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H Morii

Publications and source records attributed to H Morii.

At least 163 records · Page 9Linked to original sources
PubMed1995

Down-modulation of c-kit mRNA and protein expression by erythroid differentiation factor/activin A.

We examined the effects of erythroid differentiation factor (EDF)/activin A on the expression of c-kit mRNA and protein in murine erythroleukemia (MEL) cells. EDF/activin A induced MEL cells to benzidine positive cells. Northern blot analysis showed that the c-kit mRNA expression was reduced synchronously with increase of beta-globin and uroporphyrinogen decarboxylase gene expression during EDF/activin A induced erythroid differentiation. Scatchard analysis indicated that the cell surface receptor number was reduced without change of affinity during differentiation. Our results suggest that EDF/activin A may act as a natural regulator of erythropoiesis with modulation of c-kit gene expression.

Activins↗
PubMed1995

Immunocytochemical localization of 155 kDa myosin light chain kinase and myosin heavy chain in bovine brain.

We immunocytochemically stained the bovine brain with monoclonal antibodies against 155 kDa MLCK and myosin heavy chain (MHC) and a polyclonal antibody against calmodulin. In the bovine brain, a strong immunoreactivity with the anti-MLCK antibody was observed in neurons in all layers of the cerebral cortex and basal ganglia, and astrocytes in the white matter. The antibody also stained Purkinje, granular and molecular cells in the cerebellum. An anti MHC antibody stained neurons and astrocytes in the cerebral cortex and Purkinje cells similarly to the anti-MLCK antibody, whereas the MHC immunoreactivity was detected in the cerebellar glomerulus and there was no immunostaining of MHC in the granular and outer stellate cells. These results suggest that the 155 kDa MLCK might be related not only to the Ca-calmodulin-myosin system but also other intracellular system.

Animals↗
PubMed1995

Influence of high glucose on 1,25-dihydroxyvitamin D3-induced effect on human osteoblast-like MG-63 cells.

Impaired bone formation due to defective osteoblast function, as reflected in a decreased serum osteocalcin (OC) concentration in the patients with diabetes, has been implicated in the development of diabetic osteopenia. The role of hyperglycemia in this decrease in serum OC concentration was investigated. 1,25-dihydroxyvitamin D3 (1,25[OH]2D3), an active form of vitamin D3, stimulated OC secretion from the human osteosarcoma cell line MG-63 in a dose-dependent manner. Exposure of the cells to high concentrations of glucose for 7 days significantly impaired 1,25(OH)2D3-induced OC secretion as compared with that observed with cells maintained under normal glucose (5.5 mM) or high mannitol conditions. The inhibitory effect of glucose was in a dose-dependent manner up to 55 mM. High glucose (55 mM) also attenuated the 1,25(OH)2D3-induced increase in OC mRNA abundance in MG-63 cells, suggesting that the inhibition of the 1,25(OH)2D3-induced increase in OC secretion by exposure to a high concentration of glucose was, at least in part, mediated at the transcriptional level. High glucose significantly decreased the number of 1,25(OH)2D3 receptors in MG-63 cells, without any change in the dissociation constant for 1,25(OH)2D3; this effect was not mimicked by high mannitol, indicating specificity for glucose. These observations suggest that a high glucose concentration significantly impairs the ability of osteoblastic cells to synthesize OC in response to 1,25(OH)2D3 by reducing 1,25(OH)2D3 receptor number, and that impaired cell function caused by sustained exposure to high glucose contributes to the defect in bone formation observed in the patients with diabetic osteopenia.

Amino Acid Sequence↗
PubMed1995

Effect of 1,25-dihydroxyvitamin D3 on induction of scavenger receptor and differentiation of 12-O-tetradecanoylphorbol-13-acetate-treated THP-1 human monocyte like cells.

