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Biomedical subjects

K Fukuo

Publications and source records attributed to K Fukuo.

At least 73 records · Page 4Linked to original sources
PubMed1991

[Cognitive function and calcium-related factors in elderly female subjects].

Calcium (Ca)-related factors were evaluated as possible related factors to senile dementia in 60 elderly female subjects (mean age +/- SD: 79 +/- 7 years). These subjects were classified by their score on Hasegawa's Dementia Screening Scale, into a non-dementia group (score 22-32.5, n = 18) and a dementia group (0-21.5, n = 42), and the latter group was further classified by ischemic score into Alzheimer-type dementia (n = 22) and vascular-type dementia (n = 20). There was no significant difference in the mean values of age or serum creatinine among the three groups. In the Alzheimer-type dementia group, the mean serum level of Ca was significantly lower, and the serum level of parathyroid hormone (PTH) and urinary Ca were significantly higher than those in the non-dementia group, respectively. In the group of vascular-type dementia, the mean serum level of calcitonin (CT) was slightly, but not significantly, lower than that in the non-dementia group. The score for cognitive subjects negatively correlated significantly with the values of serum PTH (r = -0.49, p less than 0.05) and urinary Ca excretion (r = -0.38, p less than 0.05), respectively, and positively correlated significantly with that of serum 1,25-dihydroxyvitamin D [1,25(OH)2D] (r = 0.31, p less than 0.05), in the combined group of non-dementia and Alzheimer-type dementia, and positively correlated significantly with the serum CT level (r = 0.40, p less than 0.05) in the combined group of non-dementia and vascular-type dementia.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

[Presence of circulating suppressive factor for muscarinic acetylcholine receptor in senile dementia].

Alzheimer's disease is one of the main causes of senile dementia. Although its pathogenesis is not clear, some evidence has revealed that the activity of acetylcholine receptor in the brains of these patients is decreased. In the present study, possible circulating factors, affecting the muscarinic acetylcholine receptor of the synaptic vesicle from the rat brain, were evaluated in the serum of 95 senile subjects (34 males and 61 females, mean +/- SD age of 77.5 +/- 8.6 years). The cognitive function of these subjects was assessed by their Mini-Mental State scores, and they subjects were divided into non-dementic-subjects with a score of 21 or more, or subjects with dementia with a score of 20 or less. The latter were further divided into senile dementia with Alzheimer type (SDAT) and vascular type dementia (VS) using Hatchinski's ischemic score. The mean suppression rate by the serum from the SDAT patients on the binding of tritiated quinuclidinyl benzilate (3H-QNB), an antagonist for muscarinic acetylcholine receptor, to the rat synaptic membrane, was 18.1 +/- 7.2% of the control value, which was significantly greater than that of the non-dementic subjects, (4.7 +/- 3.8%). However, that in the VD group (8.4 +/- 6.8%), was not significantly different from the control value. Moreover the suppression rate of the serum on 3H-QNB binding showed significant positive correlated with score for the Mini-Mental State (r = 0.480, p less than 0.01) in the SDAT group. These data support the hypothesis that circulating suppression factors may participate in the pathogenesis of SDAT.

Aged↗
PubMed1991

[The influence of aging on parathyroid hormone-induced enhancement in (Ca2+ + Mg2+)-ATPase activity of rabbit renal basolateral membrane].

We studied the influence of aging on the stimulatory effect of parathyroid hormone (PTH) to (Ca2+ + Mg2+)-ATPase activity of rabbit renal basolateral membrane (BLM). Stimulated by PTH, (Ca2+ + Mg2+)-ATPase activity of BLM from aged rabbits was lower than those from young rabbits. However, the stimulatory effect of cyclic AMP (cAMP) showed no differences in terms of (Ca2+ + Mg2+)-ATPase activity in BLM from aged and young rabbits. As cAMP production in BLM caused by PTH stimulation was not measured, it is unclear whether cAMP production is different in BLM from young and aged rabbits. From these results, we concluded that in BLM from aged rabbit, the lower effect of PTH on (Ca2+ + Mg2+)-ATPase is due to lower production of cAMP or some other disorder of the PTH signal transduction mechanism. As (Ca2+ + Mg2+)-pump plays an important role in Ca2+ reabsorption in kidney, its lower activity in aged rabbit may be one reason for aberration of renal calcium handling.

