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Biomedical subjects

H Morii

Publications and source records attributed to H Morii.

At least 217 records · Page 12Linked to original sources
PubMed1993

[Isolated ACTH deficiency associated with Hashimoto disease].

Isolated ACTH deficiency is a rare cause of secondary adrenocortical insufficiency. The diagnosis is made by the demonstration of low cortisol production with low plasma ACTH, absent adrenal responses to stimulation for pituitary or hypothalamus with intact adrenal response to exogenous ACTH, and normal secretory indices of other pituitary hormones. Although the pathogenesis of isolated ACTH deficiency is uncertain in most cases, autoimmune process is intimately involved as suggested by the histological evidence of lymphocytic hypophysitis and frequent observation of circulating antipituitary antibodies. In isolated ACTH deficiency, there have been occasional associations with Hashimoto disease which is characterized by the presence of a autoimmune mechanism. This suggests the possibility of common autoimmune process affecting both the pituitary and the thyroid gland.

Adrenocorticotropic Hormone↗
PubMed1993

Levels of urinary polyamines in patients with rheumatoid arthritis.

OBJECTIVE: To compare urinary polyamine levels in patients with rheumatoid arthritis (RA), with osteoarthritis (OA), and in healthy controls and examine the relationship between urinary polyamine levels and several disease variables in patients with RA. METHODS: We determined the concentrations of urinary polyamines in 33 patients with RA, 24 with OA, and 20 healthy controls, using the enzymatic assay method. For patients with RA relevant clinical and laboratory variables were obtained and functional and radiologic scores determined for the joints. RESULTS: Urinary polyamine levels were significantly higher in patients with RA versus those with OA and healthy controls. In patients with RA the levels of urinary polyamines correlated significantly with the concentrations of serum C-reactive protein (CRP); there was also a statistically significant negative correlation between their urinary polyamine levels and average grip strength in either hand. Moreover, the levels of urinary polyamines in patients with RA showed an increase in proportion to the degree of joint functional damage and radiologic progression. CONCLUSION: Our results confirm our previous report of an increase in the amount of free putrescine in synovial fluids and a significant correlation between the putrescine contents of synovial tissues and the serum CRP concentrations in patients with RA; they also suggest that urinary polyamine levels may be related to the activity and progression of RA, indicating that polyamine may play an important role in RA.

Adult↗
PubMed1993

Effect of transforming growth factor-beta on extracellular matrix production by cultured rat mesangial cells.

The effects of transforming growth factor-beta (TGF-beta) on the protein synthesis and gene expression of collagen I (CI), III (CIII), IV (CIV) and laminin (LM) in cultured rat mesangial cells (MCs) were examined to determine whether or not TGF-beta could modulate the formation of extracellular matrix (ECM) constituents, employing immunocytochemistry, enzyme-linked immunoadsorbent assay (ELISA) and Northern blotting. Although TGF-beta did not modulate MC proliferation, it induced slight enhancement of immunoperoxidase staining for CIV in the cytoplasm. ELISA demonstrated a significant increase in the amounts of CIV and LM, a tendency for CIII to increase, and a significantly lower amount of CI at 4 days after TGF-beta administration. Northern blotting showed that the mRNA expression displayed different patterns among the 4 matrix components during a 24-hr period. These findings suggest that a single growth factor, TGF-beta, in vitro modulates the synthesis of individual ECM constituents in MCs differently at the level of both genetic expression and protein production. The specific effects of TGF-beta on the increase in amounts of CIV and LM indicate that TGF-beta may contribute to glomerular remodeling and ECM accumulation in various kinds of glomerular injuries.

Animals↗
PubMed1993

Chronic parathyroid hormone administration reverses the antihypertensive effect of calcium loading in young spontaneously hypertensive rats.

