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T Kiriyama

Publications and source records attributed to T Kiriyama.

At least 37 records · Page 2Linked to original sources
PubMed1995

Expression of parathyroid hormone-related peptide in human thyroid tumours.

The purpose of this study was to evaluate the distribution of parathyroid hormone-related peptide (PTHrP) in human thyroid tissues. The presence of PTHrP was studied immunohistochemically in 107 consecutive patients with human thyroid tumours. PTHrP expression was revealed in 97.6 per cent of carcinomas, but not in paranodal normal thyroid epithelial cells. Although there were no differences in the incidence of PTHrP positivity among papillary, follicular, and anaplastic carcinoma cases, PTHrP expression levels were correlated with the growth pattern of thyroid cancer. Strong immunopositivity was detected in 67.3 per cent of papillary growth tissues in papillary carcinomas. A tissue growth pattern consisting of colloid-absent follicles had a high incidence of strong immunopositivity irrespective of the histological type of tumour. Anaplastic carcinoma without colloid production also showed strong immunoreactivity in all cases. In contrast, a growth pattern of colloid-rich follicles did not show strong immunopositivity in either papillary or follicular carcinomas. Follicular adenomas showed positive immunostaining in only one case, and no adenomatous goitres showed PTHrP antigens. In situ hybridization and reverse transcription-polymerase chain reaction (RT-PCR) revealed strong PTHrP mRNA in thyroid cancer tissues, but not in normal thyroid tissues. PTHrP expression was not associated with metastasis, calcification, or hypercalcaemia in thyroid cancers. These results suggest that the expression of PTHrP in human thyroids is closely related to the malignant alteration of normal thyroid epithelial cells, especially in the growth pattern of thyroid carcinoma tissues.

Base Sequence↗
PubMed1995

Suppressive doses of thyroxine do not accelerate age-related bone loss in late postmenopausal women.

To examine whether suppressive doses of thyroxine have any adverse effects on bone, we evaluated various bone metabolic markers (lectin-precipitated alkaline phosphatase, osteocalcin, carboxyl-terminal region of type I collagen propeptide, tartrate-resistant alkaline phosphatase, and urinary excretion of hydroxyproline and pyridinium crosslinks), incidence of vertebral deformity, total body and regional (lumbar spine and radius) bone mineral densities (BMDs), and rates of bone loss in 24 late postmenopausal (more than 5 years after menopause) women who were treated with levothyroxine (L-T4) after total thyroidectomy for differentiated carcinoma. Depending on the clinical records, including serum TSH levels measured by immunoradiometric assay, these patients were divided into two groups. One group of patients was given suppressive doses of L-T4 (TSH < 0.1 mU/L, n = 12) and the other group was given nonsuppressive doses of L-T4 (TSH > 0.1 mU/L, n = 12). There was no difference in bone metabolic markers and incidence of vertebral deformity between the groups. In patients with TSH suppression, Z-scores of BMDs calculated from age-matched healthy women (n = 179, aged 55 to 80) were nearly in the zero range of values (0.077 at total body, 0.228 at lumbar spine, and -0.117 at trabecular region of lumbar spine). The rate of bone loss in TSH-suppressed patients (-0.849 +/- 0.605%/year) was not significantly different from that of nonsuppressed patients (-0.669 +/- 0.659). These prospective and cross-sectional data suggest that long-term levothyroxine therapy using suppressive doses has no significant adverse effects on bone.

Aged↗
PubMed1995

Attenuation of postmenopausal high turnover bone loss in patients with hypoparathyroidism.

