopsy revealed a large-cell carcinoma. We performed chemoradiotherapy before surgery. Radiation (total 48 Gy) and 3 courses of chemotherapy with docetaxel (60 mg/m2) in combination with carboplatin (AUC = 6,600 mg) resulted in a remarkable reduction in the size of the mass, to less than 50%, and normalized serum CEA. Left upper lobectomy, lymphadenectomy and costectomy were performed. However, no tumor cells were detectable in the ablative specimen pathologically. These findings suggest the efficacy of chemoradiotherapy including docetaxel with carboplatin in patients with large-cell lung cancer.

Antineoplastic Agents↗