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Biomedical subjects

N Itoh

Publications and source records attributed to N Itoh.

At least 523 records · Page 29Linked to original sources
PubMed1988

The Effect of Diminazene Aceturate on Spienectomized Dogs with Babesia gibsoni Infection.

The effect of diminazene aceturate on splenectomized and nonspienectomized dogs with Babesia gibsoni (B. gibsoni) infection was investigated. In splenectomized dogs, the fissional and multiplicational stages of B. gibsoni were observed in peripheral blood films, and hemoglobinuria was frequently observed. These findings were different from previous reports and were not changed by administration of diminazene aceturate. It is clear that the intramuscular administration of diminazene aceturate at the dose of 3 mg/kg body weight for 3 days is not effective against B. gibsoni infection in splenectomized dogs.

Journal Article↗
PubMed1988

Influences of pressure surrounding the heart and intracardiac pressure on the diastolic coronary pressure-flow relation in excised canine heart.

We investigated the change in the instantaneous diastolic left coronary pressure-flow relation (DPFR) when the pressure surrounding the heart (SHP), right heart pressure (RHP), and left heart pressure (LHP) were systematically varied. Eight excised and maximally vasodilated canine hearts placed in an air-tight chamber were used. To obtain a capacitance-free DPFR, coronary perfusion pressure was slowly decreased (about 2 mm Hg/sec) during a prolonged diastole. The zero-flow pressure (Pf = 0) and the slope of the DPFR were analyzed. The mean values of the slope did not change significantly throughout the interventions. The mean value of Pf = 0 in the control state (SHP = RHP = LHP = 0 mm Hg) was 6.0 +/- 2.0 mm Hg (mean +/- SD, n = 8), significantly higher than the venous outflow pressure, RHP (p less than 0.001), and the other two pressures (p less than 0.001). When SHP was raised to 15 and 30 mm Hg, while the other pressures remained at 0 mm Hg, the mean values of Pf = 0 increased to 20.9 +/- 2.4 and 35.6 +/- 3.1 mm Hg (p less than 0.001 and p less than 0.0005, respectively, vs. control). The mean values of Pf = 0 when only RHP was elevated to 15 and 30 mm Hg were 16.0 +/- 1.5 and 29.3 +/- 1.5 mm Hg (p less than 0.001 and p less than 0.0005 vs. control). On elevation of LHP to 15 and 30 mm Hg, the mean values of Pf = 0 were 12.0 +/- 2.8 and 17.3 +/- 3.6 mm Hg (p less than 0.01 and p less than 0.01 vs. control). When both SHP and LHP were almost evenly elevated to about 15 and 30 mm Hg, the mean values of Pf = 0 were raised to 22.0 +/- 2.9 and 35.3 +/- 3.2 mm Hg, respectively. These mean values were not significantly different from those when only SHP was elevated to the comparable levels. The observation that Pf = 0 exceeded RHP in the control state and that RHP, which was elevated above the preceding Pf = 0, was identical with the present Pf = 0 supports the vascular waterfall mechanism when RHP is low. Furthermore, the evidence that the degree of DPFR shift was almost linearly dependent on the SHP level rather than on the LHP level indicates that the pressure on the epicardial side is one of the factors that determines the pressure at the top of the vascular waterfall.

Animals↗
PubMed1988

Stable prostacyclin analogue preventing microcirculatory derangement in experimental cerebral ischemia in cats.

We evaluated the effect of a stable synthetic prostacyclin analogue, TRK-100, on the microcirculatory derangement occurring in feline pial vessels with endothelial damage after middle cerebral artery occlusion. Fifteen adult cats were divided into an untreated group (Group 1, n = 8) and a treated group (Group 2, n = 7). Thirty minutes after 10 minutes of ultraviolet irradiation, which selectively damaged endothelium in the pial vessels, the middle cerebral artery was occluded in both groups and maintained for 30 minutes. In Group 2, 50 ng/kg/min TRK-100 was continuously infused intravenously following ultraviolet irradiation. In both the pial arteries and veins, platelet aggregate adhesion to the endothelium with subsequent thrombus formation was significantly (p less than 0.01 and p less than 0.05, respectively) inhibited during middle cerebral artery occlusion in Group 2 compared with Group 1. Similarly, blood flow stasis in the pial veins was effectively prevented in Group 2 during occlusion. Furthermore, the pial artery diameter returned to the control level during the late period of occlusion, whereas in Group 1 the pial artery remained constricted. Our data suggest that TRK-100 can prevent microcirculatory derangement in the acute stage of ischemic stroke.

Animals↗
PubMed1987

Thiol proteinase inhibitor in the ascitic fluid of sarcoma 180 tumor-bearing mice.

A thiol proteinase inhibitor (TPI) has been purified from the ascitic fluid of Sarcoma 180 tumor-bearing mice. The molecular weight of the inhibitor was estimated to be 67,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and the substance inhibited papain, cathepsins B and L, but not cathepsins H and D and trypsin. The inhibitor also liberated kinin upon treatment with trypsin or mouse glandular kallikrein, indicating that the inhibitor is a kininogen, and the kinin liberated upon trypsinization was identified as bradykinin. An immunoreactive TPI with a molecular weight indistinguishable from that of the ascites TPI was found in plasma of non-tumor-bearing mice as well as that of tumor bearers. Plasma levels of immunoreactivity were increased up to twice the normal levels in tumor bearers inoculated with Sarcoma 180 or 3LL tumor cells. Supplementation of the purified ascites TPI into Sarcoma 180 culture medium caused a significant suppression of cell growth as well as [3H]thymidine incorporation at a concentration below that normally present in plasma. In contrast, addition of ascites-TPI to cultured mouse embryonic cells caused enhancement of cell growth as well as [3H]thymidine incorporation. These results indicate that in mice responding to tumor growth, a TPI corresponding to a kininogen is induced which may regulate tumor growth by countering tumor-related proteolytic activity.