To investigate the role of parathyroid hormone (PTH) in the development of hypertension, the long-term administration of human PTH (hPTH) was performed in 7-week-old male spontaneously hypertensive rats maintained on a standard calcium diet (1.1% calcium) or a high calcium diet (2.8% calcium). The hPTH was infused subcutaneously at 0.9 U/h over 2 weeks using a minipump. Two weeks after minipump implantation, rat PTH (rPTH) and 1,25-dihydroxy vitamin D (1,25-D) levels were measured and the pressor response to norepinephrine (NE) was examined. Calcium loading both attenuated the development of hypertension and reduced the pressor response to norepinephrine. Chronic hPTH administration accelerated the development of hypertension and increased the pressor response to norepinephrine in rats fed a high calcium diet, but did not affect either parameter in rats fed a standard calcium diet. The serum concentrations of rat PTH and 1,25-D were significantly lower in rats fed a high calcium diet than in those fed a standard calcium diet (rat PTH: 351 +/- 16 v 430 +/- 1 pmol/L; 1,25-D: 125 +/- 19 v 206 +/- 31 pg/mL). Chronic administration of hPTH increased the serum 1,25-D concentration in rats fed a high calcium diet (186 +/- 35 pg/mL), but did not affect that of rats fed a standard calcium diet (165 +/- 16 pg/mL). It is concluded that PTH prevented the antihypertensive effect of calcium loading in young SHR, perhaps by enhancing blood pressure reactivity through causing an increase of 1,25-D.

Animals↗
PubMed1993

[A case of dextrocardia concomitant with tetralogy of Fallot, patent ductus arteriosus and bronchiectasia].

We report a case of dextrocardia concomitant with tetralogy of Fallot (TOF), patent ductus arteriosus (PDA), bronchiectasia, and pulmonary tuberculosis. A 24-years-old man without surgical operation for TOF, whose diagnosis had been made at infancy, was admitted to the Osaka City University Hospital because of massive hemoptysis. The diagnosis of pulmonary tuberculosis was made. He received anti-tuberculotic drugs and bronchial arterial embolization improved his symptoms. A case of mirror-image dextrocardia concomitant with TOF, PDA, and bronchiectasia, as seen in our case, has a low incidence rate, and, moreover, such a case concomitant with pulmonary tuberculosis is rarer still.

Adult↗
PubMed1993

Effect of cisapride on gastric emptying of indigestible solids and plasma motilin concentration in diabetic autonomic neuropathy.

To investigate the role of motilin in diabetic gastroparesis, we evaluated gastric emptying and plasma concentrations of motilin in diabetic patients. Gastric emptying of radiopaque marker was significantly delayed in the diabetics with autonomic neuropathy (n = 14) compared with the healthy controls (n = 6) (p < 0.01). Mean plasma motilin concentrations were significantly higher in the diabetics with autonomic neuropathy compared with the healthy controls (p < 0.01). A positive correlation was observed between gastric emptying and plasma motilin concentrations in the healthy controls (r = 0.955, p < 0.01), whereas these values were inversely correlated in the diabetics (r = 0.620, p < 0.01). Oral administration of cisapride (15 mg/day.14 day) significantly accelerated gastric emptying without an effect on plasma motilin concentration (p = 0.03). These observations suggest that gastric emptying in the diabetics with autonomic neuropathy is delayed despite elevated levels of motilin, and that cisapride accelerates gastric emptying, independent of the plasma motilin concentration.

Autonomic Nervous System Diseases↗
PubMed1992

[A case of esophageal carcinoma with hypercalcemia caused by PTH-rP--the effect of therapy on the bone and calcium metabolism].

The changes in the bone and in calcium metabolism during cisplatin or bisphosphonate administration is reported in a 50-year-old patient with esophageal carcinoma who had humoral hypercalcemia of malignancy (HHM). Laboratory findings on admission showed that ionized calcium was 1.65mmol/L, phosphorus was 2.4mg/dl, and PTH-rP was 151pmol/L, without any evidence of bone metastasis. After admission, cisplatin and/or bisphosphonate were administrated for hypercalcemia. These administrations ameliorated serum ionized calcium, urinary pyridinoline and hydroxyproline level within a few days. Although cisplatin administration decreased the serum osteocalcin level, bisphosphonate administration kept up the level, suggesting that bisphosphonate maintained bone formation and cisplatin decreased its formation. The discrepancy may be due to the coupling with the reduction of bone resorption and/or direct toxic effect on osteoblasts during cisplatin administration, and preservation of osteoblastic activity during bisphosphonate administration. Cisplatin and bisphosphonate may have different effects on bone formation. Serum 1,25(OH)2D level was slightly decreased or unchangeable after cisplatin administration, although the level was increased after bisphosphonate administration. Direct toxic effect on 1 alpha-hydroxylase of the kidney or increase in phosphrous level may explain the change of 1,25(OH)2D after cisplatin administration. These results suggested that cisplatin and bisphosphonate have the same effect of preventing bone resorption but different effects on bone formation and/or serum 1,25(OH)2D level.