Aging↗
PubMed1990

Participation of both intracellular free Ca2+ and protein kinase C in tonic vasoconstriction induced by prostaglandin F2 alpha.

The roles of intracellular free Ca2+ and protein kinase C in the tonic contraction induced by prostaglandin were studied. Prostaglandin F2 alpha induced tonic contraction of rat thoracic aorta in both control and Ca2(+)-free solution. Close correlations were observed between the contractile response of aortic strips and the changes in intracellular free Ca2+ concentration in vascular smooth muscle cells assessed with the fluorescent Ca2+ indicator fura 2, both in control and Ca2(+)-free solutions. Prostaglandin F2 alpha also enhanced the production of inositol 1,4,5-trisphosphate in vascular smooth muscle cells before the rise of the intracellular free Ca2+ concentration. Moreover, 1-(5-isoquinoline-sulfonyl)-2-methylpiperazine, an inhibitor of protein kinase C, inhibited the tonic contractions induced by PGF2 alpha and 12-O-tetradecanoyl phorbol-13-acetate, a direct activator of protein kinase C, at similar concentrations. These results suggest that both intracellular free Ca2+ and protein kinase C participate in prostaglandin F2 alpha-induced tonic contraction.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

[A case of recessive dystrophic epidermolysis bullosa associated with dwarfism with special reference to pathophysiological role of growth hormone].

Epidermolysis bullosa is a group of disorders whose common primary feature is the formation of blisters following trivial trauma. Recessive dystrophic epidermolysis bullosa (RDEB), a subtype of epidermolysis bullosa, is frequently associated with growth retardation. This growth retardation has been reported to be caused by trophopathy following protein loss through skin lesions. Endocrine disorders as the cause of growth retardation in RDEB have not been clearly described. An 11-year-old female had a typical RDEB with dwarfism. Her height was 125 cm and weight was 21 kg, both of which were 2.5 SD below the average. The skin lesions were generalized and probably caused by undernourishment, infection, and blood loss through the skin. However, her serum albumin was at the lower normal limit, and the rapid turnover proteins were slightly decreased. Endocrinological examinations revealed that all the basal levels of pituitary, thyroid, and adrenal hormones were normal. Results of the exercise test, the insulin tolerance test, and the growth hormone-releasing factor test indicated the presence of hypothalamic disorder in secretion of growth hormone. This is the first report of RDEB in which hypothalamic disorder in growth hormone secretion was investigated. On the other hand, growth hormone is known to be involved in collagen metabolism, and a decrease in collagen fibrils and an increase in collagenase activities are found in the skin of RDEB. This implies that this hypothalamic disorder in growth hormone secretion may be involved in the pathophysiology of both dwarfism and the skin lesions in RDEB.

Child↗
PubMed1990

Inverse relation between severity of psoriasis and serum 1,25-dihydroxy-vitamin D level.

The serum levels of calcium, inorganic phosphate, parathyroid hormone, calcitonin, 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were measured in 34 patients with psoriasis vulgaris and compared with the severity of skin lesions. Severity of psoriasis was evaluated by three indices, the area-severity index (ASI), the area index (AI) and the severity index (SI), determined as the product of the area and severity, the area, and the severity of the individual skin lesions, respectively. The mean basal levels of these serum parameters were within the normal range. ASI and SI showed significant inverse correlations (r = -0.387, P less than 0.05 and r = -0.638, P less than 0.01, respectively) with the serum level of 1,25-dihydroxyvitamin D, but not with any other serum parameters, but AI was not correlated with any of these serum parameters. These data suggest that psoriatic patients are not deficient in 1,25-dihydroxyvitamin D, but that development of this skin disease may be related to a slightly decreased level of active metabolites of vitamin D or abnormalities in the responsiveness of the skin cells to them.