To elucidate the role of PTH in postmenopausal bone loss, we studied 33 postmenopausal patients who received total thyroidectomy due to thyroid carcinoma. Among these patients, 13 were patients with hypoparathyroid function (HPf), and 20 retained normal parathyroid function (NPf) after thyroidectomy. Bone mineral density (BMD), the rate of BMD loss, and incidence of spinal deformity as well as varying bone metabolic markers were analyzed in all patients. The age-matched BMD was clearly higher, and the incidence of spinal deformity was significantly lower in HPf than in NPf. The rate of BMD loss in HPf was significantly lower than in NPf during the early postmenopausal period (within 5 yr after menopause; mean +/- SD, -0.567 +/- 3.05% vs. -2.49 +/- 1.86%/yr, P < 0.05). In contrast, the rates were similar between the two groups during the late postmenopausal period (> 5 yr after menopause). Bone metabolic markers indicated that an accelerated bone turnover occurred during the early postmenopausal period in NPf, but not in HPf. These results suggest that the hypoparathyroid condition provides protection against age-related bone loss. This is due in part to attenuation of the high turnover bone loss that occurs early in menopause.

Adult↗
PubMed1995

Untreated Graves' disease patients without clinical ophthalmopathy demonstrate a high frequency of extraocular muscle (EOM) enlargement by magnetic resonance.

12 of 17, a significant frequency (71%), of untreated Graves' disease patients with no clinical ophthalmopathy showed extraocular muscle (EOM) enlargement by Magnetic Resonance Imaging (MRI). Enlargement was bilateral in 41% and unilateral in 29% in these patients. Apparent enlargements of EOM were also detected, by MRI, in all of 11 Graves' disease patients with clinical ophthalmopathy, bilateral in 73% and unilateral in 27% of patients in this group. Both group showed the inferior rectus muscle as the most frequently involved (56% and 77% respectively). In 16 patients without autoimmune thyroid disorders or ophthalmopathy who served as normal controls, only 2 of these patients (12%) demonstrated mild EOM enlargement. The severity and patterns of EOM enlargement revealed no correlation with abnormalities in serum thyroid function tests or serum thyroidal autoantibodies. In conclusion, a high frequency of Graves' disease patients without clinical eye signs or symptoms harbor EOM abnormalities, as demonstrated by MRI. This suggests that present clinical examination methods are insufficient to diagnose varying degrees of ophthalmopathy in patients with autoimmune thyroid disorders who do not initially present with clinical ophthalmopathy.

Adolescent↗
PubMed1995

Improvement of hypothyroidism after glucocorticoid replacement in isolated adrenocorticotropin deficiency.

We report a 50-year-old female who suffered from reversible hypothyroidism accompanied by isolated ACTH deficiency. There were no findings indicating a complication of autoimmune thyroiditis. Replacement of maintenance dose of glucocorticoid not only led to improvement of thyroid function, but also caused a transient decrease in T3 and an increase in reverse T3, suggesting that chronic cortisol deficiency may impair thyroid function, and that the maintenance dose, as well as pharmacological doses of glucocorticoids may influence T4 deiodination. The findings of this case suggest that thyroid function should be re-evaluated to avoid unnecessary replacement of thyroid hormone, a few months after glucocorticoid replacement.

Adrenocorticotropic Hormone↗
PubMed1995

Parathyroid hormone-related peptide expression in endocrine tumors.

Parathyroid hormone-related peptide (PTHrP) expression is associated with the histological type in pituitary tumor, but not in thyroid carcinoma. However invasive and metastatic tumors showed intense PTHrP staining in both pituitary and thyroid tumors. Analysis of the established metastatic rat pituitary tumor cell line showed that PTHrP plays a crucial role in in vivo cell proliferation closely related to worsening of malignant transformation and neovascularization in a paracrine fashion.

Animals↗
PubMed1994

Acquired nephrogenic diabetes insipidus secondary to distal renal tubular acidosis and nephrocalcinosis associated with Sjögren's syndrome.

A 52-year-old woman was referred to our hospital because of 16-year history of polyuria and polydipsia. Hyposthenuria, hyperchloremic metabolic acidosis and the inabilities to acidify the urine after acid-loading test and to concentrate the urine in responses to water-deprivation and antidiuretic hormone administration allowed us to diagnose renal tubular acidosis and nephrogenic diabetes insipidus. Radiographic examinations revealed bilateral nephrocalcinosis. The patient was also found to have clinical and laboratory findings characteristic for Sjögren's syndrome. Thus the longstanding, poorly monitored distal renal tubular acidosis associated with Sjögren's syndrome was considered to result in very rare renal complications-nephrocalcinosis and nephrogenic diabetes insipidus. In patients with renal tubular acidosis and/or nephrogenic diabetes insipidus of unknown etiology, therefore, Sjögren's syndrome should be considered as one of primary disorders.