Bone Resorption↗
PubMed1992

Adenosine(5')hexaphospho(5')adenosine stimulation of a Ca(2+)-induced Ca(2+)-release channel from skeletal muscle sarcoplasmic reticulum.

Stimulation of a Ca(2+)-induced Ca(2+)-release channel from skeletal muscle sarcoplasmic reticulum by various adenosine(5')oligophospho(5')adenosines (ApnA, n = 2-6) by a rapid quenching technique using radioactive calcium was studied. Ap4A, Ap5A and Ap6A, as well as adenosine 5'-[beta, gamma-methylene]triphosphate (AdoPP [CH2]P), a non-hydrolyzable ATP analogue, stimulated the Ca(2+)-release channel, whereas Ap2A and Ap3A had no effect. At a concentration of 0.5 mM, the order of stimulation was AdoPP[CH2]P less than Ap4A less than Ap5A much less than Ap6A. As well as having the highest affinity (0.44 mM for half-maximal stimulation), Ap6A showed an extraordinarily high Hill coefficient of 3.3 (1.9 for AdoPP[CH2]P, 2.1 for Ap5A). The stimulating effect of Ap6A was reversible, yet its dissociation proceeded very slowly. Stimulation of Ca2+ release by Ap6A was counteracted by Mg2+ and ruthenium red. A 2',3'-dialdehyde derivative of Ap6A, which is a chemical probe for amino groups, stimulated irreversibly the Ca(2+)-release channel and modified some high-molecular-mass sarcoplasmic reticulum proteins, possibly including the channel protein. Our data suggest that Ap6A stimulates the Ca2+ channel by binding to the activation site of the channel subunit and simultaneously preventing the spontaneous decay of the Ca2+ channel by keeping together two of the four channel subunits by bridging them with its two adenosine groups.

Animals↗
PubMed1992

Dibutyryl cAMP enhances the effect of 1,25-dihydroxyvitamin D3 on a human promyelocytic leukemia cell, HL-60, at both the receptor and the postreceptor steps.

1,25-Dihydroxyvitamin D3 (1,25-(OH)2D3) induces differentiation of a human promyelocytic leukemia cell line, HL-60, into monocytes/macrophages, and 25-hydroxyvitamin D3- and 1,25-(OH)2D3-24-hydroxylase activities in HL-60 mitochondria via a steroid-hormone receptor mechanism. Dibutyryl cyclic adenosine monophosphate (dbcAMP), a granulocyte inducer, significantly augmented the differentiation-inducing effect of 1,25-(OH)2D3 along the monocyte/macrophage pathway. Furthermore, dbcAMP significantly potentiated the effect of 1,25-(OH)2D3 on HL-60 cells to hydroxylate 1,25-(OH)2[26,27-3H]D3 to form 1,24,25-(OH)3[26,27-3H]D3. DbcAMP seemed to augment the effect of 1,25-(OH)2D3 in part through upregulation of the 1,25-(OH)2D3 receptor, because 10(-7) M dbcAMP increased 1,25-(OH)2D3 receptor levels approximately 2.3-fold, which was similar to a 1.9-fold augmentation by the same concentrations of dbcAMP of 1,25-(OH)2D3-induced cell characteristics to hydroxylate C-24 of 1,25-(OH)2[26,27-3H]D3. However, dbcAMP is also known to enhance HL-60 cell differentiation caused by other differentiation inducers. We have established another HL-60 clone which acquires resistance to 1,25-(OH)2D3 in the induction of cell differentiation by a defect at the postreceptor step, as reflected by resistance to other differentiation inducers, such as retinoic acid and dimethyl sulfoxide. Even in this resistant clone, dbcAMP significantly enhanced the differentiation-inducing effect of 1,25-(OH)2D3. Of interest, this clone showed resistance to dbcAMP in the induction of cell differentiation. Furthermore, we have demonstrated that intracellular cAMP levels were significantly lower in uremic serum-treated cells than in cells treated with normal human serum and that a significant positive correlation was found between intracellular cAMP levels and 1,25-(OH)2D3-induced cell differentiation. These data indicated that the intracellular cAMP level is one of the major determinants of 1,25-(OH)2D3-induced HL-60 cell differentiation and that dbcAMP could enhance the effects of 1,25-(OH)2D3 on HL-60 cells not only by increasing 1,25-(OH)2D3 receptor levels but also at the postreceptor step.

