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Biomedical subjects

M Shiraki

Publications and source records attributed to M Shiraki.

At least 73 records · Page 4Linked to original sources
PubMed1995

[Bone mineral density in postmenopausal elderly women with type 2 diabetes].

We measured lumbar bone mineral density (L2-4 MBMD) in the postmenopausal elderly diabetic women and made comparisons with age-matched controls in terms of the age, body mass index (BMI) and % BMD of age-matched. In addition we evaluated the correlation between BMD and menarche age, menopause age, HbA1c, serum calcium, serum phosphate, serum alkaline phosphatase (S-Alp) and the ratio of urine calcium to urine creatinine (UCa/Cr). Moreover we divided non-insulin dependent diabetic patients (NIDDM) into two groups; the high BMD group and the low BMD group. Serum Alp and the ratio of UCa/Cr were compared in these two groups. The relationships between regimen of therapy and BMD were also analyzed in female NIDDM. There were no significant differences of BMD and background factors between controls and NIDDM. The ratio of UCa/Cr in the high BMD group were significantly less than that in low BMD group (p < 0.05). BMD in NIDDM with retinopathy was lower, but not significantly, than that in NIDDM without retinopathy. The methods of therapy for NIDDM such as diet alone, an oral hypoglycemic agent and insulin did not influence BMD in elderly postmenopausal diabetics. These results indicated that BMD in elderly postmenopausal diabetics are dependent on UCa/Cr and retinopathy.

Aged↗
PubMed1995

[Time course changes in bone metabolic markers after menopause--a cross-sectional study].

To clarify the clinical significance of the measurement of bone metabolic markers in postmenopausal subjects, a cross-sectional study of 546 healthy women (215 premenopausal, 164 bilateral oophorectomized and 167 natural menopausal) was conducted. All the subjects had their lumbar bone (L2-4 mineral density measured by means of DEXA. Bone metabolic markers (bone formation markers: serum alkaline phosphatase, osteocalcin and intact osteocalcin; bone resorption markers: urine excretion of hydroxyproline, pyridinoline and deoxypyridinoline) were also evaluated. After dividing the subjects according to the length of time after menopause, the time course changes in the Z-score values for bone metabolic markers were calculated. A triphasic pattern of lumbar bone loss was seen: there was a rapid phase in the first 5 years after menopause, a plateau phase in the second 5 years and a slow phase beginning 10 years menopause. The changes in bone metabolic markers coincided closely with the rapid phase of bone loss. In the plateau and slow phases, there were no markers which significant changed greatly. One possible clinical application of bone metabolic markers is in assessing the results of treatment for postmenopausal osteoporosis.

Adult↗
PubMed1994

Effects of 1 alpha,25-dihydroxyvitamin D3 on macrophage colony-stimulating factor production and proliferation of human monocytic cells.

1 alpha-25-Dihydroxyvitamin D3 [1 alpha,25(OH)2D3] stimulates the proliferation of human monocytes in vitro. In the present study, we investigated a possible role of macrophage colony-stimulating factor (M-CSF) in 1 alpha,25(OH)2D3-induced proliferation of human circulating monocytes and the effects of 1 alpha,25(OH)2D3 on M-CSF production by human monocytic cells. Both 1 alpha,25(OH)2D3 and recombinant human M-CSF increased 2.5-fold the nucleus number of human circulating monocytes on day 6 of the culture. These effects were inhibited by antihuman M-CSF antibody as well as by anti-c-fms antibody, although these antibodies themselves did not affect the nucleus number when added to control culture. These results indicated that M-CSF is required for 1 alpha,25(OH)2D3-stimulated monocyte proliferation. In addition, 1 alpha,25(OH)2D3 stimulated M-CSF secretion from human circulating monocytes. Secretion and mRNA expression of M-CSF by 12-0-tetradecanoylphorbol-13-acetate (TPA)-treated THP-1 cells (human monocytic leukemia cell line) and TPA-treated HL-60 cells (human promyelocytic leukemia cell line) were also increased by 1 alpha,25(OH)2D3. M-CSF secretion from TPA-treated THP-1 cells was increased by 1 alpha,25(OH)2D3 in a dose-dependent and metabolite-specific manner. The present study demonstrates that 1 alpha,25(OH)2D3 is a potent stimulator for M-CSF production by human monocytic cells and that the proliferative effect of 1 alpha,25(OH)2D3 on human monocytes may be attributed, at least in part, to the stimulated secretion of M-CSF.

Blotting, Northern↗
PubMed1994

Effects of 1 alpha-hydroxyvitamin D3 on lumbar bone mineral density and vertebral fractures in patients with postmenopausal osteoporosis.

