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Biomedical subjects

Y Morimoto

Publications and source records attributed to Y Morimoto.

At least 307 records · Page 17Linked to original sources
PubMed1994

Effects of KB-5492, a new anti-ulcer agent with a selective affinity for the sigma-receptor, on aspirin-induced disruption of the rat gastric mucosal barrier.

The effect of KB-5492, a new anti-ulcer agent with a selective affinity for the sigma-receptor, on aspirin-induced disruption of the gastric mucosal barrier was studied in rats. Intragastric instillation of aspirin at 200 mg/kg rapidly decreased the gastric transmucosal potential difference (PD) in anesthetized rats. The PD recovered gradually following the removal of aspirin from the instillation solution. Aspirin, administered orally at 200 mg/kg, also reduced the amount of gastric covering mucus and induced a decrease in gastric H+ concentration and an increase in gastric Na+ concentration in pylorus-ligated rats. KB-5492, administered intraduodenally at 200 mg/kg, significantly prevented the aspirin-induced decrease in PD and accelerated the recovery of PD. In addition, KB-5492 at 200 mg/kg significantly prevented the reduction of gastric covering mucus, the decrease in gastric H+ concentration and the increase in gastric Na+ concentration induced by aspirin. These effects were similar to those of 0.01 mg/kg of 16,16-dimethyl prostaglandin E2 (dmPGE2). Teprenone at 200 mg/kg did not show any effect except for the inhibitory effects on the changes in gastric H+ and Na+ concentration. In the histological study, marked reduction of PAS-positive epithelial mucus and the exfoliation of surface epithelial cells were observed in the gastric mucosa exposed to aspirin. KB-5492 and dmPGE2 almost completely prevented the former, whereas both drugs prevented the latter incompletely. These findings indicate that KB-5492 protects the gastric mucosal barrier against the disruption by aspirin, which may be mainly exerted by retention of the gastric covering mucus.

16,16-Dimethylprostaglandin E2↗
PubMed1994

Purification of inulin fructotransferase (DFA I-producing) from Arthrobacter sp. MCI2493 and production of DFA I from inulin by the enzyme.

An extracellular enzyme that produces di-D-fructofuranose-2',1;2,1' dianhydride from inulin was purified from the culture broth of Arthrobacter sp. MCI2493. The molecular weight of the enzyme was 40,000 by gel filtration and SDS polyacrylamide gel electrophoresis. The enzyme had maximum activity at pH 6.0 and 50 degrees C. Using this purified enzyme, 100 g/liter inulin was converted into 60 g/liter of DFA I, nystose, and 1-F-fructofuranosyl-nystose after incubation for 30 h.

Arthrobacter↗
PubMed1994

Evaluation of serum uric acid to creatinine ratio in fulminant hepatitis.

Of the eight patients with fulminant hepatitis placed under total parenteral nutrition with an amino acid solution rich in branched chain amino acids and treated by plasma exchange, four survived and four died from hepatic failure. Serum uric acid levels in the non-survived group were significantly lower on days 1-6 compared with the survived group. The concentration ratios of uric acid to creatinine and prothrombin time were significantly lower on days 5-8 and days 3-8, respectively, in a similar comparison. Thus, the uric acid to creatinine ratio, which corrects for the possible renal dysfunction associated with acute hepatic failure, may serve as a clinically useful prognostic indicator for patients with fulminant hepatitis.

Adolescent↗
PubMed1994

Administration of a branched-chain amino acid preparation during hepatic failure: a study emphasizing ammonia metabolism.

We administered a branched-chain amino acid (BCAA) infusion to 16 patients with hepatic failure and two healthy subjects, and then evaluated its effects on ammonia metabolism and amino acid metabolic pool. Immediately after the BCAA infusion, the venous blood ammonia concentration increased in 12 of 15 patients with hepatic failure and in both two healthy subjects. Glutamine (Gln) also rose in all cases following the BCAA infusion, and this rise was particularly marked in the hepatic failure group. The increase in Gln due to the BCAA infusion and the arteriovenous difference in the pre-administration ammonia concentration showed a good correlation. These results suggest an increase in glutamine cycle capacity in patients with hepatic failure.