Acidosis, Renal Tubular↗
PubMed1994

Dexamethasone regulation of parathyroid hormone-related protein (PTHrP) expression in a squamous cancer cell line.

Dexamethasone regulation of PTHrP expression has been studied in an epidermal squamous cancer cell line COLO 16, which secretes immunoreactive PTHrP into conditioned medium. Dexamethasone was found to suppress PTHrP expression in a time- and dose-dependent manner, which was reversible upon removal of dexamethasone. The half-maximal effective concentration of dexamethasone was 1 nM and an effect of dexamethasone on PTHrP mRNA was first observed after 2 h of treatment, with maximal inhibition by 6 h. Dexamethasone action on PTHrP expression was steroid specific since progestin, 5alpha-dihydroxytestosterone and oestrogen did not regulate PTHrP expression in COLO 16 cells. The gluocorticoid/progesterone receptor antagonist RU486 inhibited the dexamethasone effect, indicating glucocorticoid receptor-mediated regulation of PTHrP expression. The half-life of PTHrP mRNA in COLO 16 cells was approximately 120 min and was not altered by treatment of cells with dexamethasone. Nuclear run-on assays revealed that dexamethasone reduced PTHrP gene transcription in COLO 16 cells. Transient transfection assays with a series of reporter gene constructs encompassing 3.5 kb of the 5' end of the PTHrP gene failed to identify a region of the gene responsible for glucocorticoid down-regulation. PCR of reverse-transcribed RNA from COLO 16 cells revealed that dexamethasone down-regulated transcripts driven from all three promoters (i.e., the TATA promoters 5' to exons I and IV and the GC-rich promoter 5' to exon III) of the human PTHrP gene.

Carcinoma, Squamous Cell↗
PubMed1994

[Personal identification of a skull by a complete denture--application of superimposition and X-ray computed tomography analysis].

Personal identification from dentures is one of the main method used in the field of forensic odontology. When examining whether a denture left at investigation scene belongs to an unknown set of skeletal remains, it is not difficult to establish identity between the partial denture and the jaw of the skull by comparison of the number and kind of defective teeth and the degree of fit of the retainer to the abutment teeth. However, it is more troublesome to demonstrate identity between a complete denture and a skull since the morphological characteristics of the denture base, including the arrangement of the artificial teeth, have to be compared with those of the surfaces of the jawbones, which cannot be observed from the outside. In cases like this, superimposition and X-ray computed tomography are effective for establishing proof of identity. The method of superimposition involves taking an impression of the upper jaw to prepare a plaster model. A photograph of the denture applied to the plaster model is then taken and another photograph of the plaster model is obtained after removal of the denture under the same conditions. The former photo is printed on a transparent film and then superimposed on the latter. This method is useful for comparison between the arrangement of artificial teeth and the crest of the alveolar ridge, and between the shape of the polished (external) surface of the denture and the shape of the alveolar ridge.(ABSTRACT TRUNCATED AT 250 WORDS)

Cephalometry↗
PubMed1993

Transforming growth factor beta stimulation of parathyroid hormone-related protein (PTHrP): a paracrine regulator?