The effects of 1 alpha-hydroxyvitamin D3 [1 alpha(OH)D3] on bone mineral density, fracture incidence, and bone metabolism were evaluated by a double-blind, placebo-controlled study. Eighty postmenopausal osteoporotic Japanese women (71.9 +/- 7.3 years, mean +/- SD) were randomly assigned to 1 microgram of 1 alpha(OH)D3 daily or inactive placebo for 1 year. All patients were given supplemental calcium (300 mg of elemental calcium daily). Lumbar (L2-L4) bone mineral density (BMD) determined by dual energy X-ray absorptiometry increased 0.65% with 1 alpha(OH)D3 treatment and decreased 1.14% with placebo (P = 0.037). BMD in both the femoral neck and Ward's triangle did not yield any significant differences between the two groups, whereas trochanter BMD in the 1 alpha(OH)D3-treated group increased 4.20% and decreased 2.37% with placebo (P = 0.055). X-ray analysis demonstrated that new vertebral fractures occurred in two patients with 1 alpha(OH)D3 and in seven patients with placebo. The vertebral fracture rate in the treated group was significantly less (75/1000 patient years) than in the control group (277/1000 patient years; P = 0.029). Hypercalcemia (12.1 mg/100 ml) occurred in one patient receiving 1 alpha(OH)D3; however, the serum calcium level in this patient promptly decreased to the reference range after cessation of the treatment. There were no significant changes in serum creatinine level in either group. A significant increase in urinary excretion of calcium was found but there was no significant change in urinary excretion of hydroxyproline in the treated group. The serum level of bone-derived alkaline phosphatase activity significantly decreased by -26 +/- 26 (mU/ml) after the treatment (P = 0.003).(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗
PubMed1994

Assessment of bone density in the distal radius with computer assisted X-ray densitometry (CXD).

A modified and improved radiographic absorptiometry of the distal radius which enables on-site analysis, called computer assisted X-ray densitometry (CXD), was evaluated from the viewpoint of quality assessment. Its precision and the correlation with dual energy X-ray absorptiometry (DXA) was evaluated in 12 volunteers (mean age 44.7 years). The profile of CXD-measured radial bone mineral density (RBMD) from 142 subjects (75 premenopausal and 67 postmenopausal women, mean ages 44.9 and 50.6 years, respectively) were compared with previous data by other methodologies of bone mineral analysis. The intra-assay coefficient of variation (CV) was 0.617%, the inter-assay CV was 2.064%, and the inter-observer CV was 0.673%. The correlation between CXD-measured RBMD and DXA-measured RBMD was of statistical significance (r2 = 0.733, P < 0.01). The correlation of CXD-measured RBMD with age, height or weight corresponded well with previous reports. CXD-measured RBMD and DXA-measured vertebral bone mineral density (VBMD) also had a significant positive correlation, but their correlation was not so close (r2 = 0.149, P < 0.01). The discriminative ability of osteoporosis by CXD was of acceptable level (odd's ratio = 5.72, P < 0.05), when assessed by comparison with bone dystrophy score (BDS) on the plain vertebral radiogram. Although some problems remain in technical standardization, CXD could be an easy, inexpensive, and widely applicable alternative of non-weight bearing cancellous bone densitometry.

Absorptiometry, Photon↗
PubMed1994

[Calcitonin physiologically regulates the postmenopausal bone loss and possibly inhibits the bone loss in fast losers].

To study the correlation between the basal serum calcitonin level and L2-4 bone mineral density (BMD), a cross sectional study of 384 healthy subjects (106 premenopausal, 88 perimenopausal and 109 postmenopausal subjects) and a longitudinal study of 42 oophorectomized subjects were conducted. A positive correlation was found in perimenopause (r = 0.219, p = 0.040) but not in premenopause (r = 0.069, p = 0.4898) and postmenopause (r = 0.141, p = 0.0554) in a cross sectional study. The percent reduction in L2-4BMD compared to the baseline also correlated with preoperative calcitonin levels at 6 months after oophorectomy (r = 0.333, p = 0.0442), but not significantly at 12 months (r = 0.224, p = 0.27). These data suggest that the basal calcitonin level correlates to L2-4BMD only at perimenopause or in the early postoophorectomized period when bone turnover is accelerated and bone resorption seems to be faster than bone formation. In addition the premenopausal basal calcitonin level may be an indicator of the fast loser after menopause.

Bone Density↗
PubMed1994

[Basic aspects of bone metabolic markers].