We investigated the effect of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on the expression of scavenger receptors in human monocytic cell line (THP-1 cells) treated for 24 h with 12-O-tetradecanoylphorbol-13-acetate (TPA) which induces their differentiation into macrophages. The capacity to degrade 125I-labeled acetyl low density lipoprotein (LDL) was developed in accordance with macrophage differentiation. The treatment with 10 nM 1,25(OH)2D3 for 72 h inhibited the degradation of acetyl LDL by THP-1 macrophages in a dose-dependent manner, suggesting that 1,25(OH)2D3 inhibits scavenging function in macrophages. In order to clarify the mechanism of its inhibitory effect on degradation of acetyl LDL, we performed the ligand binding assay using 125I-labeled acetyl LDL. Scatchard analysis revealed that 1,25(OH)2D3 decreased the number of scavenger receptors without changing the affinity for acetyl LDL. We next examined the effect of 1,25(OH)2D3 on the expression of scavenger receptor mRNA. The mRNA of type I scavenger receptor was first detected in THP-1 cells 4 days after the treatment with TPA, the mRNA level increased up to 6 days, and then decreased. The treatment with 1,25(OH)2D3 for 72 h dramatically decreased the mRNA levels after the acquisition of macrophage phenotypes as evidenced by nonspecific esterase staining. However, 1,25(OH)2D3 did not affect the activity of nonspecific esterase nor the induction of interleukin-1 beta mRNA by lipopolysaccharide in THP-1 macrophages. These findings suggest that 1,25(OH)2D3 exclusively decreases the expression of scavenger receptors in TPA-induced THP-1 macrophages without affecting the basic cellular functions as macrophages.

Base Sequence↗
PubMed1995

A case of primary and generalized allergy to human insulin with no history of any prior insulin exposure.

A generalized hypersensitivity reaction against human insulin was demonstrated in a non-insulin dependent diabetic man treated with only human insulin. The patient had no history of previous insulin exposure or atopy. Because of negative reactions to intracutaneous tests of constituents of the formulation and the presence of insulin-specific IgE antibody, this generalized allergic reaction seems to have been caused by the human insulin itself. Although desensitization was not effective, this allergic reaction was improved both by the treatment with oral antihistamines and desensitization. Cases of generalized and primary allergy against human insulin have been rarely reported making this a very rare case.

Diabetes Mellitus, Type 2↗
PubMed1995

Heat-insoluble cryoglobulin in a patient with essential type I cryoglobulinemia and massive cryoglobulin-occlusive glomerulonephritis.

We report a case of type I essential cryoglobulinemia with massive cryoglobulin-occlusive glomerulonephritis, in which the clinical course and the physical characteristics of the cryoglobulin were unusual. Nine years before appearance of cryoglobulin, this 54-year-old man noted edema and purpura of the lower extremities. Renal biopsy performed 2 years later showed large amounts of amorphous, weakly eosinophilic, weakly periodic acid-Schiff (PAS)-positive materials occluding the glomerular capillaries. Immunostaining showed the material to be weakly immunoglobulin (Ig) G positive, and electron microscopy showed homogeneous, electron-dense deposits. Nephrotic syndrome and azotemia did not respond to steroid treatment, and dialysis was begun 5 years after the biopsy. A small amount of cryoglobulin was first detected 2 years later, 9 years after the onset of disease. The cryoglobulin had a white gelatinous appearance, was resistant to resuspension, and did not redissolve when rewarmed to 37 degrees C. Immunoelectrophoresis of the cryoglobulin, which partially dissolved at 54 degrees C, showed it to be composed of monoclonal IgG-kappa and a small amount of albumin. We consider that the unusual physical characteristics of the cryoglobulin in this case precipitated a massive cryoglobulin-occlusive glomerulonephritis, which progressed to end-stage renal failure in the absence of significant cryoglobulinemia during the initial onset of disease.

Cryoglobulinemia↗
PubMed1995

High-resolution B-mode ultrasonography in evaluation of atherosclerosis in uremia.