Animals↗
PubMed1987

Identification of T-kininogen in rat urine.

Studies were carried out in order to characterize the kininogen in rat urine. Rat urine contained a component which was cross-reactive with antibody to rat plasma T-kininogen. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of rat urine revealed a single antigenic band corresponding to the molecular weight of plasma T-kininogen. Induction of acute inflammation in rats by an injection of lipopolysaccharide caused an increase in the urinary excretion of immunoreactive T-kininogen in parallel with an elevation of plasma T-kininogen. Kininogen partially purified from rat urine by affinity chromatography using S-carboxymethylated papain-agarose liberated only T-kinin upon trypsinization, but not upon treatment with rat glandular kallikreins. From these results, we conclude that T-kininogen is the major kininogen present in rat urine.

Animals↗
PubMed1987

Acute phase responses of plasma angiotensinogen and T-kininogen in rats.

Acute phase responses of plasma angiotensinogen and kininogen were studied in rats. Plasma angiotensinogen levels increased about 3-fold during the first 8 hr, and returned to normal at 48 hr, following the induction of acute inflammation by lipopolysaccharide (LPS). Plasma kininogen reached maximum levels at 48 hr following LPS administration. In adrenalectomized rats, plasma angiotensinogen levels decreased significantly, and the administration of LPS did not elevate plasma angiotensinogen levels. In contrast, plasma kininogen levels were increased by adrenalectomy, as well as by sham-operation. Dexamethasone significantly increased plasma angiotensinogen levels in adrenalectomized rats as well as in normal rats, but aldosterone did not. Plasma kininogen levels of normal rats were not changed by the administration of dexamethasone or aldosterone. From these results, it was concluded that the acute phase response of plasma angiotensinogen is mediated by glucocorticoid, but that of plasma kininogen is not.

Acute-Phase Reaction↗
PubMed1987

Characterization of nonheme iron and reaction mechanism of bromoperoxidase in Corallina pilulifera.

The properties of the nonheme iron of bromoperoxidase from Corallina pilulifera were studied. The enzyme lost its activity when reduced with formamidine-sulfinic acid and recovered it when oxidized by air. Incubation of the enzyme with ferric or ferrous ion-chelating agents indicated that its nonheme iron was ferric. Analyses of circular dichroism and proton NMR spectra suggested that the ferric ion tightly bound to cysteine, histidine, or tyrosine residues of the enzyme. The enzyme catalyzed Br--dependent catalase reactions to yield 1 mol of O2 from 2 mol of H2O2. No O2 evolution was observed when bromination reaction of monochlorodimedone occurred. From these results, together with previous knowledge of this enzyme, it was concluded that it activated bromide anion (Br-) to bromonium cation (Br+) using one molecule of H2O2, and this Br+OH- formed at the active site then decomposed another H2O2 to yield O2 in the absence of halogen acceptors (substrate). When substrate was present in the reaction mixture, it and H2O2 competitively reacted with the reaction intermediate (Br+OH-) to give brominated products.

Circular Dichroism↗
PubMed1987

Involvement of leukocyte and glucocorticoid in the acute-phase response of angiotensinogen.

Plasma levels of angiotensinogen were significantly increased in rats following treatment with lipopolysaccharide (LPS). However, no such acute-phase response in the plasma angiotensinogen level was induced in hypophysectomized rats. Implantation of peritoneal exudate cells (PEC), which had been collected from rats treated with i.p. injection of LPS and glycogen, into the peritoneal cavities of normal rats also caused elevation of plasma angiotensinogen levels. No significant changes in plasma levels of corticosterone were observed in rats receiving either LPS or LPS-stimulated PEC. These results indicate that the acute-phase response of angiotensinogen is mediated by leukocytes-derived cytokine, and glucocorticoid is essential for its stimulatory effect on the hepatic production of angiotensinogen.

Angiotensin I↗
PubMed1987

Genistein, a specific inhibitor of tyrosine-specific protein kinases.

Tyrosine-specific protein kinase activity of the epidermal growth factor (EGF) receptor, pp60v-src and pp110gag-fes was inhibited in vitro by an isoflavone genistein. The inhibition was competitive with respect to ATP and noncompetitive to a phosphate acceptor, histone H2B. By contrast, genistein scarcely inhibited the enzyme activities of serine- and threonine-specific protein kinases such as cAMP-dependent protein kinase, phosphorylase kinase, and the Ca2+/phospholipid-dependent enzyme protein kinase C. When the effect of genistein on the phosphorylation of the EGF receptor was examined in cultured A431 cells, EGF-stimulated serine, threonine, and tyrosine phosphorylation was decreased. Phosphoamino acid analysis of total cell proteins revealed that genistein inhibited the EGF-stimulated increase in phosphotyrosine level in A431 cells.

Cell Line↗
PubMed1987

Significant effects of Z-Gln-Val-Val-OME, common sequences of thiol proteinase inhibitors on thiol proteinases.

The first studies on a series of the small synthetic thiol proteinase inhibitors, conservative common sequences in several thiol proteinase inhibitors, are described. Among the many interesting findings with synthetic thiol proteinase inhibitors was the observation that the most effective analogue, Z-Gln-Val-Val-Ala-Gly-OMe, whose amino and carboxyl groups were protected with Z and OMe, respectively, showed inhibitory activity on papain and cathepsin B and protected papain from egg cystatin, human low-molecular-weight kininogen and T-kininogen-induced inhibition but not from leupeptin-induced inhibition. Moreover, it was revealed that Z-Gln-Val-Val-OMe was the smallest peptide to exhibit a protective effect on papain.

Amino Acid Sequence↗