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Biomedical subjects

H Morii

Publications and source records attributed to H Morii.

At least 235 records · Page 13Linked to original sources
PubMed1992

Plasma 1,5-anhydroglucitol concentration in patients with end-stage renal disease with and without diabetes mellitus.

The plasma concentration of 1,5-anhydroglucitol, a new clinical marker of glycemic control in diabetic patients, was evaluated as a marker of glycemia in 83 diabetic and nondiabetic patients with end-stage renal disease. Plasma 1,5-anhydroglucitol concentration decreased and correlated inversely with blood glucose, hemoglobin A1c, or fructosamine in 48 diabetic patients with normal renal function. In 13 nondiabetic patients with end-stage renal disease not on dialysis, plasma 1,5-anhydroglucitol concentrations were lower than in 23 healthy subjects (6.22 +/- 2.10 vs. 24.20 +/- 7.50 micrograms/ml, respectively). The plasma concentration of 1,5-anhydroglucitol concentration in nondiabetic patients with end-stage renal disease was inversely correlated to the urinary N-acetyl-beta-D-glucosaminidase activity (r = -0.634) but not to blood glucose, hemoglobin A1c, or fructosamine. Renal tubular damage may contribute to the low plasma concentration of 1,5-anhydroglucitol in this group. The plasma concentrations of this polyol decreased in both diabetic (4.63 +/- 1.08 micrograms/ml) and nondiabetic patients on hemodialysis (4.71 +/- 0.87 micrograms/ml). In these two groups, there was no correlation between plasma concentration of this polyol and blood glucose, hemoglobin A1c, or fructosamine. The plasma concentration of 1,5-anhydroglucitol decreased after a single hemodialysis session. The results showed that impaired renal function and removal of 1,5-anhydroglucitol by dialysis may contribute to its decreased concentration in patients with end-stage renal disease, but that glycemic control does not. Therefore, we should consider renal function when we use plasma 1,5-anhydroglucitol concentration as a marker of glycemic control in diabetic patients.

Adult↗
PubMed1992

Evidence for the presence of differently glycosylated forms of prorenin in the plasma of anephric man.

Previously, we unexpectedly observed that plasma inactive renin (trypsin-activatable renin) in bilaterally nephrectomized rats is not prorenin. To determine whether plasma inactive renin in anephric man is prorenin, we examined the immunological and biochemical properties of plasma inactive renin from five anephric patients. There were significant concentrations of inactive renin (5.33 +/- 2.08 ng/L.s) in plasma of anephric patients, while active renin was negligible (0.06 +/- 0.01 ng/L.s). The inactive renin from anephric patients could be immunoprecipitated 97 +/- 1% by specific antiserum against the prosegment portion of prorenin. Specific antimature renin serum completely inhibited the angiotensin-I-generating activity of inactive renin induced by trypsin treatment. The molecular mass of inactive renin from anephric patients (49.0 +/- 0 kDa), estimated by gel permeation high performance liquid chromatography, was similar to that of normal human plasma prorenin (48.2 +/- 0.8 kDa). These results indicate that plasma inactive renin in anephric man is prorenin, findings different from our previous observations obtained in anephric rats. Concanavalin-A chromatography separated inactive renin from anephric patients into three forms, including the column-unbound form, the loosely bound form, and the tightly bound form. Thus, in anephric man, differently glycosylated multiple forms of prorenin are released into the circulation from an extrarenal organ(s).

Adult↗
PubMed1992

Radioimmunoassay for calcitonin gene-related peptide and its measurement in sera of patients with thyroid disease.