Adult↗
PubMed1994

[Anesthetic management for urological surgery of patients with chronic spinal cord injury].

We evaluated retrospectively the anesthetic management and perioperative complications of 47 patients with chronic spinal cord injury for genitourinary procedures. Of the 69 cases, 38 were performed under general anesthesia, 21 cases under spinal anesthesia, one case under epidural anesthesia, four cases under axillary block, and five cases under either sedation or standby. In preoperative laboratory findings, anemia was observed in 41%, hypoproteinemia in 38%, renal insufficiency in 23%, and restrictive pulmonary dysfunction in 69%. Hypotension and bradycardia were seen in 25% and 16% of patients, respectively. Autonomic hyperreflexia was seen in four cases with cervical cord injury: two under spinal anesthesia and two under either sedation or standby. Patients with chronic spinal cord injury have disorders of various organ systems. Careful preoperative evaluation and anesthetic management are required for prevention and prompt treatment of perioperative complications related to the disorders. Autonomic hyperreflexia can be successfully prevented by either general anesthesia or spinal anesthesia. The increased anesthesia safety can be obtained by the successful management of the cardiovascular instability during surgery.

Adolescent↗
PubMed1994

Evaluation of laboratory parameters reflecting activity of lupus nephritis in children: indicators of severe renal lesions.

Assessment of activity of lupus nephritis is critical in the management and ultimate prognosis of patients. Clinical and laboratory data of 18 children with lupus nephritis were examined to determine what factors reflect activity of renal lesions. Using a histologic scoring system with an activity index (AI) and a chronicity index (CI), correlations between histologic scores and laboratory parameters were analyzed. Serum total protein, albumin and complement at the time of renal biopsy inversely correlated with the AI, but not parameters correlated with the CI. Serum complement levels correlated inversely with the amount of glomerular immune deposits, while the AI and CI correlated with the amount of immune deposits. These results suggest that hypoalbuminemia and hypocomplementemia are indicators of severe, active lupus nephritis, pointing to the need for early renal biopsy and intensive therapy.

Adolescent↗
PubMed1994

[Clinico-pathological study of carried-over patents with Henoch-Schönlein nephritis].

Fifty-two (49.5%) of 105 children with Henoch-Schönlein purpura developed nephritis. Eleven (21.1%) of 52 nephritic patients were carried over beyond childhood, while 21 (40.4%) cases had normalized urinalyses in childhood. The carried-over patients had a higher incidence of severe proteinuria and tubular atrophy compared to those of patients with normalized urinalyses (p < 0.05). These results suggest that patients with severe proteinuria and tubular atrophy tend to have persistent urinary abnormalities beyond childhood.

Adolescent↗
PubMed1993

Crystallization and preliminary X-ray studies of wild type and catalytic-site mutant alpha-amylase from Bacillus subtilis.

Recombinant alpha-amylase (EC3.2.1.1) from Bacillus subtilis has been crystallized by the hanging drop vapor diffusion method using polyethylene glycol as precipitant. Crystals of wild-type protein diffract to at least 2.2 A resolution, and belong to the space group P2(1)2(1)2(1) with a = 72.2 A, b = 74.9 A, c = 116.1 A with probably one molecule in the asymmetric unit. A catalytic site mutant created by site-directed mutagenesis has also been grown as isomorphous crystals with a = 72.6 A, b = 74.4 A, c = 116.7 A. Structural studies of both wild-type and mutant proteins will provide a basis for understanding the catalytic mechanism of alpha-amylase.

Bacillus subtilis↗
PubMed1993

Activation of the zymogen of hepatocyte growth factor activator by thrombin.

