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Biomedical subjects

H Yasuda

Publications and source records attributed to H Yasuda.

At least 307 records · Page 17Linked to original sources
PubMed1995

Plasma copper and antioxidant status in Wilson's disease.

It has been demonstrated that the level of serum copper unbound to ceruloplasmin (loosely bound copper) is increased in Wilson's disease, although the total serum copper concentration is usually low, reflecting a low ceruloplasmin level. To assess the contribution of free radical reactions catalyzed by nonceruloplasmin copper to the development of complications in this disease, we investigated copper and antioxidant status in four untreated patients who had hepatic dysfunction with or without hemolytic anemia and made a comparison with five patients controlled on penicillamine therapy and 19 age-matched healthy children. We found that loosely bound copper in plasma measured by the phenanthroline assay was detectable in three of four untreated patients with Wilson's disease, but was not detectable in the patients during therapy or in the healthy controls. Among the various antioxidants, the ascorbate and urate levels were markedly reduced before treatment (mean +/- SD, 23 +/- 16 microM for ascorbate and 90 +/- 59 microM for urate) compared with the values in the patients during treatment with penicillamine (67 +/- 19 and 302 +/- 78 microM, p < 0.05) and in control children (60 +/- 8 and 254 +/- 48 microM, p < 0.05). We also demonstrated that the plasma concentration of allantoin, an oxidation product of uric acid and a possible marker of radical generation in vivo, was markedly elevated in the untreated patients (11.0 +/- 1.8 versus 4.3 +/- 0.5 microM in patients on therapy and 6.5 +/- 0.8 microM in controls, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Allantoin↗
PubMed1995

Ubiquitin-activating enzyme, E1, is phosphorylated in mammalian cells by the protein kinase Cdc2.

The ubiquitin-activating enzyme (E1) is the first enzyme in the pathway leading to formation of ubiquitin-protein conjugates. E1 was found to be phosphorylated in cells of a mouse mammary carcinoma cell line, FM3A. Peptide mapping of trypsin digests of labeled E1 indicated that two oligopeptides were mainly phosphorylated in vivo. The same oligopeptides were also labeled in vitro on Cdc2 kinase-mediated phosphorylation of E1, affinity-purified from the same cell line. The Cdc2 kinase is a key enzyme playing a pivotal role in G2/M transition in the cell cycle. The phosphorylation of one of the two oligopeptides was prominent at the G2/M phase of the cell cycle, and dependent upon the Cdc2 kinase activity in vivo since it was significantly reduced in tsFT210, a mutant cell line deficient in Cdc2 kinase. Mutation analysis indicated that the serine residue at the fourth position of the E1 enzyme was a phosphorylation site of Cdc2 kinase. These findings suggest that E1 is a target of Cdc2 kinase in the cell, implying that the ubiquitin system may be dynamically involved in cell cycle control through phosphorylation of this key enzyme.

Amino Acid Sequence↗
PubMed1995

[Postoperative pulmonary stenosis after arterial switch operation, comparison in three methods of pulmonary reconstruction: modified Pacifico, autologous pericardial patch, and equine pericardial patch].

To prevent postoperative pulmonary stenosis in arterial switch operation for transposition of the great arteries, pulmonary reconstruction without patch augmentation (modified Pacifico method: Pa-group) and reconstruction using W-shaped fresh autologous pericardium (AW-group) were introduced instead of the former method using equine pericardium (XW-group). Postoperative pulmonary stenosis (RV-PA pressure gradient greater than 30 mmHg) was not seen among the 17 cases in the Pa-group (0%), and was seen in 2/14 (14.3%) in the AW-group and in 4/14 (29%) in the XW-group. Progressive increase in pressure gradient was seen in the XW-group in the midterm cardiac catheterization (p < 0.01), but such tendency was not observed in the Pa-group and the AW-group. Sectional area at the pulmonary valve ring, at the anastomotic site in the main pulmonary artery, and at the pulmonary branches just distal to the bifurcation, standardized by the body surface area, increased in the Pa-group and the AW-group, but were unchanged or slightly decreased in the XW-group in the midterm cardiac angiography. We believe that postoperative pulmonary stenosis can be best avoided if modified Pacifico method is used. The cases in which postoperative pulmonary stenosis or coronary artery compression is anticipated such as those with side-by-side aortopulmonary relationship or after pulmonary artery banding, should be operated upon using fresh autologous pericardial patch.

Humans↗
PubMed1995

[Surgical results of valvuloplasty for common atrioventricular valve regurgitation in single ventricle].