To investigate serum levels of calcitonin gene-related peptide (CGRP), we developed a sensitive radioimmunoassay (RIA). RIA for CGRP in serum can present some problems: the serum may degradate the tracer during incubation and suppress the antigen-antibody reaction. We avoided these problems by using aprotinin and CGRP-free serum instead of a buffer for the standard curve. We detected serum CGRP in all 39 healthy subjects when CGRP-free serum was not used for the standard curve, but 34 of these subjects had serum CGRP levels below the detection limit (less than 80 pmol/l) when CGRP-free serum was used for the standard curve. We defined the normal range for serum CGRP as below 100.8 pmol/l, which was the maximum level found in the healthy subjects. We studied serum levels of this peptide in patients with thyroid diseases, because the thyroid may be one origin of circulating CGRP. Four of 10 patients with medullary thyroid carcinoma had elevated serum levels of CGRP. Seven of 24 patients with subacute thyroiditis had elevated serum levels of CGRP, but at least one year after clinical recovery, CGRP was undetectable in all. Seven of the 37 patients with hypothyroidism had elevated serum levels of CGRP. None of the patients with hyperthyroidism, adenomatous goiter, thyroid adenoma, or thyroid carcinoma had elevated serum CGRP levels. It is necessary to use a standard curve obtained by the addition of aprotinin and CGRP-free serum to the assay standards to measure serum CGRP levels. Some patients with subacute thyroiditis, hypothyroidism, or medullary thyroid carcinoma had elevated serum CGRP levels.

Adult↗
PubMed1992

Magnesium deficiency enhances secretion of parathyroid hormone in normal and 5/6-nephrectomized uremic rats.

Hypercalcemia, rather than hypocalcemia, has been observed in conjunction with severe magnesium (Mg) depletion in rat, in contrast to the development of hypocalcemia in Mg deficiency in various animal models. In the present study, a possible involvement of parathyroid hormone (PTH) in the development of hypercalcemia in rat was studied by using a newly-developed sensitive and specific radioimmunoassay system for the determination of rat PTH. In normal rat model, hypercalcemia occurred in association with a decrease of serum phosphate levels in Mg deficiency. However, serum PTH levels were not suppressed despite the occurrence of hypercalcemia, suggesting PTH as an important factor for the development of hypercalcemia. Of interest, in 5/6-nephrectomized uremic model, hypocalcemia, rather than hypercalcemia, was observed in Mg-deficient rats. Serum PTH levels seemed to be higher, but not statistically significant probably due to a small number of rats. However, infusion study clearly demonstrated that PTH secretion was significantly increased in Mg-deficient uremic rats compared with Mg-replete counterparts. The reason for an increase of serum PTH responses might be explained by Mg depletion itself in addition to a fall in serum Ca levels, because infusion study revealed that the magnitude of the stimulation of PTH secretion was increased in Mg deficiency despite the similar degrees of changes in serum Ca levels and that the set point for the suppression of PTH secretion by Ca might be altered in Mg deficiency. Taken these data together, it was strongly suggested that Mg depletion might enhance PTH secretion in rat.

Animals↗
PubMed1992

[Vitamin D3].

With the application of biochemical technique came the discovery that vitamin D is metabolized sequentially to 25-hydroxyvitamin D in liver and then to 1.25-dihydroxyvitamin D (1.25D), the hormonal form of vitamin D, in kidney. The latter process is strictly controlled with the demand of calcium and phosphorus. The produced 1.25D binds its specific receptor probably located in the nuclei. With the application of modern tools of molecular biology came the discovery that vitamin D receptor (VDR), which belongs to steroid receptor family, acquires increased affinity for DNA when it binds to 1.25D and then VDR complexes bind to DNA with its two zinc-finger projections. VDR complexes recognize vitamin D responsive element on DNA, two tandemly repeated hexanucleotide sequences separated by three base pairs. Furthermore, to interact with the VDRE, VDR complexes require nuclear accessory factor, which might be retinoid X receptor (RXR). As above, molecular biology helps us to extend our knowledge in the field of vitamin D.

Calcitriol↗
PubMed1992

A two-site immunochemiluminometric assay for intact parathyroid hormone and its clinical utility in hemodialysis patients.

