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Biomedical subjects

M Shiraki

Publications and source records attributed to M Shiraki.

At least 145 records · Page 8Linked to original sources
PubMed1987

Reduced occurrence of vertebral crush fractures in senile osteoporosis treated with 1 alpha (OH)-vitamin D3.

To examine whether the administration of 1 alpha (OH)-vitamin D3 (1 alpha (OH)D3) could prevent the occurrence of vertebral crush fractures in senile osteoporosis, crush fractures of the thoracic or lumbar spine in senile osteoporosis treated with 1 alpha (OH)D3, 1.0 microgram/day (22 cases), 1 alpha (OH)D3 1.0 microgram/day + Ca 1.0 g/day (16 cases) or Ca 1.0 g/day (23 cases) were compared with those in non-treated controls (25 cases). The average treatment periods were 1.7 +/- 0.7 years in the 1 alpha (OH)D3 group, 2.1 +/- 1.0 years in the 1 alpha (OH)D3 + Ca group and 1.7 +/- 0.9 years in the Ca group. Occurrence of spinal crush fractures per 1000 patient years was significantly less in the 1 alpha (OH)D3 + Ca group (P less than 0.01) than in the non-treated control group. These findings suggest that administration of 1 alpha (OH)D3 is effective in preventing the occurrence of pathological fractures in senile osteoporosis.

Aged↗
PubMed1986

An enzyme immunoassay for osteocalcin.

A sensitive and specific enzyme immunoassay for bovine osteocalcin was developed with the use of enzyme-labeled antigen. Bovine osteocalcin was conjugated with beta-D-galactosidase for use in the immunoassay. The minimum amount of osteocalcin detectable by this method was 5-10 pg/assay. The enzyme immunoassay could detect immunoreactive osteocalcin levels in normal human sera, giving a value of 6.58 +/- 0.72 ng/ml (mean +/- SE of 16 human subjects). The correlation coefficient between the levels measured by this method and radioimmunoassay was 0.94.

Animals↗
PubMed1986

Parathyroid hormone stimulates phosphate efflux through an apparently adenosine 3',5'-monophosphate-independent process in rat parotid cell aggregates.

The effects of PTH on phosphate fluxes and cAMP and protein secretion in rat parotid cell aggregates were studied. PTH-(1-34) as well as PTH-(1-84) stimulated phosphate efflux in a dose-dependent [5 X 10(-7) to 7 X 10(-6) M for human (h) PTH-(1-34), 2 X 10(-7) to 5 X 10(-6) M for bovine (b) PTH-(1-34), and 3.8-114 U/ml for bPTH-(1-84)] and time-dependent [detectable by 15-30 min after incubation with N-terminal PTH and 30-45 min after incubation with bPTH-(1-84)] manner. The effect of PTH on phosphate efflux was saturable, with maximal stimulation at 10(-6) M above for N-terminal PTH and at 57.8 U/ml and above for bPTH-(1-84). Half-maximal stimulation of phosphate efflux by hPTH-(1-34), bPTH-(1-34), and bPTH-(1-84) was achieved at 5.7 X 10(-7) M, 10(-7) M, and 40 U/ml, respectively. Neither bPTH-(1-34) nor bPTH-(1-84) had any effect on phosphate uptake by parotid cell aggregates at the concentrations examined. bPTH-(1-34) and bPTH-(1-84) also stimulated amylase secretion, with a significant increase in cAMP production (70-90% over basal). However, (BU)2cAMP did not stimulate phosphate efflux. Isoproterenol (10(-5) M) markedly stimulated cAMP production and amylase secretion without causing a significant increase in phosphate efflux. Oxidized bPTH-(1-84) and the C-terminal fragment of hPTH had no stimulating effect on phosphate efflux. The present results suggest, therefore, that PTH may play an important role in regulating rat parotid cell phosphate metabolism through an apparently cAMP-independent process.

Amylases↗
PubMed1986

Hypercalcemia due to spontaneous hemorrhage in a parathyroid adenoma during recovery from acute renal failure.

A 89-year-old woman showed transient and mild hypercalcemia (11.0 mg/dl) at the phase of recovery from acute renal failure. Serum PTH level elevated to 2.1 ng/ml when hypercalcemia was observed, and decreased to 1.1 ng/ml. Autopsy study revealed the bleeding within parathyroid adenoma. The transient and mild hypercalcemia seen in the patient was considered as the result of the bleeding within parathyroid adenoma. This unusual manifestation of parathyroid adenoma, bleeding, usually causes hypercalcemic crisis. The mild hypercalcemia observed in this patient despite of bleeding into parathyroid adenoma might be due to old age of the patient and the existence of renal failure in the patient.

Acute Kidney Injury↗
PubMed1985

Evaluation of bleomycin, chlorozotocin, MGBG, and bruceantin in patients with advanced soft tissue sarcoma, bone sarcoma, or mesothelioma.