Bone formation and bone resorption are altered in most metabolic bone diseases. Recent advances in measurement of bone metabolic markers arrows as the non-invasive investigation of bone metabolic balance. The rate of formation or degradation of the bone matrix can be assessed by the measurement of bone specific proteins and it's degradative products. Among the posturated products, osteocalcin, carboxy-terminal propeptide of type I collagen (PICP) are considered to be more specific indices to know the osteoplastic function. On the other hand, pyridinoline or deoxypyridinoline in urine strongly reflects bone resorption rate. However some criticisms still exist in the evaluation of serum or urinary levels of bone metabolic markers, especially in formation markers. In adults, bone formation marker such as osteocalcin negatively correlated with their bone mineral density. On the other hand, in children, osteocalcin positively correlated with height velocity. Therefore we have to pay special attention to dysfunction of osteoblast, such as retarded calcification in evaluation of serum level of bone formation markers.

Biomarkers↗
PubMed1994

[Bone metabolic markers in osteoporosis].

Since osteoporosis has been defined as "state of low bone mass", the bone mineral measurement has been utilized as a golden standard. However some limitations in bone mineral measurement such as expensive machine, very small extent in bone mineral change and/or required long term observation to detect significant change in bone mass, are prohibited extensive use. On the other hand, recent advances in the measurement of bone metabolic markers arrows us to utilize in the diagnosis of osteoporosis as well as in the monitoring of drug efficacy for osteoporosis. Especially in the monitoring of osteoporosis under some treatment, the magnitude of the change in bone metabolic markers are about 10 times higher than that in bone mineral density. Therefore, the measurement of bone metabolic markers may be utilized more widely in the clinical field of not only osteoporosis but also the other metabolic bone diseases in near future.

Amino Acids↗
PubMed1994

Levels of parathyroid hormone and calcitonin in serum among atomic bomb survivors.

To examine the potential causes of increased levels of calcium in serum with increasing dose of atomic bomb radiation, which was obtained from the previous preliminary analysis, levels of parathyroid hormone (PTH) and calcitonin in serum were examined among 1459 subjects in Hiroshima and Nagasaki. A significant effect of radiation on levels of calcium, PTH and calcitonin in serum was found, even after patients with hyperparathyroidism were excluded. The level of calcium in serum increased with radiation dose; this can be explained partly by the increase in the level of PTH with radiation dose. However, the dose effect on calcium remained even after adjustment for PTH, calcitonin and confounding factors such as renal function, serum albumin level and medication. Parathyroid hormone increased initially by 6.8% per gray, but the dose response leveled off after about 1 Gy. The level of calcitonin increased with radiation dose, probably in part due to feedback mechanisms stimulated by the increase in calcium. However, after adjustment for the level of calcium, the increase in the level of calcitonin with dose was still found. Although the etiological mechanisms of the effect of radiation on serum levels of calcium, PTH and calcitonin are unclear, radiation exposure may affect secretion of PTH and calcitonin and regulation of calcium a long time after atomic bomb exposure.

Adult↗
PubMed1993

Vitamin K2 (menatetrenone) inhibits prostaglandin synthesis in cultured human osteoblast-like periosteal cells by inhibiting prostaglandin H synthase activity.

Prostaglandin (PG) E2, a potent bone-resorbing agent, is synthesized in osteoblast-like cells. Since vitamin K reportedly plays an important role in bone metabolism, we investigated the effects of vitamin K2 (menatetrenone) on PGE2 production by human osteoblast-like periosteal cells. In cells incubated with menatetrenone (1 microgram/mL = 2.25 x 10(-6) M) for 2 days, PGE2 production was reduced to 50% of that in untreated control cells. This inhibition was dose and time dependent for up to 10 micrograms/mL and 20 days, respectively, and involved two major steps. In one of these menatetrenone at doses of 0.5-10 micrograms/mL dose dependently inhibited the calcium ionophore A23187-induced release of arachidonic acid (AA) from membrane phospholipids, and in the other the conversion of AA to PG was inhibited, as evidenced by the PG-synthesizing activity in the homogenates of menatetrenone-treated cells with AA being lower than that in untreated cells. The inhibitory effect was almost identical to that for PG production. The PG synthesizing activity in cell homogenates was inhibited only by a high concentration of menatetrenone (10 micrograms/mL) when this was added directly. Menatetrenone (1 microgram/mL) also inhibited 52% of the purified PGH synthase activity from a ram seminal vesicle. This study shows that menatetrenone inhibited PGE2 release from cells by inhibiting both PG production steps, AA release from the membrane and PG synthesizing activity with AA. Inhibition of PGE2 production by menatetrenone might be important in improving bone metabolism.