Measurement of serum parathyroid hormone (PTH) concentrations is complicated by the fact that there are several fragments of the hormone in the circulating as a result of the metabolism of PTH. The best way to study the secretory activity of the parathyroid glands directly may be to measure the biologically active intact PTH molecule. Recently, it has become possible to overcome these limitations by application of the two-site immunoradiometric assay (IRMA) to the measurement of intact PTH. The two-site immunometric technique has been applied to the two-site immunochemiluminescent assay (ICMA) for the measurement of circulating intact PTH. To evaluate the utility of measurements of serum intact PTH by two-site ICMA in hemodialysis patients, two-site ICMA and IRMA were compared in 104 hemodialysis patients. We found a good correlation (r = 0.93) between values obtained by ICMA and by IRMA. Although serum intact PTH by ICMA was significantly suppressed by rising plasma ionized calcium after a session of hemodialysis in 29 patients, mid-region PTH did not show a significant change. This result suggests the intact PTH assay is more suitable for the earlier detection of secondary hyperparathyroidism than the mid-region assay and may be useful for precise assessment of clinical status and response to therapeutic intervention designed to correct the progressive bone disease in hemodialysis patients. We conclude that two-site ICMA for serum intact PTH which could be measured without radioisotopes nor scintillation counter is as useful as IRMA in hemodialysis patients.

Humans↗
PubMed1992

High serum lipoprotein(a) concentrations in uremic patients treated with continuous ambulatory peritoneal dialysis.

We measured serum lipoprotein(a) [Lp (a)] concentrations in 50 uremic patients treated on continuous ambulatory peritoneal dialysis (CAPD) and compared them with those in 29 uremic patients on hemodialysis (HD) and those in 62 normal controls. The median values were 47.9 mg/dl in CAPD patients, 25.2 mg/dl in HD patients, and 11.7 mg/dl in controls, respectively. These differences were statistically significant when assessed by Kruskal-Wallis test (p < 0.0001). Thirty-five out of 50 patients on CAPD (70%) and 12 out of 29 patients on HD (41%) had Lp(a) concentrations above 30 mg/dl, whereas these high values were observed in only 15% of normal controls. This difference in prevalence of high Lp(a) was also significant by 2 x 3 chi-square test (p < 0.01). There was a significant positive correlation between Lp(a) and apolipoprotein B (r = 0.517, p < 0.0001). In CAPD patients, 9 with ischemic heart disease had a significantly higher median Lp(a) than those without it (67.4 vs 40.9 mg/dl, p < 0.01 by Mann-Whitney U-test). These results suggest that high levels of serum Lp(a) might contribute to an increased risk for ischemic heart disease in CAPD patients, and that there may be a relationship between Lp(a) and apolipoprotein B metabolism in CAPD patients.

Adult↗
PubMed1992

Inhibitory effect by 1,25-dihydroxyvitamin D3 on concanavalin A-stimulated proliferation of rat thymic lymphocytes.

It has been reported that vitamin D3 derivatives promote the differentiation of monocytes into macrophages, while the derivatives suppress mitogen-stimulated proliferation of human peripheral blood-mononuclear cells (PBMC). However, their effect on thymic lymphocytes which are in the course of differentiation and maturation into T cells has not been thoroughly examined. The authors studied the inhibitory effect by 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] on concanavalin A (Con A)-stimulated proliferation of rat thymic lymphocytes and explored its mechanism. The proliferation of rat thymic lymphocytes stimulated with Con A was suppressed by 1,25-(OH)2D3 in a dose-dependent manner between a range of 10(-10) M to 10(-8) M. Because this suppressive action of 1,25-(OH)2D3 was markedly reduced by removal of coexisting adherent cells or by treatment with indomethacin which suppresses the prostaglandin E2 (PGE2) synthesis, it seems likely that PGE2, released from macrophages with the stimulation of 1,25-(OH)2D3, is involved in the suppressive action. Further studies on the inhibitory mechanism clarified that PGE2 from the contaminated macrophages suppressed the formation and release of interleukin-2 (IL-2), whereas the expression of IL-2 receptors on thymic lymphocyte with Con A stimulation was not affected. These results suggest that vitamin D3 derivatives might possibly contribute to regulation of in vitro proliferation of thymic lymphocytes.

