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Biomedical subjects

H Morii

Publications and source records attributed to H Morii.

At least 307 records · Page 17Linked to original sources
PubMed1989

Late-phase accumulation of inositol phosphates stimulated by prostaglandins D2 and F2 alpha in neuroblastoma x glioma hybrid NG108-15 cells.

The accumulation of inositol phosphates (IPs) in response to prostaglandins (PGs) was studied in NG108-15 cells preincubated with myo-[3H]inositol. As a positive control, bradykinin caused accumulation of IPs transiently at an early phase (within 1 min) and continuously during a late phase (15-60 min) of incubation in the cells. PGD2 and PGF2 alpha did not significantly cause the accumulation of IPs at an early phase but significantly stimulated inositol bisphosphate (IP2) and inositol monophosphate (IP) formation at late phase of incubation. The maximum stimulation was obtained at greater than 10(-7) M concentrations of these PGs, the levels being three-and twofold for IP2 and IP1, respectively. 9 alpha, 11 beta-PGF2 has a slight effect but PGE2 and the metabolites of PGD2 and PGF2 alpha have no effect up to 10(-6)M. The effects of PGD2 and PGF2 alpha were not additive, but the effect of each PG was additive to that of bradykinin at a late phase of incubation. Inositol 1-monophosphate was mainly identified in the stimulation by 10(-5) M PGD2 and 10(-5) M PGF2 alpha, whereas both inositol 1-monophosphate and inositol 4-monophosphate were produced in the stimulation by 10(5) M bradykinin. Depletion of extracellular Ca2+ diminished the stimulatory effect of PGD2 and PGF2 alpha and late-phase effect of bradykinin, but simple Ca2+ influx into the cells by high K+, ionomycin, or A23187 failed to cause such late-phase effects. These results suggest that PGD2 and PGF2 alpha specifically stimulate hydrolysis of inositol phospholipids.

Animals↗
PubMed1989

Clinical availability of serum fructosamine measurement in diabetic patients with uremia. Use as a glycemic index in uremic diabetes.

Serum fructosamine levels were investigated in patients with uremia undergoing various modes of treatment. The serum fructosamine levels correlated positively with the blood glucose levels determined a week or two earlier. The fructosamine levels were significantly affected by the protein concentration, and those corrected for protein concentrations had a closer correlation to the blood glucose levels than did the uncorrected levels. The corrected fructosamine levels were not significantly different between healthy volunteers and nondiabetic patients with uremia on conservative treatment. In an in vitro system, fructosamine concentrations were hardly affected by urea, which is known to influence the level of hemoglobin A1. These results suggest that serum fructosamine measurement can provide us with reliable information on a short-term glycemic condition, even in azotemic patients. To be more precise, the serum level of fructosamine corrected for protein concentration can be an excellent glycemic index which is not susceptible to over- or dehydration and is of high clinical value, especially in the management of diabetic patients with chronic renal failure.

Adult↗
PubMed1989

Evidence against the importance in the disease process of antibodies to bovine thyroid-stimulating hormone found in some patients with Graves' disease.