From 1988 through 1994, 18 patients who had common atrioventricular valve regurgitation associated with single ventricle underwent valvuloplasty. All patients had isomerism heart (right isomerism: 16, left isomerism: 2). The preoperative degree of regurgitation was 3.3 +/- 0.4 (Sellers). Valvuloplasty was performed by two different procedures. Semi-circular annuloplasty was used in nine patients. Dividing the common atrioventricular valve orifice into two parts (bivalvation) with or without annuloplasty was used in nine. The concomitant procedures varied: three patients underwent systemic pulmonary shunt, two underwent repair of total anomalous pulmonary venous drainage, one underwent pulmonary arterial banding, five underwent bidirectional Glenn, shunt, and four underwent Fontan operation. One early death and three late deaths have occurred. The early postoperative degree of regurgitation was reduced to 1.3 +/- 1.0. In nine patients, however, the degree of regurgitation increased late postoperatively. Seven patients were reoperated on because of regurgitation: three patients had valve replacement and four had reannuloplasty. Increased incidence of deterioration of regurgitation in late period was seen in patients under 2 years old and those receiving a concomitant Blalock shunt. Lower event-free rate after 2 years was seen in patients with double inlet right or indeterminate ventricle and those underwent the annuloplasty alone. We conclude that the dividing common atrioventricular valve orifice into two parts with annuloplasty could effectively reduce the regurgitation in most patients with isomerism heart, and the concomitant ventricular unloading operation seems to offer promise for improving long-term results.

Adolescent↗
PubMed1994

SV40 large T antigen reinduces the cell cycle in terminally differentiated myotubes through inducing Cdk2, Cdc2, and their partner cyclins.

Terminally differentiated skeletal muscle myotubes are arrested in G0 phase of the cell cycle and are unable to be released from this arrest by stimulation with mitogens including serum and growth factors. To inspect a possibility of reversing the quiescence at the G0 phase, we have exploited the mouse skeletal muscle cell line C2SVTts11, which is a clone of C2 cells transfected with the SV40 T antigen gene (encoding thermolabile large T and wild-type small t) fused to an inducible promoter. When the large T is induced in the myotubes, the terminally differentiated cells reenter the cell cycle and proceed to S and M phases. To elucidate how large T forces the myotubes to traverse each phase of the cell cycle, we examined the expression and activity of Cdk2 and Cdc2, which in complex with cyclin A and cyclin B are essential for S and M phases, respectively in undifferentiated cells. The levels of their mRNAs and proteins and histone H1 kinase activity, which was ascribed to Cdc2-cyclin B, were high in the proliferating myoblasts but gradually decreased during terminal differentiation. In contrast, they were reinduced in the myotubes reentering the cell cycle. Stimulation of the myotubes with serum failed to evoke these factors. These results indicate that large T, but not mitogens, is able to drive terminally differentiated myotubes to pass each phase of the cell cycle through eliciting these factors as do mitogens on proliferating undifferentiated cells. Since large T is a nuclear protein, signals generated by the protein in the nucleus are likely to be sufficient to induce each phase of the cell cycle in the terminally differentiated cells.

Animals↗
PubMed1994

Depressed responsiveness to angiotensin II in ventricular myocytes of hypertrophic cardiomyopathic Syrian hamster.

Electromechanical responsiveness to angiotensin II (Ang II) receptor stimulation in ventricular myocardium and myocytes of hypertrophic cardiomyopathic Syrian hamsters (BIO 14.6) was examined and compared with that in preparations of normal hamsters (F1B) using conventional microelectrode and patch clamp techniques. Action potential duration (APD) and developed tension (DT) corrected for the cross-sectional area of the papillary muscles of 14-20 week-old BIO 14.6 hamsters were significantly smaller than those in preparations of age-matched normal hamsters. An Ang II (1 microM)-induced increase in DT in BIO 14.6 papillary muscles (24.7 +/- 11.0%) was significantly smaller than that in F1B papillary muscles (53.8 +/- 8.5%), which was associated with a smaller increase in APD in BIO 14.6 papillary muscles. In ventricular myocytes of both BIO 14.6 and F1B hamsters. Ang II increased the calcium current (ICa) following a transient decrease in ICa. However, the magnitude of the Ang II-induced increase in ICa in BIO 14.6 myocytes (35.5 +/- 7.5%) was significantly smaller than that in F1B myocytes (86.0 +/- 19.7%), suggesting a causal relationship between ICa and mechanical response to Ang II in these hamsters. The depressed responsiveness to Ang II receptor stimulation in hypertrophic cardiomyopathic hamster is in a marked contrast with the enhanced responsiveness to alpha 1-adrenergic stimulation, which was demonstrated by previous studies, and may be one of adaptational changes to the activated renin-angiotensin system in the cardiomyopathy.

Action Potentials↗
PubMed1994

Involvement of Ca(2+)-calmodulin in platelet-derived growth factor-, fibroblast growth factor-, and insulin-induced ornithine decarboxylase in NIH-3T3 cells.