Animals↗
PubMed1992

Extracellular matrix protein: gene expression and synthesis in cultured rat mesangial cells.

Production of extracellular matrix (ECM) by mesangial cells (MCs) contributes to progressive glomerulosclerosis. Our previous immunocytochemical studies on ECM production by MCs [1] were extended by examining the gene expression and protein synthesis using Northern blotting and ELISA. ELISA demonstrated that fetal calf serum (FCS) stimulated the synthesis of collagen I (CI), III (CIII) and IV (CIV), and laminin (LM). At and after confluence, the amounts of CIII, CIV and LM per DNA amount began to decrease, whereas that of CI did not. Northern blotting indicated that the mRNA expressions for CIV and LM were transiently increased by FCS. The mRNA expressions for CI and CIII decreased until confluence and then returned to the initial levels. These results suggest that FCS and cellular confluence affected the synthesis of ECM at both the level of gene expression and protein synthesis. The mRNA expressions for CIV and LM paralleled the protein synthesis and appeared tightly regulated. CI and CIII synthesis and mRNA expression were not coordinate and were not regulated in the same manner as the basement membrane matrix components.

Animals↗
PubMed1991

Fluctuation and rotation of human growth hormone-releasing factor in the presence and the absence of phospholipid bilayer analyzed by time-resolved fluorescence depolarization.

Time-resolved fluorescence depolarization measurements were carried out for human growth hormone-releasing factor analog ([Trp10]-hGRF (1-29) NH2), where the Trp10 residue was incorporated as a fluorescent probe, in the presence and the absence of 1,2-dimyristoyl-sn-glycero-3-phospho-rac- glycerol(DMPG) liposome and in aqueous 2,2,2-trifluoroethanol (TFE) solution. The fluorescence lifetimes and the rotatory correlation times of the peptide in each medium were determined. The apparent volumes of the rotatory Brownian motion unit calculated from these fluorescent parameters indicate the different mode of the fluctuation and/or the rotation of the peptide in each medium, such as: (i) In the aqueous solution, several segments of the peptide fluctuate individually. (ii) In the DMPG bilayer, both the local fluctuation of Trp residue alone and the rotation of the whole molecule exist. (iii) In the aqueous TFE solution, the monomeric peptide rotates as a rigid ellipsoid.

Amino Acid Sequence↗
PubMed1991

A possible mechanism of mitochondrial dysfunction during cerebral ischemia: inhibition of mitochondrial respiration activity by arachidonic acid.

The dramatic increase in the arachidonic acid (AA) level in the brain is a well-known molecular event during cerebral ischemia. As mitochondria are known to be one possible site of the cell damage, the effects of AA on the respiratory activity of rat brain mitochondria were investigated in vitro using an oxygen electrode. In NAD-linked respiration, respiratory control ratio was decreased significantly by AA, with an IC50 of 6.0 microM. AA had the dual effect on mitochondrial respiration, a decrease in state 3 and uncoupled state and an increase in state 4 (i.e., uncoupling) as reported by Hillered and Chan (J. Neurosci. Res. 19, 94-100, 1988). Furthermore, we found that other unsaturated long-chain free fatty acids (C18:1-C18:3, C20:1-C20:5) also showed such a dual effect. Cyclooxygenase metabolites of AA such as prostaglandins (D2, E2, F2 alpha, E1) and thromboxane B2, and lipoxygenase metabolites such as leukotrienes (D4, B4) and 5- or 12-hydroperoxyeicosatetraenoic acid had no significant effect. The inhibition of the uncoupled state by AA was more marked in NAD-linked than that in FAD-linked respiration, while the degree of uncoupling by AA were the same in both respirations. In spectrophotometrical measurement, the reduction of cytochromes and flavo-protein was markedly inhibited by AA in NAD-linked respiration, but not in the FAD-linked one. In addition, the activity of cytochrome c oxidase was scarcely inhibited by AA. These data suggest that AA itself, not its metabolites, may inhibit mitochondrial ATP production during brain ischemia and that AA may act on the site(s) closely related to NAD-linked respiration, but not the FAD-linked one, in addition to its uncoupling effect.