The antibody to TSH (TSH-Ab) found in some patients with Graves' disease may be either an antiidiotype (anti-id-Ab) to the TSH receptor antibody (TRAb) or the antigen (idiotype) for which the anti-id-Ab is in fact TRAb. Four groups have found antibodies to bovine TSH (bTSH-Ab) in Graves' disease patients in a TSH binding-inhibiting immunoglobulin (TBII) RRA that uses [125I]bTSH. In this assay serum samples containing bTSH-Ab give highly negative TBII values. The purpose of this study was to look for any clinical significance of potential idiotypic-antiidiotypic network regulation related to bTSH-Ab. Twenty-one (0.49%) of 4285 Graves' disease patients had TBII values less than the mean -4 SD of normal subjects. In all 21, bTSH-Ab was found by incubation of [125I]bTSH with the patient's serum, and significant inhibition of binding of bTSH-Ab to bTSH by human TSH was found in only 3 of these serum samples. We investigated next whether the binding site of the anti-TSH-Ab mimicked the TSH receptor-binding site. Binding of [125I]bTSH to bTSH-Ab-positive serum was not inhibited by bTSH-Ab-negative, thyroid-stimulating immunoglobulin-positive [(+)], and/or TBII(+) immunoglobulin G. In one patient with human TSH-Ab, TSH-Ab appeared and disappeared, and when TSH-Ab was negative, TBII was positive. Inhibition of [125I]bTSH binding to TSH-Ab by the same patient's serum when that patient was serum thyroid-stimulating immunoglobulin(+), TBII(+), and TSH-Ab-negative was sought but not found. Changes in serum TSH-Ab activity and disease activity were not correlated in this patient. In six untreated patients with Graves' hyperthyroidism with bTSH-Ab, the serum T3 and T4 concentrations and the time required to become euthyroid during antithyroid drug treatment were not significantly different from those in 52 such patients without bTSH-Ab. These data suggest that bTSH-Ab is not an anti-id-Ab to TRAb and that TSH-Ab does not directly modulate the activity of Graves' disease.

Animals↗
PubMed1989

Thyroid peroxidase activity-inhibiting immunoglobulins in patients with autoimmune thyroid disease.

The thyroid microsomal antibody (M-Ab) has been found to be an antibody against thyroid peroxidase (TPO), and such antibodies have been reported not only to bind TPO but also to directly inhibit TPO activity. In this study we investigated the relationship between TPO activity-inhibiting immunoglobulin (TPII) and thyroid function in 55 untreated patients with hyperthyroidism due to Graves' disease and 35 untreated patients with Hashimoto's disease. TPO partially purified from the microsomal fraction of Graves' thyroid tissue by Sephacryl S-300 gel filtration was incubated with immunoglobulin (Ig) fractions of serum prepared by precipitation with 15% polyethylene glycol. At the end of incubation, TPO activity was measured by a guaiacol assay. The TPII level was expressed as the TPII index, defined as the inhibition of TPO activity by patient Ig divided by inhibition produced by a known positive Ig. We also measured serum free T4, free T3, and TSH concentrations and anti-M-Ab titers, the latter by a microenzyme-linked immunosorbent assay. When a positive TPII index was defined as more than the mean + 2 SD of the TPII index (0.38) for 15 normal subjects, 13 patients with Graves' disease and 14 patients with Hashimoto's disease had positive TPII index values. There was a positive correlation between the TPII index values and the M-Ab titers in patients with either Graves' disease (r = 0.38; P less than 0.01) or Hashimoto's disease (r = 0.52; P less than 0.01). The mean TPII index in patients with Hashimoto's disease was significantly higher than that in patients with Graves' disease [0.38 +/- 0.42 (+/- SD) vs. 0.19 +/- 0.41; P less than 0.05]. The slope of the regression line between the TPII index values and the M-Ab titers for patients with Hashimoto's disease was steeper than that for patients with Graves' disease. The mean serum free T4 concentration was significantly lower in those patients with Hashimoto's disease who had positive TPII index values than in those with negative TPII index values (14.0 +/- 5.0 vs. 9.6 +/- 3.7 pmol/L; P less than 0.01). There was no significant difference in thyroid function between the patients with Graves' disease with positive and negative TPII index values. TPII appears to inhibit thyroid function in some patients, but no simple relationship between TPII and thyroid function in autoimmune thyroid disease was demonstrated. Understanding the factors that control access of anti-TPO antibody to its antigen may help to elucidate the significance of circulating anti-TPO antibody.

Adolescent↗
PubMed1989

Serum parathyroid hormone concentration measured by highly sensitive assay in post-thyroidectomy hypocalcemia of patients with Graves' disease.