Bucladesine↗
PubMed1992

A new, highly sensitive assay for 1,25-dihydroxyvitamin D not requiring high-performance liquid chromatography: application of monoclonal antibody against vitamin D receptor to radioreceptor assay.

A new, highly sensitive radioreceptor assay, which does not require high-performance liquid chromatography, has been developed for the determination of 1,25-dihydroxyvitamin D3 (1,25-(OH2)D3) in serum. The assay involves rapid extraction of serum, Sep Pak silica purification, and addition of 1,25-dihydroxyvitamin D3 receptor, radiolabeled 1,25-dihydroxyvitamin D3, bovine serum albumin, and monoclonal antibody to specifically precipitate the receptor. This method is sensitive to 0.3-0.6 pg/tube, with B50 occurring at 5.8 pg/tube. This sensitivity combined with overall recovery of 1,25-dihydroxyvitamin D3 (81.5 +/- 5.2%, n = 50, mean +/- SD) allows the measurement of serum 1,25-(OH)2D3 in duplicates with only 0.5 ml of serum. Intra- and interassay coefficient of variation were 9.5 and 14.6%, respectively. Dilution analysis, analytical recovery of added 1,25-dihydroxyvitamin D3, and comparison with a standard method using HPLC have been used to validate the assay. Serum 1,25-dihydroxyvitamin D3 level was for normal adults, 36.6 +/- 10.5 pg/ml (n = 14); in primary hyperparathyroidism, 98.9 +/- 19.9 pg/ml (n = 16); in chronic renal failure, 17.8 +/- 5.1 pg/ml (n = 12). This method allows large numbers of samples to be processed at once. Further, the method is rapid and provides an accurate assay using small amounts of serum.

Administration, Oral↗
PubMed1992

A possible role of carbohydrate moieties in prostaglandin D2 and prostaglandin E2 receptor proteins from the porcine temporal cortex.

The binding activities of prostaglandins (PGs) D2 and E2 were measured after deglycosylation of P2 membranes prepared from the porcine temporal cortex in order to investigate the role of carbohydrate moieties in the receptor binding. PGD2 and PGE2 binding activities were significantly decreased by pretreatment with various exoglycosidases, such as neuraminidase for PGE2 binding, alpha-mannosidase and beta-galactosidase for PGD2 binding, and beta-N-acetylhexosaminidase for both. Further, peptide N-glycohydrolase F and endo-alpha-N-acetylgalactosaminidase, which are specific for the cleavage of N-glycan and O-glycan linkages, respectively, in glycoproteins were used. Pretreatment with either of them also reduced both PGD2 and PGE2 binding activities. The reduction was dependent on the pretreatment time and enzyme concentration. The time courses of the reduction were typically characterized by a marked increase in the nonspecific bindings. Scatchard plot analysis revealed that the reduction was caused by a decrease in the affinity rather than one in the maximal binding capacity. The specificity of the binding sites thereby shifted to be more nonspecific without affecting the order of the relative affinities among PGs for the binding sites. These results suggest that the carbohydrate moieties on PG receptor proteins of the brain are essential for the expression of their binding activities.

Amidohydrolases↗
PubMed1992

Partial protection of 1 alpha-hydroxyvitamin D3 against the development of diabetes induced by multiple low-dose streptozotocin injection in CD-1 mice.