Hepatocyte growth factor activator (HGF activator) is a serine protease which converts single-chain HGF to the active two-chain form. HGF activator purified from human serum has a molecular mass of 34 kDa and consists of two chains held together by a disulfide bond. The nucleotide sequence of HGF activator cDNA shows that HGF activator is derived from the COOH-terminal region of a precursor of 655 amino acids by proteolytic cleavage of the bonds between Arg372 and Val373 and between Arg407 and Ile408 and that the precursor consists of multiple domains homologous to those observed in blood coagulation factor XII. In this study, we identified the precursor of HGF activator in human plasma using an enzyme-linked immunosorbent assay system. The precursor was purified from plasma by a five-step procedure. The purified precursor did not activate single-chain HGF. The precursor was efficiently cleaved in vitro by thrombin, at the bond between Arg407 and Ile408, in the presence of negatively charged substances. The cleaved precursor activated single-chain HGF. These findings led us to conclude that HGF activator is present in plasma as an inactive zymogen and that the zymogen is activated by the cleavage of the bond between Arg407 and Ile408 by thrombin. Characteristic structural domains in the NH2-terminal region of the zymogen may be involved in the binding of the zymogen to negatively charged substances, which stimulates the activation of the zymogen by thrombin.

Amino Acid Sequence↗
PubMed1993

Hepatocyte heterogeneity in response to extracellular adenosine.

Metabolic and haemodynamic effects of adenosine were studied in antegrade and retrograde rat liver perfusions with influent nucleoside concentrations either below (i.e. 20 microM) or exceeding (i.e. 200-300 microM) the single-pass clearance capacity of the liver. Adenosine (20 microM) increased in antegrade perfusions the perfusion pressure and markedly stimulated prostaglandin D2, thromboxane B2 and glucose output, whereas in retrograde perfusions no pressure and eicosanoid response occurred and glucose output was stimulated only slightly. The perfusion-direction-dependent differences in the glucose and pressure response to adenosine (20 microM) were fully abolished in presence of ibuprofen (50 microM). When the adenosine concentration in influent was raised to 200-300 microM, i.e. to a concentration exceeding single-pass clearance of the nucleoside, the adenosine-induced prostaglandin D2 release was about 10-fold higher in retrograde perfusions than in antegrade perfusions. On the other hand, both adenosine (20-300 microM)-induced cyclic AMP (cAMP) and K+ release from the liver were not affected by the direction of perfusion, and maximal effects on cAMP release were observed at influent adenosine concentrations of 100 microM. The basal rate (adenosine absent) of prostaglandin D2 and thromboxane B2 release was about 10-fold higher in retrograde than in antegrade perfusion experiments, whereas the basal cAMP release from the liver was not affected by the direction of perfusion. Maximal adenosine-stimulated glucose output was significantly higher in antegrade than in retrograde perfusions at all adenosine concentrations tested (range 10-300 microM). Ibuprofen abolished this difference, indicating that eicosanoids liberated under the influence of adenosine contribute to the glycogenolytic response in antegrade, but not in retrograde, perfusion. Desensitization occurred following repetitive adenosine infusion; this was more pronounced for adenosine-induced prostaglandin release than for cAMP or K+ efflux. The data suggest the following. (i) Both cAMP and eicosanoids are involved in the stimulation of glycogenolysis by adenosine. (ii) Eicosanoids are probably liberated under the influence of extracellular adenosine from a portal pre-sinusoidal compartment and accordingly stimulate glycogenolysis only in antegrade perfusions. Thus signals derived from portal vein structures can modulate hepatocellular function. (iii) Contractile elements are probably located also inside the liver acinus. (iv) Eicosanoids released into the hepatic vein reflect less than 10% of hepatic eicosanoid formation, because of marked clearance by perivenous hepatocytes.

Adenosine↗
PubMed1993

Molecular cloning and sequence analysis of the cDNA for a human serine protease reponsible for activation of hepatocyte growth factor. Structural similarity of the protease precursor to blood coagulation factor XII.