We sought to determine whether artherosclerosis may be accelerated in uremic patients on maintenance hemodialysis and investigated the risk factors for carotid and femoral atherosclerosis in such patients. High-resolution B-mode ultrasonography was used to determine the intima-media thickness (IMT) of the carotid and femoral arteries in 199 hemodialysis patients and 81 age-matched healthy controls subjects. The IMT values of the carotid and femoral arteries in the hemodialysis patients were significantly higher than in age-matched control subjects in most age groups. The IMT values of the carotid or femoral artery were significantly correlated with age in both the hemodialysis patients and the control subjects. There was a significant relationship between the IMT values of the two arteries in the hemodialysis patients (r = 0.418, P = 0.0001) and in the control subjects (r = 0.321, P = 0.0037). Multiple regression analysis showed that age, cigarette smoking, and uremic state were independent risk factors for atherosclerosis of both arteries in the patients and the control subjects (R2 = 0.174, P < 0.0001; R2 = 0.205, P < 0.0001, respectively). In the hemodialysis patients, the independent risk factors associated with the extent of the IMT of the carotid artery were age, cigarette smoking, and serum phosphorus level (R2 = 0.230, P < 0.0001), while those associated with the extent of the IMT of the femoral artery were age, cigarette-smoking, and serum m-PTH level (R2 = 0.230, P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Inhibition of intestinal tumor development in rat multi-organ carcinogenesis and aberrant crypt foci in rat colon carcinogenesis by 22-oxa-calcitriol, a synthetic analogue of 1 alpha, 25-dihydroxyvitamin D3.

The modifying effects of 22-oxa-calcitriol (OCT), a synthetic analog of 1 alpha,25-dihydroxyvitamin D3, were assessed in a multi-organ carcinogenesis model using male F344 rats initially treated with five kinds of carcinogens. In experiment 1 the rats were given OCT intraperitoneally at doses of 30 micrograms/kg (25 rats) or 3 micrograms/kg (25 rats), three times a week for 24 weeks after initial carcinogen exposure over 4 weeks and a 2 week non-treatment period. Twenty-two rats received the five carcinogens and were given the vehicle intraperitoneally as a control. A further group of 10 rats was given the 30 micrograms/kg dose of OCT without prior carcinogen application. At the end of the total observation period of 30 weeks the carcinoma incidence in the small intestine of rats given 30 micrograms/kg OCT after carcinogen treatment was 0%. This incidence was significantly smaller when compared with the control group. The incidence of large intestine carcinomas in the 30 micrograms/kg OCT group showed a tendency to decrease. The numbers of small and large intestinal carcinomas per rat were also significantly lower in the group given 30 micrograms/kg OCT than after 3 micrograms/kg OCT or carcinogens alone. Attention was, therefore, focused on colon carcinogenesis and in experiment 2 30 micrograms/kg OCT administered six times a week to rats for 8 weeks after the last injection of N,N'-dimethylhydrazine (DMH) exposure. OCT significantly reduced the formation of DMH-induced aberrant crypt foci, considered to be putative preneoplastic lesions. In experiment 3 30 micrograms/kg OCT was administered six times a week to rats for 4 weeks without prior carcinogen treatment. The proliferating cell nuclear antigen labeling index for the colonic epithelium of rats given 30 micrograms/kg OCT was decreased. Ornithine decarboxylase and spermidine/spermine N1-acetyltransferase activities in colonic epithelium, assayed as indicators of cell proliferation, were not significantly decreased as compared with control group values. Furthermore, vitamin D receptors in colonic epithelium were not significantly increased. Thus the present study indicates that OCT can exert inhibitory effects on tumor development in the small and large intestines, although the mechanism is unclear.

Acetyltransferases↗
PubMed1995

Beta-glycerophosphate accelerates calcification in cultured bovine vascular smooth muscle cells.

Calcification is a common feature of advanced atherosclerotic lesions and is being reemphasized as a clinically significant element of vascular disease. However, the scarcity of in vitro models of vascular calcification preclude studying its molecular and cellular mechanism. In the present study, we describe an in vitro calcification in which diffuse calcification can be induced by culturing bovine vascular smooth muscle cells (BVSMC) in the presence of beta-glycerophosphate, ascorbic acid, and insulin in a manner analogous to in vitro mineralization by osteoblasts. Calcification was confirmed by von Kossa staining and 45Ca accumulation. Factor analysis revealed that beta-glycerophosphate is the most important factor for this calcification process, suggesting that alkaline phosphatase (ALP) may be involved. As predicted, high levels of ALP expression were detected by ALP assay and Northern blot analysis. Functional significance of ALP was confirmed by demonstrating that levamisole, a specific inhibitor of ALP, inhibited BVSMC calcification in a dose-dependent manner. Bisphosphonates such as etidronate and pamidronate potently inhibited BVSMC calcification, suggesting that hydroxyapatite formation may be involved. Importantly, expression of osteopontin mRNA was dramatically increased in calcified BVSMC compared with uncalcified control cells. These data suggest that beta-glycerophosphate can induce diffuse calcification by an ALP-dependent mechanism and that this in vitro calcification system is useful for analyzing the molecular and cellular mechanisms of vascular calcification.