Patients with objectively measurable soft tissue sarcoma, bone sarcoma, or mesothelioma who had failed at least one prior chemotherapy regimen received either bleomycin (20 U/M2 i.v. day 1 each week), chlorozotocin (150 mg/M2 i.v. q6 weeks), MGBG (500 mg/M2 i.v. each week, escalated in 50 mg/M2 weekly increments to a maximum dose of 700 mg/M2), or bruceantin (5.5 mg/M2 days 1, 8, 15, and 22, with cycles repeated every 6 weeks). One hundred eighty patients were evaluable: 53 on bleomycin, 51 on chlorozotocin, 38 on MGBG, and 38 on bruceantin. Two partial responses resulted from bleomycin, and one each from chlorozotocin and MGBG. Both responders on bleomycin had mesothelioma. Seventy-four percent of the patients were of ECOG performance status 0 or 1, and over half on each arm had moderate or worse toxicity. At these doses and schedules, none of the four drugs tested was active against previously treated sarcomas. Bleomycin, however, should be considered for further evaluation in mesothelioma patients.

Adolescent↗
PubMed1985

Platelet thromboxane synthesizing activity in non-insulin-dependent diabetes: correlation with diabetic retinopathy and diabetic treatment.

Since elevated thromboxane A2 synthesis could be expected to lead to microvascular injury in diabetic patients, it is important to determine the relationship between thromboxane A2 synthesis and diabetic microvascular complications. In the present study, the activity of thromboxane A2 synthesis in platelets was assessed in 57 Type 2 (non-insulin-dependent) diabetic patients by measuring the conversion of exogenously added 14C-arachidonic acid into 14C-thromboxane B2. The activity of thromboxane synthesis was significantly higher in diabetic patients than in 16 age-matched control subjects (2.61 +/- 0.07 vs 1.95 +/- 0.12 microgram . 10(9) platelets-1 . 3 min-1, respectively, p less than 0.001). When the diabetic patients were divided into three groups (nil, background, and proliferative retinopathy) on the basis of severity of diabetic retinopathy, there was a trend to increased thromboxane synthesizing activity as diabetic retinopathy develops. However, no statistically significant changes were demonstrated among these three groups. In the diabetic patients, a positive correlation was found between thromboxane synthesizing activities and glycosylated hemoglobin values (biochemical indicator of long-term glycemic control), but not between the activities and plasma glucose levels. To ascertain the effect of desirable diabetic treatment on thromboxane synthesizing activity in platelets, 9 newly diagnosed patients and 6 poorly controlled patients were examined. During treatment, all patients had declining plasma glucose and glycosylated hemoglobin levels. Thromboxane synthesizing activities in 6 patients treated by insulin decreased significantly during treatment (3.16 +/- 0.17 to 2.49 +/- 0.22 microgram . 10(9) platelets-1 .3 min-1, p less than 0.01), but 9 diabetic patients treated by diet or sulphonylureas still maintained their elevated thromboxane synthesizing activity levels (2.76 +/- 0.24 to 2.66 +/- 0.25 microgram . 10(9) platelets-1 .3 min-1,NS). These results suggest that the increased thromboxane synthesizing enzyme system is involved in the abnormal platelet function in diabetes independently of diabetic retinopathy, and that appropriate metabolic control using insulin might be successful in lowering the increased thromboxane synthesizing activity.

Aged↗
PubMed1985

Long-term treatment of postmenopausal osteoporosis with active vitamin D3, 1-alpha-hydroxycholecalciferol (1 alpha-OHD3) and 1, 24 Dihydroxycholecalciferol (1, 24(OH)2D3).

The effects of active vitamin D3 analogues on radial mineral content (RMC) in postmenopausal osteoporosis were examined. Seventy eight subjects with postmenopausal osteoporosis were divided into 5 groups; Group 1 (n = 23) as the control group and Group 2 (n = 27), Group 3 (n = 8), Group 4 (n = 9) and Group 5 (n = 11) which were given 1 microgram of 1, 24(R) (OH)2D3 per day, 1 microgram of 1, 24(S)(OH)2D3 per day, 0.5 and 1 microgram of 1 alpha-OHD3 per day for 6 to 24 months, respectively. After 3-months administration of these drugs, RMC values were significantly increased in Groups 2 (102.8 +/- 1.8%), 4 (103.9 +/- 3.3%) and 5 (114.2 +/- 3.6%), when compared with the controls (97.9 +/- 2.4%). RMC in Group 3 (97.9 +/- 2.4%) was not significantly different from the control value. The administration of 1 alpha-OHD3 caused in increase in RMC in a dose-related manner. A rapid decrease in RMC was observed after withdrawal of the treatment in Groups 2, 4, and 5. A subsequent increase in RMC was observed after re-administration of 1 alpha-OHD3 and 1, 24(R)(OH)2D3. Serum Ca levels were increased in the group treated with 1, 24(R)(OH)2D3 and were decreased after the discontinuation of 1 alpha-OHD3 administration. Serum A1-P activity was decreased by treatment with 1 alpha-OHD3 (1 microgram per day) and a subsequent increase was observed in both groups treated with 1, 24(R)(OH)2D3 and 1 alpha-OHD3. Serum PTH levels were decreased by the administration of 1, 24(R)(OH)2D3 and 1 alpha-OHD3. In the group treated with 1 microgram of 1 alpha-OHD3 per day, hypercalcemia (2 out of 11 cases and these patients took calcium tablets) and an increase in BUN (1 out of 2 hypercalcemic patients) were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