Hepatocyte growth factor (HGF) is a potent mitogen for parenchymal liver cells, epithelial cells, and endothelial cells and may play an important role in liver regeneration following hepatic injury. HGF is homologous to plasminogen and is first synthesized and secreted as an inactive single-chain precursor and then activated to a heterodimeric form by endoproteolytic processing. Recently, a novel serine protease responsible for this processing (HGF activator) has been purified from fetal bovine serum (Shimomura, T., Ochiai, M., Kondo, J., and Morimoto, Y. (1992) Cytotechnology 8, 219-229). In this study, we purified HGF activator from human serum and determined its partial amino acid sequence. Based on the amino acid sequence, we have molecularly cloned the cDNA for human HGF activator. The nucleotide sequence of the cDNA revealed that HGF activator is derived from the COOH-terminal half region of a precursor protein of 655 amino acids and that the precursor consists of multiple putative domains homologous to those observed in blood coagulation factor XII. These domains may be involved in the conversion of the precursor to the active form of HGF activator.

Amino Acid Sequence↗
PubMed1993

In vivo conversion of recombinant human proapolipoprotein AI (rh-Met-proapo AI) to apolipoprotein AI in rabbits.

In vivo conversion of recombinant human proapolipoprotein AI (rh-Met-proapo AI) from E. coli to apolipoprotein (apo) AI was investigated. rh-Met-proapo AI was labeled with 125I, and then administered intravenously to rabbits. Blood was sampled periodically for 6 days. The plasma decay curves of radioiodinated rt-Met-proapo AI were similar to those of human mature apo AI (fractional catabolic rate (FCR); 1.018 +/- 0.090/day vs. 0.976 1 0.031/day, respectively). In vivo conversion of rh-Met-proapo AI to mature apo AI was examined by autoradiography of the isoelectric focusing (IEF) slab gel, i.e., the HDL fraction from each sampling point was semiquantitatively applied to IEF. It was found that the radioactivity of rh-Met-proapo AI migrated to more acidic isoproteins, the conversion was complete within 24 h, and the FCR of rh-Met-proapo AI was 9.20 +/- 1.34/day. Although the plasma decay curves of both human pro (rh-Met-proapo AI) and mature apo AI were significantly steeper than those of rabbit mature apo AI4 and apo AI5 (FCR; 0.703 +/- 0.027/day and 0.795 +/- 0.031/day, respectively), the conversion rate of human rt-Met-proapo AI to mature apo AI in rabbit was assumed to be 1:1. In vitro incubation of rh-Met-proapo AI with rabbit serum produced mature apo AI isoproteins, as determined by the apo AI immunoblotting method. Prediction of the amino acid sequence at the NH2 terminus of rabbit proapo AI showed that the prosegment consisted of an alpha helix with a high probability of a beta turn at Pro9, which is close to that in humans. Thus, (1) the proteolytic cleavage of proapo AI is an extracellular event, (2) the converting enzyme in rabbits can also process human proapo AI, (3) this converting enzyme does not specifically and directly attack the Gln6-Asp7 bond which links the carboxyl-terminal residue of the hexapeptide to the amino-terminal residue of human mature apo AI. The conformation of proapo AI at the NH2 terminus (alpha helix of the prosegment and a beta turn at Pro9) may have a key role in this cleavage, and (4) the examination of rh-Met-proapo AI in rabbits helps to explain the early events of HDL biogenesis.

Amino Acid Sequence↗
PubMed1993

The structural barrier of absorptive mucosae: site difference of the permeability of fluorescein isothiocyanate-labelled dextran in rabbits.

The permeability of fluorescein isothiocyanate-labelled dextran (FD, M.W. 4400-71,200) across nasal, buccal, duodenal, jejunal, ileal, colonic, and rectal mucosae excised from rabbits has been measured to estimate the structural barrier of absorptive mucosae using Ussing-type diffusion chambers. The permeability coefficient of FD in all these mucosae decreased with increasing molecular weight. The rank order of FD permeability did not always correlate with the electrical resistance of the mucosae. Among components of the small intestine (duodenum, jejunum, ileum) and the large intestine (colon, rectum), however, the rank order of FD permeability corresponded to the magnitude of the electrical resistance in each instance; the upper colonic mucosa showed the highest permeability, especially in FD of low molecular weight, and permeability of the rectal mucosa was lowest except for the duodenal mucosa. The nasal mucosa showed the lowest electrical resistance and the highest permeability of those studied, suggesting that it has a leaky structural barrier.

Animals↗