Alkaline Phosphatase↗
PubMed1995

Impaired retinal artery blood flow in IDDM patients before clinical manifestations of diabetic retinopathy.

OBJECTIVE: To determine whether hemodynamic changes in retinal arteries precede clinical manifestations of diabetic retinopathy and to examine the effects of control of hyperglycemia on retinal artery blood flow. RESEARCH DESIGN AND METHODS: We assessed blood flow in bilateral central retinal arteries in 50 insulin-dependent diabetes mellitus (IDDM) patients without retinopathy and 20 sex- and age-matched control subjects using duplex Doppler sonography. We determined the peak systolic velocity (PSV), end-diastolic velocity (EDV), time-averaged velocity (TAV), resistance index (RI), and pulsatility index (PI). RESULTS: PSV, EDV, and TAV were significantly lower in IDDM patients than in control subjects (P < 0.05, P < 0.01, and P < 0.01, respectively). The RI was significantly higher in IDDM patients than in control subjects (P < 0.01) and was significantly correlated with plasma levels of glucose in IDDM patients (r = 0.0.310, P = 0.0248). Multiple regression analysis identified the plasma levels of glucose as a significant determination of RI in IDDM patients. After 14 days of intensive insulin therapy in 7 IDDM patients, the RI and plasma levels of glucose showed significant decreases (P = 0.018, P = 0.001, respectively). CONCLUSIONS: Our results showed that changes in retinal hemodynamics were present before the clinical detection of overt diabetic retinopathy and suggest that the presence of short-term hyperglycemia partly contributes to impaired retinal circulation.

Adolescent↗
PubMed1995

Involvement of polyamines in the proliferation of bovine parathyroid cells.

An active form of vitamin D, 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], is involved in the regulation of parathyroid cell proliferation as well as of parathyroid hormone synthesis. We examined the effects of 1,25-(OH)2D3 on the proliferation of parathyroid cells in relation to their effects on ornithine decarboxylase (ODC) activity. Exposure of bovine parathyroid cells to serum caused an elevation in [3H]thymidine incorporation, which was preceded by a rise in ODC activity. The biodegradative enzyme, spermidine/spermine N1-acetyltransferase (SAT) activity did not change by 12 h after serum exposure. Preincubation of the cells with 10(-8)M 1,25-(OH)2D3 for 48 h attenuated the serum-induced rise in ODC activity by 12 h. alpha-Difluoromethylornithine (DFMO), a specific inhibitor of ODC, inhibited the serum-stimulated [3H]thymidine incorporation. Simultaneous addition of 25 microM putrescine reversed the inhibitory effect of DFMO. In summary, it was strongly suggested that polyamine is intimately involved in the proliferation of parathyroid cells and that 1,25-(OH)2D3 inhibited parathyroid cell growth through suppression of ODC activity.

Animals↗
PubMed1995

Impaired response of human osteosarcoma (MG-63) cells to human parathyroid hormone induced by sustained exposure to high glucose.

It is known that osteopenia is frequently associated with diabetes mellitus. Although its mechanism is not well understood, impaired bone formation due to an osteoblast deficit seems to be a major factor as reflected by a fall in serum levels of osteocalcin and by the findings of low bone formation with bone histomorphometry. In the present study, we studied the effect of high glucose conditions on osteoblast by examining the responsiveness of human osteosarcoma (MG-63) cells to human parathyroid hormone 1-34 [hPTH-(1-34)]. MG-63 cells were cultured either with 5.5 mM glucose (normal glucose), 55.0 mM glucose (high glucose) or 5.5 mM glucose plus 49.5 mM mannitol (high mannitol) condition for 7 days. Both an increase in cAMP levels and an immediate increase in [Ca2+]i, induced by hPTH(1-34), were significantly lower in high glucose-treated cells than in those treated with normal glucose or high mannitol. Basal cAMP levels in the cells after a 7-day culture in high glucose conditions were significantly higher than in those in the other two groups. We concluded that high glucose specifically impaired the response to hPTH(1-34). This impairment seemed to arise from an increase in intracellular cAMP levels, which is reported to induce downregulation of PTH receptors.