1 alpha-Hydroxyvitamin D3 (1 alpha-OH-D3), a precursor of active vitamin D3, 1 alpha,25-dihydroxyvitamin D3, was tested in CD-1 mice for its in vivo effect against the development of diabetes induced by administering multiple low doses of streptozotocin (STZ). Daily intraperitoneal (IP) injections of 35 mg/kg body weight of STZ administered for 5 consecutive days to mice from 7 weeks of age induced a delayed-onset hyperglycemia, insulitis, and beta-cell degranulation in 26 of 28 mice. Only 12 of 29 mice developed diabetes when treated with simultaneous daily IP injections of 1 alpha-OH-D3 for 14 consecutive days, with diabetes defined as a plasma glucose level greater than 200 mg/dL. A daily dose of 0.3 micrograms/kg 1 alpha-OH-D3 also protected against the development of hyperglycemia in five of 13 mice, whereas 0.2 micrograms/kg 1 alpha-OH-D3 was ineffective, indicating a dose-related effect. Histological study showed that, among the 1 alpha-OH-D3-treated mice, the pancreatic islets of euglycemic mice showed neither massive islet infiltration nor beta-cell degranulation, whereas those of the hyperglycemic mice showed insulitis. However, when diabetes was chemically induced with a single high dose of STZ, the simultaneous administration of 1 alpha-OH-D3 to mice failed to protect against the development of hyperglycemia; all five mice so treated developed hyperglycemia. Their pancreatic islets did not show insulitis. Therefore, it is suggested that 1 alpha-OH-D3 may protect against the development of diabetes following administration of multiple low doses of STZ, probably via an immune mechanism.

Animals↗
PubMed1992

Segmental gut transit in diabetes mellitus: effect of cisapride.

Gut transit using radiopaque markers was assessed in 5 healthy subjects and 24 diabetic patients. In the diabetics, various parameters including duration of the disease and diabetic complications, such as neuropathy, retinopathy and nephropathy, were determined, and the relationships between gut transit times and these complications were evaluated. The effect of cisapride on gut transit was studied in 10 diabetic patients. Large intestinal, descending colon, distal colon, and whole gut transit times were delayed in diabetics with autonomic neuropathy compared to controls and to diabetics without autonomic neuropathy (P less than 0.01). There was no difference in proximal colon transit times among them. An inverse correlation was observed between CVRR and the transit times for descending colon, distal colon, large intestine and whole gut. Large intestinal and whole-gut transit times were delayed in diabetics with retinopathy or with nephropathy compared to diabetics without those complications (P less than 0.01). In the diabetics, oral administration of 7.5 mg/day of cisapride for 2 weeks significantly accelerated descending colon transit (P less than 0.05) and partially accelerated distal colon, large intestinal and whole-gut transit. It is concluded that diabetics with autonomic neuropathy have delayed transits for the whole gut and that this finding is apparent to some extent in the distal colon but not in the proximal colon. Chronic oral administration of cisapride, a gastrointestinal prokinetic drug, was effective to improve these gastrointestinal motility disorders in diabetics with autonomic neuropathy.

Administration, Oral↗
PubMed1992

Impaired metabolism of high density lipoprotein in uremic patients.