Animals↗
PubMed1991

Inhibition of rat brain prostaglandin D synthase by inorganic selenocompounds.

Various inorganic selenocompounds dose-dependently inhibited the rat brain prostaglandin (PG) D synthase, both in the purified enzyme preparation and in the crude brain supernatant. All of the quadrivalent selenium compounds tested had a very limited range of IC50 values in the purified enzyme (11-12 microM) and in the brain supernatant (9-15 microM). A divalent selenium compound was also inhibitory, but a hexavalent selenium compound was ineffective. In contrast, organic selenocompounds such as selenomethionine and selenourea had no effect on the PGD synthase activity. Furthermore, sodium sulfate and sodium sulfite up to 10 mM did not inhibit the activity. The inhibition by selenium required the preincubation of the metal with sulfhydryl compounds such as dithiothreitol (DTT), indicating that the formation of selenotrisulfide or some other adduct(s) is essential for the inhibition. Furthermore, the inhibition was reversed by an excess amount of dithiothreitol, suggesting that the selenotrisulfide derivative of DTT binds to the SH group of the PGD synthase. The kinetic analysis revealed the inhibition by selenite to be noncompetitive with a Ki value of 10.1 microM. On the other hand, glutathione-dependent PGD synthase from rat spleen was much less inhibited, and PGF synthase and PGD2 11-ketoreductase activities were not inhibited by the selenium compound.

Animals↗
PubMed1991

Selective inhibition of NADH-CoQ oxidoreductase (complex I) of rat brain mitochondria by arachidonic acid.

The effects of arachidonic acid on the enzyme complexes in the electron transport system were investigated using submitochondrial particles from rat brain. Arachidonic acid irreversibly inhibited NADH-CoQ oxidoreductase (complex I) activity, but had no effect on the activities of succinate-CoQ oxidoreductase (complex II), CoQH2-cytochrome c oxidoreductase (complex III), cytochrome c oxidase (complex IV), ATPase (complex V), glutamate dehydrogenase, and malate dehydrogenase up to 50 microM. The inhibition was dose-dependent with an IC50 value of 110 nmol/mg protein. The Lineweaver-Burk plot revealed that the inhibition by arachidonic acid was noncompetitive against CoQ with a Ki value of 33 microM and uncompetitive against NADH with a Ki value of 22 microM.

Animals↗
PubMed1991

Effects of parathyroid hormone on ornithine decarboxylase activity in human osteosarcoma cells.

Ornithine decarboxylase (ODC) is a rate-limiting enzyme of the biosynthesis of polyamines, which are important in cell growth and differentiation. Here, we studied whether parathyroid hormone (PTH) affects the induction of ODC and the proliferation of the human osteoblast-like cell line SaOS2, which is sensitive to PTH. In confluent cells, ODC activity was not detected, but activity was significantly induced by fresh medium, with maximum activity 6 h after the change. PTH potentiated this enzyme induction in a dose-dependent manner at 10(-9) and 10(-8) M at which range the intracellular cAMP level also rose. Dibutyryl cAMP, cholera toxin, and 3-isobutyl-1-methylxanthine each caused an increase in ODC activity similar to that with PTH. The half-life of enzyme activity was about 30 min and was not changed by the addition of PTH. mRNA coding for ODC was detected in the confluent cells and its concentration was increased two- to threefold by the fresh medium. No further increase in mRNA occurred when PTH was added. At 48 h after the change of medium, PTH inhibited the DNA synthesis induced by fresh medium. These results suggest that the increase in ODC activity caused by PTH was caused by enhancement of cAMP synthesis, and that this augmentation involves post-transcriptional regulation.

Bucladesine↗