The regulation of PTHrP expression and production by transforming growth factor-beta (TGF beta) has been investigated in an epidermal squamous cancer cell line COLO 16. TGF beta 1 treatment increased steady-state levels of PTHrP mRNA and concentrations of PTHrP immunoreactivity in conditioned medium in a time- and dose-dependent manner with a half-maximal effect at 40 pM. An effect of TGF beta 1 on PTHrP mRNA was observed first after 4 h treatment and continued to increase up to 48 h with a concomitant increase in PTHrP immunoreactivity in the culture medium. TGF beta 1 was found to stabilize PTHrP mRNA as assessed by actinomycin C1 experiments. In addition, a direct effect of TGF beta to increase PTHrP transcription was indicated by nuclear run-on and transient transfection experiments using a CAT promoter/expression construct encompassing the region -1100 bp to -20 bp from the initiating AUG of the human PTHrP gene. The conditioned medium from COLO 16 cells was also shown to contain both latent and active TGF beta at concentrations of 160 pM and 16 pM, respectively, in 72 h conditioned medium. A neutralizing antibody to TGF beta 1 (and TGF beta 2) decreased the level of immunoassayable PTHrP in the medium.

Base Sequence↗
PubMed1993

[Anesthesia for a patient with red cell aldolase deficiency].

Aldolase deficiency of red blood cell is a rare cause of hereditary hemolytic anemia and now there exists only three patients in the world. We had a 24-year-old man operated on for gallbladder stone secondary to this uncommon disease. He underwent a cholecystectomy under general anesthesia combined with thoracic epidural block, using isoflurane, fentanyl, vecuronium, midazolam and lidocaine. During the surgery serum concentrations of bilirubin, free hemoglobin and LDH showed no change, suggesting a lower incidence of drug-induced hemolysis in the case of aldolase deficiency than in other enzyme deficiency. This fact also provides a useful guide to the choice of anesthetics and related agents. In the postoperative period, however, we found a hemolytic response to fever with a drop in hemoglobin level to 2.5 g.dl-1. Aldolase activity of his red cell is heat labile and an increase in body temperature may aggravate a disturbance in the glycolytic pathway leading to hemolytic crisis. It is thus important to prevent the body temperature from rising when a patient is suffering from hemolytic anemia due to red cell aldolase deficiency.

Adult↗
PubMed1991

Mechanism of action of newly developed vitamin D analogue.

26,27-F6-1,25(OH)2D3 has a higher potency both in vivo and in vitro systems, and longer duration of action in vivo, instead of almost equal binding to 1,25(OH)2D3 receptor and comparatively short serum half-life. To date, the mechanism of higher action is not known, but using these analogues as a mirror we might be able to elucidate the mechanism of action or the metabolism of the kidney hormone, 1,25(OH)2D3.

Animals↗
PubMed1991

Effect of a highly potent fluoro analog of 1,25-dihydroxyvitamin D3 on human bone-derived cells.

The fluorine introduced analog of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], 26,26,26,27,27,27-hexafluoro-1,25-dihydroxyvitamin D3 [26,27-F6-1,25-(OH)2D3] is 5-10 times more potent than 1,25-(OH)2D3 in vitamin D-deficient rats and chicks. In this study we established cultures of human bone cells in order to elucidate the mechanisms responsible for the higher activity of this compound. The effects of 26,27-F6-1,25-(OH)2D3 and 26,26,26,27,27,27-hexafluoro-1,23(S),25-trihydroxyvitamin D3[26,27-F6-1,23(S),25-(OH)3D3], the postulated main metabolite of 26,27-F6-1,25-(OH)2D3, were assessed by the response of alkaline phosphatase (ALP) activity. 26,27-F6-1,25-(OH)2D3 increased ALP activity in a dose-related fashion, from a concentration of 10(-11) M and caused a 3-fold elevation at a concentration of 10(-9) M. To achieve the same stimulating effect on ALP activity, the required dose of 26,27-F6-1,25-(OH)2D3 was 100 times less than that of 1,25-(OH)2D3. Analysis of the receptors of these cells revealed that they have specific receptors for 1,25-(OH)2D3, which have a dissociation constant of 0.9 x 10(-10) M. The competitive binding assays of 26,27-F6-1,25-(OH)2D3 on these receptors showed that binding ability of 26,27-F6-1,25-(OH)2D3 is almost the same as that of 1,25-(OH)2D3. Therefore, receptor binding affinity does not account for the higher potency of 26,27-F6-1,25-(OH)2D3. The trihydroxylated compound, 26,27-F6-1,23(S),25-(OH)3D3 revealed almost the same stimulatory activity on ALP activity in these cells. The most likely explanation for the higher activity of 26,27-F6-1,25-(OH)2D3 than 1,25-(OH)2D3 is that 26,27-F6-1,25-(OH)2D3 is metabolized to 26,27-F6-1,23(S),25-(OH)3D3, which has almost the same activity as 26,27-F6-1,25-(OH)2D3 in target tissues, whereas 1,25-(OH)2D3 is degraded to less active metabolites such as 1,24,25-(OH)3D3.