To investigate the role of parathyroid function in transient hypocalcemia after subtotal thyroidectomy for Graves' disease, the serum parathyroid hormone (PTH) concentration and nephrogenous (N) cAMP were measured in 16 patients before and after surgery. Serum PTH was measured with two commercially available kits (PTH-M, PTH-C), PTH-M is a recently developed highly sensitive assay using an antibody recognizing the mid-portion of human PTH and a synthetic 125I-tyr45-human PTH (43-68) as a radioligand. One of the 16 patients had severe clinical tetany and had a markedly lower PTH-M concentration and NcAMP after thyroidectomy. However, no significant change in serum PTH-M, PTH-C and NcAMP were observed in the other patients, although their serum calcium (Ca) concentrations decreased significantly. The Data were analyzed by dividing the patients according to the change in serum Ca or PTH. Serum PTH-M and PTH-C significantly decreased in 4 patients whose serum Ca clearly decreased after surgery. Serum Ca on the first postoperative day was significantly lower in patients whose serum PTH decreased after thyroidectomy than in patients whose serum PTH did not. Furthermore, the serum Ca concentration was significantly correlated with PTH-M, and with NcAMP on the third postoperative day. These data proved that hypofunction of the parathyroid gland is important in transient hypocalcemia after subtotal thyroidectomy for Graves' disease. The pathogenetic mechanism of transient hypocalcemia was discussed in comparison with the data from a patient who had overt parathyroid injury.

Calcium↗
PubMed1989

Biological activity of 26,26,26,27,27,27-hexafluoro-1,25-dihydroxyvitamin D3 in the chick.

A newly synthesized fluorinated analogue of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), 26,26,26,27,27,27-hexafluoro-1,25-dihydroxyvitamin D3 (26,27-F6-1,25-(OH)2D3) has been compared with 1,25(OH)2D3 as to its biological activity in vitamin D-deficient chicks. One day-old, white Leghorn cockerels were fed a rachitogenic diet for 5 weeks. They were then given vehicle or 32.5, 130 or 325 pmol of 26,27-F6-1,25(OH)2D3 or 1,25(OH)2D3 in a solution of propylenglycol:ethanol (95:5 v/v) sc every day for 2 weeks. Twenty-four hours after the last dose, the animals were sacrificed and their femurs were removed. 26,27-F6-1,25(OH)2D3 was more active than 1,25(OH)2D3 in stimulating growth, healing of rachitic cartilage visualized by soft X-ray radiography, elevation of serum inorganic phosphorus, and mineralization of rachitic bone. These biological differences between two compounds were observed only for the dose of 130 pmol. However, this fluorinated compound has less binding ability than 1,25(OH)2D3 to fetal chick intestinal cytosol receptors. The mechanism of the higher potency of this analogue is still unknown, but its affinity to the 1,25(OH)2D3 receptor does not account for the higher activity. Since 26-hydroxylation can be postulated as the inactivation step in vitamin D metabolism, these results suggest that the reason for increased activity of this fluorinated analogue is most likely its slower metabolism.

Animals↗
PubMed1989

[Analysis of the result of thyroid microsomal particle agglutination test by ELISA].

No accurate method to detect thyroid microsomal (MC) antibody (Ab) in serum has been generalized. In this study, the titer of MC Ab obtained by the method of MC autoantibody particle agglutination (MCPA) was analyzed by enzyme linked immunosorbent assay (ELISA). MC and thyroglobulin (Tg) were prepared from Graves' thyroid. ELISA was done by coating the plate with MC, adding Tg to buffer and using peroxidase-conjugated anti-h IgG. 1) The titer of MCPA correlated with the MC Ab ELISA index in serum without Tg Ab, but it did not in serum with Tg Ab. MC Ab was negative by ELISA while it was positive by MCPA in some of the sera with Tg Ab. 2) When ELISA was done using buffer without Tg, the amount of IgG bound to MC was greater in serum with TGPA: + and MCPA: - than in serum with MCPA: + and TGPA: -. 3) The zone phenomenon observed in MCPA did not always indicate an excess of MC Ab. 4) MC Ab was positive by ELISA in some of the negative MCPA sera obtained from patients with Hashimoto's disease in which diagnosis was confirmed by biopsy. In conclusion, the result obtained in MCPA now in use is strongly influenced by Tg Ab. Furthermore, since binding of Ab to MC is judged by agglutination of particles in MCPA, ELISA is superior in sensitivity and accuracy in detecting MC Ab.

