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Biomedical subjects

M Inaba

Publications and source records attributed to M Inaba.

At least 127 records · Page 7Linked to original sources
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

The effects of intracerebroventricular administration of adrenergic agonists and antagonists on adrenaline secretion from the adrenal medulla in stressed conscious rats.

The effects of intracerebroventricular (i.c.v.) administration of adrenergic agonists and antagonists on the increase in serum adrenaline (Ad) induced by immobilization stress were examined in unanesthetized, unrestrained rats. The serum Ad of rats showed a significant linear increase as time elapsed after the induction of immobilization stress. This immobilization stress-induced increase was inhibited by the i.c.v. administration of a small amount of noradrenaline (NA) and phenylephrine. Isoproterenol and clonidine failed to inhibit the immobilization stress-induced increase. The inhibition of the immobilization stress-induced increase by i.c.v. administration of NA was antagonized by pretreatment with phentolamine and prazosin, but not by pretreatment with yohimbine and propranolol. These results suggested that NA administered via an i.c.v. route may inhibit the stress-induced increase in adrenomedullary Ad secretion by an action on the central alpha 1-adrenoceptor.

Adrenal Medulla↗
PubMed1988

Effect of intracerebroventricular administration of opioid peptides on basal serum adrenaline levels in conscious rats.

It is considered that adrenomedullary secretion of adrenaline is centrally regulated by various endogenous substances. Recently, opioid peptides have been reported as one of this group of endogenous substances. However, the receptor through which these endogenous opioid peptides regulate adrenomedullary adrenaline secretion has not been elucidated. In the present study, various opioid peptides were administered intracerebroventricularly in conscious, unrestrained rats, and blood catecholamine levels were measured at various periods to determine which cerebral opioid peptide receptor is involved in the mechanism of basal adrenomedullary adrenaline secretion. The results indicate that delta-receptor stimulation has a positive effect on basal adrenomedullary adrenaline secretion, while mu- and kappa-receptors are not involved in this mechanism.

Adrenal Medulla↗
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↗
PubMed1988

[Potentiation of the antitumor activity of 5-fluorouracil by biochemical modulators].

About 30 kinds of biochemical modulators of 5-fluorouracil (5-FU) are described. They modify the metabolism and cytotoxic action of 5-FU through an alteration in (1) intracellular concentration of 5-FU or its metabolites, (2) intracellular pool of co-substrates essential for 5-FU metabolism, and (3) intracellular pool of normal substrates which compete with 5-FU metabolism. As a result, they affect either its inhibitory effect on thymidylate synthase or incorporation into RNA, or both. Thus, some of these modulators can improve antitumor activity of 5-FU by potentiating its tumor-selective toxicity or reducing its host toxicity selectively. From such various points of view, a variety of biochemical modulators of 5-FU are reviewed.

Animals↗
PubMed1988

[P388].

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Animals↗
PubMed1988

Corneal endothelial changes associated with herpetic stromal keratitis.

Wide-field specular microscopy was performed on both eyes of 33 patients with unilateral herpetic stromal keratitis. Endothelial changes were quantitated by computerized morphometric analysis of individual cells. In the 16 patients with disciform keratitis, the corneal endothelium of the affected eyes showed no difference in cell density but demonstrated significant increases of variation in cell size (polymegathism) and shape (pleomorphism) when compared to the cells in the fellow unaffected eyes. The eyes with keratouveitis (17 patients), however, had marked polymegathism and pleomorphism of the endothelium and a distinctly lower endothelial cell density (mean, 19%) than the healthy fellow eyes.

Adolescent↗
PubMed1987

Biological activity of fluorinated vitamin D analogs at C-26 and C-27 on human promyelocytic leukemia cells, HL-60.

Vitamin D compounds added to the culture medium induce HL-60 cells to differentiate into macrophage/monocytes via a receptor mechanism. This system provides a biologically relevant assay for the study of biopotency of vitamin D analogs. Using this system, the biological activity of various fluorinated derivatives of vitamin D3 was compared with that of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3). As assessed by cell morphology, nitroblue tetrazolium reduction and nonspecific esterase activity, 26,26,26,27,27,27-hexafluoro-1,25-dihydroxyvitamin D3 (26,27-F6-1,25-(OH)2D3) and 26,26,26,27,27,27-hexafluoro-1,24-dihydroxyvitamin D3 (26,27-F6-1,24-(OH)2D3) were about 10 times as potent as 1,25-(OH)2D3 in suppressing HL-60 cell proliferation and inducing cell differentiation. The biological activity of 26,26,26,27,27,27-hexafluoro-1-hydroxyvitamin D3 (26,27-F6-1-OH-D3) was equal to that of 1,25-(OH)2D3 in this system. 1,25-(OH)2D3 and its fluorinated analogs exerted their effects on HL-60 cells in a dose-dependent manner. HL-60 cells have a specific receptor for 1,25-(OH)2D3 with an apparent Kd of 0.25 nM, identical with that of chick intestinal receptor. While the binding affinities of 26,27-F6-1,25-(OH)2D3 and 26,27-F6-1,24-(OH)2D3 for chick intestinal receptor were lower than that of 1,25-(OH)2D3 by factors of 3 and 1.5, respectively, they were as competent as 1,25-(OH)2D3 in binding to HL-60 cell receptor. The ability of 26,27-F6-1-OH-D3 to compete for receptor protein from HL-60 cells and chick intestine was about 1/70 that of 1,25-(OH)2D3. These results indicate that trifluorination of carbons 26 and 27 of vitamin D3 can markedly enhance the effect on HL-60 cells.