Adolescent↗
PubMed1990

Effects of prostaglandin F2 alpha on the mobilization of cytosolic free calcium in vascular smooth muscle cells and on the tension of aortic strips from rats.

The possible mechanism of action of prostaglandin F2 alpha on vascular smooth muscle was investigated. Prostaglandin F2 alpha induced sustained tonic vasoconstriction of rat aortic strips, accompanied by rapid increase in the cytosolic free Ca2+ concentration [( Ca2+]i) in the vascular smooth muscle cells. Prostaglandin F2 alpha also evoked rapid increase in production of inositol 1,4,5,-trisphosphate (Ins-P3). Moreover, it increased release of Ca2+ from nonmitochondrial pools in digitonin-permeabilized vascular smooth muscle cells, although this effect was much weaker than that of Ins-P3. These results suggest that the sustained action of prostaglandin F2 alpha may involve not only a rise in [Ca2+]i mediated by Ins-P3, but also a direct stimulation of Ca2+ from intracellular stores.

Animals↗
PubMed1990

Comparison of the production of cyclic AMP in response to parathyroid hormone in fibroblasts from aged subjects and young subjects: lack of an age-dependent decrease.

An age-dependent effect on the ability to produce cyclic AMP in response to parathyroid hormone (PTH) stimulation was examined using culture skin fibroblasts from both young and elderly female subjects. The mean values of both absolute and comparative production of intracellular cyclic AMP due to various concentrations of PTH administration did not differ between the two age groups, although the mean serum PTH level was significantly higher in the elderly subjects. These results indicate that the decreased response of the target organ to PTH in aged subjects can be explained mainly by the decreased number of intact cells rather than a decreased response of individual cells to PTH.

Adolescent↗
PubMed1990

Nicorandil is a potent dilator of endothelin-induced vascular contraction.

Nicorandil, an antianginal drug, is known to open K+ channel and to increase cGMP production. The effects of nicorandil on vascular contraction induced by endothelin (ET), a potent newly discovered vasoconstrictor peptide, were investigated using helical strips from rat thoracic aorta. ET at a concentration of 5 x 10(-9) M induced strong and persistent contraction in the presence of extracellular Ca2+ and similar persistent but smaller contraction in the absence of extracellular Ca2+. Nicorandil at concentrations greater than 10(-7) M, strongly and dose-dependently inhibited ET-induced contraction in the presence of extracellular Ca2+. Nicorandil also suppressed ET-induced contraction in the presence of 10(-4) M methylene blue, an inhibitor of cGMP production, in the presence of extracellular Ca2+ but not in the absence of extracellular Ca2+. ET-induced contraction was also inhibited to lesser extents by the Ca2+ channel blockers nicardipine and verapamil. Nicorandil also strongly suppressed ET-induced increase in cytosolic free Ca2+ concentration in cultured vascular smooth muscle cells. These results suggest that nicorandil is a potent dilator of ET-induced vasoconstriction.

Animals↗
PubMed1990

Stimulatory effect of 1,25-dihydroxyvitamin D3 on transferrin synthesis in primary cultures of adult rat hepatocytes.

The effect of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] on protein synthesis was studied in primary cultures of adult rat hepatocytes, in comparison with those of dexamethasone (DEX). The transferrin (TF) level in the culture medium assayed by a radioimmunoassay (RIA), after incubation for 24 hr was increased in the presence of 1,25-(OH)2D3, significantly at concentrations of more than 10(-12) M and maximally to about 140% of that in control cultures at 10(-8) M, without change in the albumin concentrations, assayed by an EIA. Other vitamin D3 metabolites had similar but weaker effects in increasing transferrin synthesis. On the other hand, incubation with 10(-6) M Dex for 24 hr enhanced the syntheses of both transferrin and albumin. Addition of 10(-7) M actinomycin D did not significantly block the effect of 1,25-(OH)2D3, but did suppress that of dexamethasone. These results indicate that 1,25-(OH)2D3 stimulates TF synthesis of cultured rat hepatocytes with different mechanism(s) of action from that of dexamethasone.