Agglutination Tests↗
PubMed1989

Nuclear binding sites for reverse triiodothyronine in human placenta.

It has been generally believed that reverse triiodothyronine (reverse T3, rT3) is biologically inactive. Nevertheless the serum rT3 level is very high in fetal life, when the serum calcium level is higher than in the maternal. For this hypercalcemia in fetal life, there is no convincing evidence that any major calcium regulating hormone is responsible. And the assumption that rT3 may be concerned in active transport of calcium at placenta could be suggested. In this study nuclear protein was isolated from human placenta by extraction with 0.4M KCl buffer and binding studies utilizing radioactive rT3 were carried out. Scatchard analysis presented a curvilinear pattern, suggesting two classes of receptors: One with a association constant (Ka) of 1.14 X 10(8) M-1 and a limited capacity (Bmax) of 32.0 X 10(-15) mol/100 micrograms DNA and the other with Ka = 4.34 X 10(6) and Bmax = 454 X 10(-15). Its relative affinities for several thyroid hormone analogues were calculated. If the affinity for rT3 was assigned l, that for triiodothyronine would be 1/40, thyroxine: 1/63, Triiodothyroacetic acid: 1/18. Sulfhydryl agents affecting these binding characteristics were also studied. The Ka was not substantially changed but the Bmax was notably decreased by dithiothreitol (43%) and 2-mercaptoethanol (26%). In liver nuclei, the binding characteristics of rT3 receptor were analyzed for comparison. In this case only a single class of low affinity-high capacity rT3 binding site with a Ka of 6.69 X 10(6) was detected, a finding which was apparently different from those in placenta.(ABSTRACT TRUNCATED AT 250 WORDS)

Binding Sites↗
PubMed1989

Protection by thymosin fraction 5 from streptozotocin-induced diabetes in mice.

Protection by thymosin fraction 5 (TF5) from subdiabetogenic-dose streptozotocin (STZ)-induced type I diabetes in CD-1 mice was investigated. Mice which received multiple subdiabetogenic-dose (35 mg/kg) injections of STZ became hyperglycemia within two weeks. Hyperglycemia was also induced in those treated with low dose of TF5 (0.01 mg/day) in addition to STZ, though it was somewhat mild. In contrast, animals given STZ plus high dose of TF5 (0.1 mg/day) remained normoglycemic throughout the whole observation period (within 4 weeks). In the pancreatic islets from these animals, histologically, the well-granulated beta cells were observed and the infiltration of lymphoid cells was absent or mild. These results suggest that the administration of TF5 prevents the induction of insulitis and hyperglycemia in the subdiabetogenic-dose STZ-treated mice.

Animals↗
PubMed1988

Biological activity of 26,26,26,27,27,27-hexafluorinated analogs of vitamin D3 in inhibiting interleukin-2 production by peripheral blood mononuclear cells stimulated by phytohemagglutinin.