Alkaline Phosphatase↗
PubMed1989

Biological activity of 26,26,26,27,27,27-hexafluoro-1,25-dihydroxyvitamin D3 in the chick.

A newly synthesized fluorinated analogue of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), 26,26,26,27,27,27-hexafluoro-1,25-dihydroxyvitamin D3 (26,27-F6-1,25-(OH)2D3) has been compared with 1,25(OH)2D3 as to its biological activity in vitamin D-deficient chicks. One day-old, white Leghorn cockerels were fed a rachitogenic diet for 5 weeks. They were then given vehicle or 32.5, 130 or 325 pmol of 26,27-F6-1,25(OH)2D3 or 1,25(OH)2D3 in a solution of propylenglycol:ethanol (95:5 v/v) sc every day for 2 weeks. Twenty-four hours after the last dose, the animals were sacrificed and their femurs were removed. 26,27-F6-1,25(OH)2D3 was more active than 1,25(OH)2D3 in stimulating growth, healing of rachitic cartilage visualized by soft X-ray radiography, elevation of serum inorganic phosphorus, and mineralization of rachitic bone. These biological differences between two compounds were observed only for the dose of 130 pmol. However, this fluorinated compound has less binding ability than 1,25(OH)2D3 to fetal chick intestinal cytosol receptors. The mechanism of the higher potency of this analogue is still unknown, but its affinity to the 1,25(OH)2D3 receptor does not account for the higher activity. Since 26-hydroxylation can be postulated as the inactivation step in vitamin D metabolism, these results suggest that the reason for increased activity of this fluorinated analogue is most likely its slower metabolism.

Animals↗
PubMed1989

[Effect of estrogen treatment on antithrombin III activity in patients with carcinoma of the prostate].

Since reduced antithrombin III (AT III) activity are associated with increased risk of thromboembolism, we have determined it in 39 patients with prostatic carcinoma. Pre-treatment levels were determined in 24 patients, 6 additional patients with prostatic carcinoma on estrogen treatment and 9 patients on chlormadinone acetate (CMA) therapy. In 12 of 24 patients we studied AT III levels before and after estrogen therapy was initiated. A significant decrease in AT III activity of 23.5% was found after one month on estrogen treatment, the patients on low doses of estrogen. Recovery of the levels of AT III was found after 6 months treatment even in in 5 of 6 patients who had shown depression of AT III levels initially. CMA treatment did not cause its depression. AT III levels was not connected with the stage of the disease or age of the patient.

Aged↗
PubMed1989

[Adjuvant chemotherapy after cystectomy of bladder tumor].

Adjuvant chemotherapy mainly consisting of cisplatin, adriamycin and mitomycin C was administered to 17 patients after cystectomy for bladder tumor (chemotherapy group). Seventeen concurrently treated patients did not receive adjuvant chemotherapy (control group). From the comparison of survival curves of these two groups, the following results were obtained. 1) Survival curves of the patients in all stages did not differ significantly between chemotherapy and control groups. 2) Among patients in stage pT3, pT4 and/or N+, survival of the chemotherapy group seemed to have some advantage over that of the control group, but the survival curves did not differ significantly between these two groups. 3) Among patients in N+, survival of the chemotherapy group was far better than that of the usual cases. Review of the literature on adjuvant chemotherapy after cystectomy for bladder tumor revealed the necessity of randomized study to determine whether adjuvant chemotherapy is effective.

Aged↗