Animals↗
PubMed1987

Treatment of type 1 diabetes mellitus in non-obese diabetic mice by transplantation of allogeneic bone marrow and pancreatic tissue.

Non-obese diabetic (NOD) mice provide a model for type 1 diabetes mellitus. We previously showed that allogeneic bone marrow transplantation (ABMT) can prevent and treat insulitis and overt diabetes in NOD mice. However, ABMT alone could not be used to treat overt diabetes in NOD mice whose islets had been completely destroyed. To provide insulin-producing cells, pancreatic tissue from newborn mice was grafted under the renal capsules in combination with ABMT. The aims of concomitant ABMT are as follows. (i) It induces immunological tolerance to the donor-type major histocompatibility complex determinants and permits the host to accept subsequent pancreatic allografts from the bone marrow donor. (ii) ABMT replaces abnormal stem cells with normal stem cells. After transplantation of bone marrow plus newborn pancreas, NOD mice showed reduction of the glycosuria and a normal response in the glucose-tolerance test. Immunohistological study revealed the presence of clustered insulin-containing beta cells in the grafted pancreatic transplants. ABMT may become a viable treatment of established type 1 diabetes mellitus in humans.

Animals↗
PubMed1987

A case of hyponatremia in panhypopituitarism caused by the primary empty sella syndrome.

A 64-year-old woman was admitted for evaluation of hyponatremia. She was maintained on hypertonic saline administration. Without this therapy, the serum Na concentration decreased progressively to 127 mEq/L and the plasma osmolality to 254 mOsm/Kg H2O, on Day 3. At that time, the concentration of antidiuretic hormone (ADH) was as high as 3.5 pg/ml. A skull radiogram revealed an enlarged sella turcica. Computed tomography (CT) revealed a low density in the sella, and magnetic resonance imaging revealed equal intensity of the sella turcica and the cerebrospinal fluid. A diagnosis of empty sella syndrome was made by metrizamide cisternography in conjunction with CT scanning. A diagnosis of panhypopituitarism was made by endocrine function tests. 123I-thyroidal uptake was 6% when her serum TSH was 10.9 microU/ml, suggesting that she might also have primary hypothyroidism. When this patient was given glucocorticoid before levothyroxine replacement, her serum Na concentration rose up to about 140 mEq/L and a normal relationship between her plasma ADH level (2.4 pg/ml) and plasma osmolality (281 mOsm/kg H2O) was restored. Therefore, it was suggested that ADH hypersecretion induced by the glucocorticoid deficiency might in part contribute to the development of hyponatremia. This is the case of primary empty syndrome associated with panhypopituitarism, in whom initial symptom was caused by hyponatremia.

17-Hydroxycorticosteroids↗
PubMed1987

The effects of aldose reductase inhibitor on the corneal endothelial morphology in diabetic rats.

Diabetic rats were produced by intravenous injection of streptozotocin. Of these, eleven rats were treated with topical instillation of 0.5% aldose reductase inhibitor (ARI), while ten received vehicle alone. The corneal endothelium of these diabetic rats was examined by specular microscopy and compared to age-matched nondiabetic rats (ten rats). Computerized morphometric analysis of individual cells demonstrated that the endothelium of the untreated diabetic rats had marked polymegathism (increased coefficient of variation in cell area) and pleomorphism (decreased percentage of hexagonal cells), as previously observed in diabetic patients. Similar endothelial changes were also noted in the ARI-treated diabetic rats, but to a significantly lesser extent. These results suggest that topically applied ARI can be effective in reducing morphologic changes of the diabetic endothelium, and that activation of the sorbitol pathway may be implicated in the etiology of such endothelial changes.

Aldehyde Reductase↗
PubMed1987

Selective IgM deficiency in adults: phenotypically and functionally altered profiles of peripheral blood lymphocytes.

Peripheral blood lymphocytes from four patients with selective IgM deficiency were examined phenotypically and functionally. Although B cell subpopulations determined by surface immunoglobulins were within normal or nearly normal range, T8+ cells were significantly increased and T4/T8 ratios were inverted in three patients. IgM specific hyporesponsiveness in the PWM-driven immunoglobulin production system was observed in all four patients. Ia-like antigen positive T cells were increased in two patients; both had increased Leu2a+ Leu15+ suppressor-effector cells. In addition, Leu3a+ Leu8+ suppressor-inducer cells were increased in one of these two patients. Excessive (either IgM-specific or isotype non-specific) suppressor activity of T cells and IgM specific hyporesponsiveness of non-T cells were observed in these two patients in the recombination plaque assay. Although these results showed the complexity of the pathogenesis of this syndrome, they suggested that suppressor-associated T cells may play a role in some patients with selective IgM deficiency.

Adult↗