Vitamin D compounds suppress the production of interleukin-2 (IL-2) by peripheral blood mononuclear cells (PBMCs) stimulated with phytohemagglutinin in a dose-dependent manner. We used this suppression to test 26,26,26,27,27,27-hexafluorinated analogs of vitamin D3 for their immunosuppressive activity in PBMCs. 26,26,26,27,27,27-Hexafluoro-1,25-dihydroxyvitamin D3 and 26,26,26,27,27,27-hexafluoro-1,24-dihydroxyvitamin D3 were approximately 10 times more potent than 1,25-dihydroxyvitamin D3 in suppressing IL-2 production. 26,26,26,27,27,27-Hexafluoro-1-hydroxyvitamin D3 was 20 to 30 times less potent than 1,25-dihydroxyvitamin D3 in causing this effect. The relative biopotency of each vitamin D3 analog toward PBMC proliferation was roughly similar to that toward IL-2 production by PBMCs. Suppression of PBMC proliferation by vitamin D3 analogs seemed to be a secondary effect of their inhibition of IL-2 production.

Calcitriol↗
PubMed1988

In vivo effect of 1 alpha-hydroxyvitamin D3 on interleukin-2 production in hemodialysis patients.

The immunoregulatory effect of 1 alpha-OHD3, a precursor form of active vitamin D3 1,25 (OH)2D3, was examined in hemodialysis patients. Peripheral blood mononuclear cells (PBM) from hemodialysis patients produced significantly less interleukin-2 (IL-2) than those from normal controls. Four weeks of oral administration of 0.5 micrograms/day of 1 alpha-OHD3 enhanced the IL-2 production of PBM from the patients. This fact suggests that 1 alpha-OHD3 therapy may be useful for the restoration of IL-2 production in hemodialysis patients, and that the vitamin D3 deficiency may be responsible for the impairment of cellular immunity associated with IL-2 production disorder in hemodialysis patients.

Adult↗
PubMed1988

Calcium/calmodulin-mediated action of calcitonin on lipid metabolism in rats.

The effects of calcitonin on lipid metabolism were investigated in three kinds of rats, one strain of rabbits, and a primary culture of rat hepatocytes. In a short-term experiment, calcitonin decreased serum cholesterol and triglycerides after injection in rats on either an ordinary or high-fat diet. In a long-term experiment, calcitonin decreased the serum cholesterol and triglycerides in uremic rats, hypothalamic obese rats, and Watanabe-heritable hyperlipidemic rabbits. In cultured hepatocytes, calcitonin reduced the incorporation of [14C]acetate into cholesterol and triglycerides in a dose-dependent way. Treatment with W7, a calmodulin inhibitor, overcame the decrease caused by calcitonin in serum lipids in rats and in the synthesis of triglycerides from acetate or palmitate in the hepatocytes, but did not alter the intracellular cAMP level or incorporation of [32P]Pi into PI in the cells. The results suggest that calcitonin lowers serum lipid levels and lipogenesis in hepatocytes in a calcium/calmodulin-dependent way.

Animals↗
PubMed1988

Effect of tolbutamide and glyburide on cAMP-dependent protein kinase activity in rat liver cytosol.

The effect of sulfonylureas tolbutamide and glyburide on adenylate cyclase- and cAMP-dependent protein kinase (A-kinase) was examined in rat liver cytosol. Both tolbutamide and glyburide inhibited the A-kinase activity in a dose-dependent manner. Half-maximal inhibition was obtained at 10 mM with tolbutamide and at 0.2 mM with glyburide, indicating that glyburide was 50-fold as potent as tolbutamide. Neither tolbutamide nor glyburide affected [3H]cAMP binding to the protein kinase, but both inhibited the activity of catalytic units of the A-kinase. Lineweaver-Burk double-reciprocal plots revealed that the inhibitory effects of these drugs were noncompetitive with respect to the protein substrate histone, as well as to the phosphate-donor substrate ATP. Thus, tolbutamide and glyburide inhibited the A-kinase activity in rat liver cytosol, and it was suggested that, through the inhibition of A-kinase, the sulfonylureas would affect the carbohydrate metabolism in the liver. In fact, the relative potencies of these two drugs on A-kinase activity corresponded well with those of their reported antidiabetic effects.

Adenosine Triphosphate↗