We measured lipoproteins, apolipoproteins, lipoprotein lipase (LPL), hepatic triglyceride lipase (HTGL), lecithin: cholesterol acyltransferase (LCAT) and parameters of calcium metabolism to evaluate the roles of these enzymes and hypertriglyceridemia for impaired high-density lipoprotein (HDL) metabolism in chronic renal failure, and to examine the impact of altered calcium homeostasis on the lipoprotein-regulating enzymes. The subjects were 25 healthy volunteers and 66 uremic patients, 24 treated with hemodialysis (HD) and 42 with continuous ambulatory peritoneal dialysis (CAPD). Lipoprotein analysis revealed: (1) reduction in HDL cholesterol especially in HDL2 subfraction; (2) increase in HDL triglyceride; and (3) decreased ratio of HDL2 cholesterol to HDL3 cholesterol in both HD and CAPD patients. Simple regression analysis showed: (1) a positive correlation between VLDL triglyceride and triglyceride/cholesterol ratio of HDL; (2) positive correlations of LPL level in post-heparin plasma to cholesterol concentrations in HDL2, HDL3 and total HDL, and to apolipoproteins A-I and A-II; and (3) inverse correlations of HTGL to HDL2 cholesterol and to the ratio of HDL2 cholesterol/HDL3 cholesterol. Multiple regression analysis of HDL cholesterol indicated positive association with LPL and inverse correlation with VLDL triglyceride. Four variables including LPL, HTGL, LCAT and VLDL triglyceride explained 51.5% of the variation of HDL cholesterol. HDL2 cholesterol was associated positively with LPL and negatively with VLDL triglyceride in the model. HDL3 cholesterol was associated positively with LPL, HTGL and LCAT and inversely with VLDL triglyceride. Stepwise multiple regression analysis indicated that independent predictors of HTGL were gender, parathyroid hormone levels by a mid-portion assay, ionized calcium and age, and that those of LCAT were ionized calcium and age.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins↗
PubMed1992

Altered calcium homeostasis accompanying changes of regional bone mineral during a very-low-calorie diet.

Calcium homeostasis during a very-low-calorie diet (VLCD) was examined. During the treatment, intact parathyroid hormone tended to decrease initially, bone Gla-protein increased significantly in the third week, and tartrate-resistant acid phosphatase decreased during the entire treatment. Serum ketone bodies showed significant correlations with intact parathyroid hormone and bone Gla-protein in some cases. Regarding bone mineral content, bone mineral content of the head increased while that of the legs decreased, resulting in no significant changes in total bone mineral content. These results suggest that VLCD treatment alters calcium homeostasis, which may cause regional bone mineral changes.

Acid Phosphatase↗
PubMed1992

High-density-lipoprotein metabolism during a very-low-calorie diet.

We examined the changes in high-density-lipoprotein (HDL) metabolism in eight female obese patients undergoing a very-low-calorie diet (VLCD). In the first half of the study, HDL cholesterol (HDL-C), apolipoprotein A-I (apo A-I), and apo A-II showed a parallel decrease. Although lipoprotein lipase (LPL) and hepatic lipase (HTGL) did not change, lecithin: cholesterol acyltransferase (LCAT) decreased. In the latter half of the protocol, HDL-C and apo A-I increased whereas apo A-II decreased, resulting in increased apo A-I-A-II ratios. There was no change in LPL, HTGL, or LCAT. LCAT and apolipoprotein composition may be important in HDL-C changes after VLCD.

Acyltransferases↗
PubMed1992

Transport of 1,5-anhydro-D-glucitol into human polymorphonuclear leukocytes.

1,5-Anhydro-D-glucitol (AG) is one of the main polyols and its structure resembles glucose. It has been proposed that decreased serum AG concentrations in diabetic patients are a novel indicator of diabetic metabolic derangement. However, the pathway of AG metabolism still remains to be clarified. In this study we investigated the transport of AG into human polymorphonuclear leukocytes (PMNLs) isolated from healthy volunteers and found that 0.1 mM 3-O-methy-D-glucose (3OMG) was equilibrated with a half saturation time of 10 s, while the uptake rate of AG was much slower. The concentration dependence of AG uptake revealed that the AG transport velocity reached a plateau, with a Km of about 50 mM and Vmax of about 25 nmol/min/10(7) cells. Transport of 14C-labeled 3OMG was inhibited by unlabeled D-glucose or AG in a dose-dependent manner. The mean inhibition constant (Ki) for D-glucose and for AG were 1.06 and 4.93 mM, respectively. Cytochalasin B (20 microM) inhibited 3OMG transport by 90% but AG transport by only 50%. S/V for 14C-labeled AG transport plotted against the concentration of unlabeled 3OMG showed a non-linear and biphasic pattern. These results suggest that AG influx into PMNLs is mediated not only by the cytochalasin B-sensitive glucose transport system but also via another facilitated transport system.

3-O-Methylglucose↗