Calcium↗
PubMed1995

Impaired vitamin D metabolism and response in spontaneously diabetic GK rats.

Several studies of diabetes mellitus patients have demonstrated abnormalities in calcium, phosphate and vitamin D metabolism. In an earlier study, the authors reported impaired renal processing of phosphate in spontaneously diabetic GK rats, an animal model of type II diabetes mellitus. In the present study, which represents an extension of the earlier study, vitamin D metabolism and response are examined in 20-week-old GK rats. Serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] was found to be lower in GK rats than in Wistar rats. After intraperitoneal administration of 0.5 micrograms/kg 1,25-(OH)2D, serum calcium increased in GK rats, but not in Wistar rats, while serum phosphate remained unchanged in GK rats, but increased in Wistar rats. Although serum 1,25-(OH)2D rose abruptly in 3 h and decreased thereafter in both GK and Wistar rats, the decrease in serum 1,25-(OH)2D at 6 h was more marked in GK rats than in Wistar rats. Serum 24,25-dihydroxyvitamin D was consistently higher in GK rats than in Wistar rats. Northern blotting and dot blotting with use of a cDNA probe for the 24-hydroxylase gene showed an increased expression of the gene in the kidney of GK rats. These results demonstrate impaired vitamin D metabolism in GK rats. Increased activity of 24-hydroxylase, in addition to impaired phosphate metabolism, may play a role in impaired vitamin D metabolism in GK rats.

Animals↗
PubMed1995

Biological activities of 26,26,26,27,27,27-hexafluoro-1,25-dihydroxyvitamin D3 on human promyelocytic leukemic HL-60 cells: effects of fetal bovine serum and of incubation time.

The hexafluorinated vitamin D3 analog, 26,26,26,27,27,27-hexafluoro-1,25-dihydroxyvitamin D3[F6-1,25-(OH)2D3] is more potent than 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] regarding various physiological effects. When the biological potencies of vitamin D3 analogs were assessed 24 h after the addition by the induction of 24-hydroxylation activity in the human promyelocytic leukemia cell line, HL-60,F6-1,25-(OH)2D3 was 6 times as potent as 1,25-(OH)2D3 in a medium containing 5% fetal bovine serum. When the cells were cultured in a serum-free medium, F6-1,25-(OH)2D3 was only equipotent to 1,25-(OH)2D3. Considering a previous report demonstrating a weaker binding of F6-1,25-(OH)2D3 to serum vitamin D-binding protein (DBP) than 1,25-(OH)2D3, it seems that the resultant greater free fraction of F6-1,25-(OH)2D3 might account for its greater activity in a serum-containing medium. As assessed by the suppression of cell proliferation and the induction of cell differentiation along the monocyte/macrophage pathway which requires as long as 96 h for their assessment, the potency ratio of F6-1,25-(OH)2D3 to 1,25-(OH)2D3 increased as the levels of fetal bovine serum increased. It was of great interest that F6-1,25-(OH)2D3 was still significantly more potent than 1,25-(OH)2D3 even in a serum-free medium. Together with the data indicating the equipotency of F6-1,25-(OH)2D3 and 1,25-(OH)2D3 in the induction of 24-hydroxylation activity, it was suggested that decreased metabolic inactivation might contribute in part to the higher potency of F6-1,25-(OH)2D3 in the long-term effect.

Animals↗
PubMed1995

Implication of parathyroid hormone for the development of hypertension in young spontaneously hypertensive rats.

The purpose of this study is to elucidate the role of parathyroid hormone (PTH) in the development of hypertension in young spontaneously hypertensive rats (SHR). Parathyroidectomy (PTX) or sham surgery was performed on 6-week-old male SHR, and 3 weeks later human PTH (hPTH) or saline was infused subcutaneously over 2 weeks using a minipump. PTX significantly attenuated the development of hypertension and reduced serum vitamin-D concentrations. PTX also augmented the depressor response to acetylcholine before N-nitro-L-arginine (L-NNA), although it remained unchanged after L-NNA. The cardiovascular reactivity to exogenous noradrenaline and angiotensin II was not affected by PTX. The chronic administration of hPTH reversed these effects. We conclude that PTH plays an important role in the development of hypertension, through modulating the release of endothelium-derived relaxing factor, in young SHR.

Acetylcholine↗