Adult↗
PubMed1993

Menatetrenone inhibits bone resorption partly through inhibition of PGE2 synthesis in vitro.

We studied the effect of menatetrenone, a vitamin K2 homolog, on bone resorption stimulated by interleukin-1 alpha (IL-1 alpha), prostaglandin E2 (PGE2), parathyroid hormone (PTH), and 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. Bone-resorbing activity was assessed by measurement of calcium and hydroxyproline in the media and calvariae. IL-1 alpha (0.1-100 U/ml), 1,25-(OH)2D3 (10(-10)-10(-7) M), PGE2 (10(-9)-10(-6) M), and PTH (3 x 10(-8)-3 x 10(-7) M) dose dependently increased the levels of calcium and hydroxyproline in the medium. Indomethacin (10(-6) M) completely inhibited bone resorption induced by IL-1 alpha and partially inhibited bone resorption induced by 1,25-(OH)2D3. However, indomethacin did not affect the action of PGE2 or PTH. Menatetrenone (3 x 10(-6)-3 x 10(-5) M) inhibited the bone resorption induced by IL-1 alpha (2 U/ml), PGE2 (10(-7) M), PTH (3 x 10(-7) M), and 1,25-(OH)2D3 (3 x 10(-10) M) in a dose-dependent manner. Menatetrenone also inhibited the PGE2 production stimulated by IL-1 alpha. These results indicate that menatetrenone may inhibit bone resorption through at least two different mechanisms; one possibly is an inhibitory effect on prostaglandin production.

Animals↗
PubMed1993

Secretion of osteocalcin and its propeptide from human osteoblastic cells: dissociation of the secretory patterns of osteocalcin and its propeptide.

Specific immunoassay systems for intact human osteocalcin (I-OC) and its 26-residue propeptide have been newly developed to assess their usefulness as biochemical markers of bone metabolism. Using human cultured osteoblastic periosteal cells, we monitored 24 h secretion of these molecules from the osteoblastic cells and also examined the deposition of Ca, P, and I-OC on the extracellular matrix. At day 5, both I-OC and its propeptide were secreted by osteoblastic cells in a concentration-dependent manner by treatment with 1,25-(OH)2D3. This propeptide was not detected in the serum of adult subjects but was detected in the serum of normal children, which confirmed this in vitro result of propeptide secretion. The secretion of I-OC into medium transiently decreased at day 11, when the rapid accumulation of I-OC, Ca, and P, namely mineralization, was observed on the extracellular matrix of osteoblastic cells, although secretion of the propeptide constantly increased throughout the culture period. Therefore, the ratio of the amount of propeptide to I-OC in the supernatant markedly increased when mineralization started. These data demonstrate the superior specificity of propeptide as a marker of osteoblastic function in vitro compared with I-OC and that monitoring the changes in propeptide to I-OC ratios in the culture supernatant may be useful for predicting the timing of mineralization on the extracellular matrix of osteoblastic cells.

Adolescent↗
PubMed1993

Effects of estrogen replacement on insulin-like growth factor I concentrations in serum and bone tissue and on interleukin 1 secretion from spleen macrophages in oophorectomized rats.

Oophorectomy (OOX) has been known to increase bone turnover, but its precise mechanism is not fully understood. In order to further investigate the mechanism, we determined insulinlike growth factor I (IGF-I) concentrations in serum and bone tissue and interleukin 1 (IL-1) release from spleen macrophages in oophorectomized rats because it has been demonstrated that IGF-I stimulates bone formation and IL-1 stimulates bone resorption. Female 8-week-old Wistar rats were divided into four groups: (1) control, (2) OOX, (3) OOX given estradiol, and (4) control given estradiol. Ten micrograms/kg of 17 beta-estradiol was given daily by subcutaneous injection. After 5 weeks of treatment, IGF-I concentrations in the extract from right femur and in serum were determined by specific radioimmunoassay. IL-1 activity released from lipopolysaccharide (LPS)-stimulated spleen macrophages was determined by bioassay. IGF-I contents in the femur and IGF-I concentrations in serum in oophorectomized rats were significantly higher than those in control rats. Treatment by estradiol inhibited the increase in IGF-I concentrations both in femur and in serum. IL-1 release from LPS-stimulated spleen macrophages in oophorectomized rats was increased, and treatment by estradiol also inhibited the stimulated IL-1 release. The ash weights and the calcium contents of left femur in oophorectomized rats were lower than those in control rats. These results suggest that both IGF-I and IL-1 may be involved in the mechanism of the regulation of bone turnover in oophorectomized rats.

Animals↗
PubMed1993

Estrogen and bone.

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Base Sequence↗