Albumins↗
PubMed1989

Association of increased intracellular free Ca2+ by platelet-derived growth factor with mitogenesis but not with proteoglycan synthesis in chondrocytes--effect of suramin.

The effects of platelet-derived growth factor (PDGF) on the intracellular free Ca2+ concentration [( Ca2+]i) in chondrocytes were studied with a fluorescent Ca2+ indicator, fura 2, and compared with the effects of PDGF on mitogenesis and proteoglycan synthesis. PDGF evoked phasic and then tonic increase in [Ca2+]i dose-dependently in quiescent cultures of chondrocytes, and it also stimulated both DNA and proteoglycan syntheses dose-dependently similar to somatomedins. Suramin, which inhibits the interaction of PDGF with its receptors, caused dose-dependent inhibition of both the PDGF-evoked increase in [Ca2+]i and stimulation of DNA synthesis by PDGF. However, suramin rather enhanced the proteoglycan synthesis induced by PDGF without affecting the basal level of proteoglycan synthesis directly. These results suggest that [Ca2+]i may be an important signal for the action of PDGF on cell proliferation in chondrocytes, and that the initial signal for proteoglycan synthesis is different from that for DNA synthesis induced by PDGF after the activation of PDGF receptor.

Animals↗
PubMed1989

Low density lipoprotein and apoprotein B induce increases in inositol trisphosphate and cytosolic free Ca2+ via pertussis toxin-sensitive GTP-binding protein in vascular smooth muscle cells.

Low density lipoprotein (LDL), a major cholesterol-carrying lipoprotein in the plasma, binds to its receptor through apoprotein B (Apo-B). The addition of LDL and Apo-B induced rapid (5 s), but transient increase in the inositol 1,4,5-trisphosphate (Ins-1,4,5-P3) level with K0.5 values of 1.1 and 0.07 microgram/ml, accompanied by increases of cytosolic free Ca2+ concentration [( Ca2+]i), in vascular smooth muscle cells (VSMC). The increases by LDL and Apo-B were both reduced by pretreatment of the VSMC with pertussis toxin. The early change in Ins-1,4,5-P3 involving a GTP-binding protein may function as an initial signal for the action of LDL in VSMC.

Animals↗
PubMed1988

[Immunoreactive parathyroid hormones in the circulation and cerebrospinal fluid from patients with renal failure: possible restriction of parathyroid hormone by the blood-brain barrier].

There are reports that patients with renal failure have elevated circulating concentrations of parathyroid hormone (PTH), which is suspected to be a causal factor of the cerebral symptoms of these patients. A positive correlation between the circulating level of immunoreactive PTH and the extent of abnormality in the electroencephalogram (EEG) in humans has been reported. Moreover, in uremic dogs normalization of the EEG was observed after parathyroidectomy, and increased abnormality of the EEG was observed on infusion of PTH. If PTH is really a causal factor of uremic encephalopathy and abnormality of the EEG in patients with renal failure, the question arises as to whether PTH acts on the brain after penetrating through the blood-brain barrier or in some other way. In this work, we measured PTH by both C-terminal-specific RIA (C-PTH) and N-terminal-specific RIA (N-PTH) in the circulation and cerebrospinal fluid (CSF) of normal subjects and patients with renal failure. Blood and CSF samples were obtained from 7 normal volunteers (31 approximately 81 years old: 4 males and 3 females) and 22 patients with chronic renal failure (25 approximately 87 years old: 12 males and 10 females). No patients had a psychotic disease or endocrinopathy other than secondary hyperparathyroidism. Samples of venous blood were collected from the subjects after an overnight fast at the time of lumbar puncture for CSF sampling. C-terminal-specific RIA for measurement of the plasma and CSF concentrations of C-PTH was carried out using a commercially available RIA kit (Eiken Laboratory Inc., Tokyo, Japan).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

1,25-Dihydroxyvitamin D3 binds specifically to rat vascular smooth muscle cells and stimulates their proliferation in vitro.

Cultured vascular smooth muscle cells (VSMC) derived from rat aorta were found to contain a specific receptor for 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. Its Kd (5.0 x 10(-11) M) and capacity (22.9 fmol/mg of cytosol protein) for 1,25-(OH)2D3, its sedimentation coefficient on a sucrose density gradient (3.2 S), its relative affinities for various vitamin D3 metabolites [1,25-(OH)2D3 greater than 25-hydroxyvitamin D3 greater than 24,25-dihydroxyvitamin D3 greater than vitamin D3] and its affinity for DNA-cellulose were similar to those reported for the 1,25-(OH)2D3 receptor in other tissues. 1,25-(OH)2D3 at concentrations of more than 10(-10) M caused dose-dependent enhancement of the proliferation of VSMC in DMEM with 10% FCS. 25-Hydroxyvitamin D3 stimulated the proliferation of VSMC only at its highest concentration tested (10(-6) M). These data show that 1,25-(OH)2D3 stimulates the proliferation of VSMC after its binding to a cytoplasmic receptor of the cells in vitro, and support the possibility that VSMC are target cells of the hormone.

Animals↗
PubMed1988

Effect of estrogens on renal responsiveness to parathyroid hormone in elderly female subjects.

The effect of estrogens on the renal responsiveness to parathyroid hormone (PTH) was examined by PTH loading tests with synthetic human-PTH (1-34) in 8 normal elderly females (mean +/- SD age, 81.0 +/- 7.1 yr) before and after administration of estrogen (Premarin 1.25 mg/day for 4 weeks). Basal urinary adenosine cyclic 3', 5'-monophosphate (cAMP) excretion showed a tendency to increase after estrogen administration (5.47 +/- 1.68 vs 6.60 +/- 2.67 nmol/100 ml GFR) and the theoretical renal phosphorous threshold showed a tendency to decrease from 3.22 +/- 0.98 to 2.73 +/- 0.56 mg/dl. The blood ionized calcium concentration did not change after estrogen administration (4.44 +/- 0.16 vs 4.32 +/- 0.20 mg/dl) and serum phosphorous (P) decreased significantly (3.65 +/- 0.47 vs 3.01 +/- 0.42 mg/dl, p less than 0.05). There was no increase in mean serum immunoreactive PTH (0.34 +/- 0.10 vs 0.34 +/- 0.05 ngeq/ml). The urinary excretions of cAMP in response to PTH loading [100 U of human-PTH (1-34), intravenously] significantly (p less than 0.05) increased (94.8 +/- 57.0 vs 196.7 +/- 118.3 nmol/100 ml GFR/h) after estrogen administration. Moreover the changes in urinary excretion of cAMP (r = 0.698, p less than 0.01) and P (r = 0.555, p less than 0.05) induced by the PTH loading were positively correlated with serum estradiol in elderly females, assessed as groups before and after estrogen administration. These results suggest that estrogens may enhance the renal responsiveness to exogenous PTH administration.

Adult↗
PubMed1988

A patient with hypogonadotropic hypogonadism successfully treated by long-term pulsatile administration of luteinizing hormone-releasing hormone.

A male patient with hypogonadotropic hypogonadism has been treated by pulsatile administration lf luteinizing hormone-releasing hormone (LHRH) (20-25 micrograms, every 2 hours, sc) for 4 years 6 months. His plasma testosterone (T) concentration began to increase after 4 weeks of treatment and reached the normal range in week 5. He showed complete secondary sexual development after 1 year of treatment. His sperm count was normalized after 1 year of treatment. He was married after 29 months of therapy, and has a healthy male child. Blood type tests showed his paternity of the child. During the long duration of pulsatile LHRH therapy, his gonadotropin secretion has been stimulated by LHRH and his T level has been maintained with no observable side effects. There are no other reports of patients treated by pulsatile LHRH injection for such a long duration, but finding in this patient indicated that long-term pulsatile LHRH therapy is a useful and safe method for treatment of hypothalamic hypogonadotropic hypogonadism.

Adult↗