Ornithine decarboxylase (ODC) was induced by platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), and insulin at doses ranging from 0.125 to 0.5 U/mL, 25 to 500 ng/mL, and 10(-8) to 10(-7) mol/L, respectively, in NIH-3T3 cells. The induction of ODC reached a plateau approximately 4 to 6 hours after addition of each mitogen. PDGF exerted a synergistic action with 10(-7) mol/L insulin until the concentration of PDGF reached 0.5 U/mL and exerted an additive action at concentrations greater than 0.5 U/mL. FGF also accelerated ODC induction by insulin (10(-7) mol/L) synergistically when it was added at doses up to 500 ng/mL. PDGF added to the intact monolayer cells caused a spike-and-plateau increase in cytosolic Ca2+ concentration ([Ca2+]i); the spike was independent of extracellular Ca2+, whereas the plateau formation was dependent on extracellular Ca2+. On the other hand, FGF caused a plateau-like increase in [Ca2+]i, exclusively dependent on extracellular Ca2+. Insulin did not affect [Ca2+]i in NIH-3T3 cells. Trifluoperazine (15 to 30 mumol/L) inhibited the induction of ODC by PDGF and FGF, but did not inhibit the effect of insulin to induce ODC. N-(6-aminohexyl)-5-chloro-1-Naphthalenesulfonamide ([W-7] 30 to 40 mumol/L) showed a more profound suppressive effect on ODC induced by PDGF and FGF than N-(6-aminohexyl)-naphthalenesulfonamide (W-5) did. There was no difference between the effects of W-7 and W-5 on ODC induction by insulin.(ABSTRACT TRUNCATED AT 250 WORDS)

3T3 Cells↗
PubMed1994

Metabolic effect of PGE1 analogue 01206.alpha CD on nerve Na(+)-K(+)-ATPase activity of rats with streptozocin-induced diabetes is mediated via cAMP: possible role of cAMP in diabetic neuropathy.

We investigated the dose-dependent effects of prostaglandin E1 (PGE1) analogue, OP1206.alpha CD (OP), on motor nerve conduction velocity (MNCV), nerve blood flow (NBF) and Na(+)-K(+)-ATPase (ATPase) activity in streptozocin-induced diabetic rats. At 10 micrograms/kg/day, OP ameliorated MNCV and NBF, but no ATPase activity, whereas at 30 micrograms/kg/day it increased MNCV and ATPase activity, but not NBF. These results suggested a possible direct metabolic effect of OP, at least at a certain dose, on ATPase activity independent of NBF. Since PGE1 exerts an effect on nerve cAMP content, we conducted an in vitro study to clarify the relationship of cAMP to the modulation of ATPase activity in diabetic nerves. We studied sciatic nerves isolated from 53 rats with streptozocin-induced diabetes that had exhibited hyperglycemia for 6 wk. OP increased the activity of ATPase and the accumulation of cAMP in a dose-dependent manner. Dibutyryl cAMP, a cAMP analogue, and aminophyline, which increases nerve cAMP content, enhanced ATPase activity in a dose-dependent manner. In addition, the increased activity of ATPase in diabetic nerves produced by OP was suppressed by a protein kinase inhibitor, H8. These results suggest that ATPase activity in diabetic nerves might be regulated or modified by cAMP and, possibly, by protein kinase A, a finding that is important for clarifying the pathogenesis of diabetic neuropathy and for developing new approaches to treatment.

Alprostadil↗
PubMed1994

Long-continuous observation of the effects of methamphetamine on wheel-running and drinking in mice.

1. Effects of methamphetamine (MAP) on wheel-running and drinking in mice, housed under 12-hr light-dark schedule (light period; 06:00-18:00), were investigated through long-continuous observation. 2. MAP (1, 2 and 4 mg/kg, s.c.) acutely increased the wheel-running and drinking for 2-4 hr in a dose-dependent manner after the administration at 11:00, midpoint of light period. 3. MAP administered at 11:00 sub-acutely suppressed the spontaneous increment during dark period (18:00-06:00) in both the behaviors. 4. Many factors, such as the time-of-day and interval of the administration as well as the dose administered, affected the behavioral suppression induced by MAP. 5. In addition to these findings, the wheel-running and drinking during the light period increased even on the days without MAP administration. 6. These results suggest that MAP have not only acute stimulant and sub-acute depressant effects, but also long-lasting effects.

Animals↗
PubMed1994

Antibacterial trichorabdal diterpenes from Rabdosia trichocarpa.

Four antibacterial diterpenes, trichorabdals A, B, C and H were isolated from the leaves of Rabdosia trichocarpa and the relationship between their conformations analysed by spectroscopic and computational methods. Their antibacterial activity is discussed.

Anti-Bacterial Agents↗
PubMed1994

Interaction between human polymorphonuclear leucocytes and bacteria released from in-vitro bacterial biofilm models.

The interactions between phagocytic cells (polymorphonuclear leucocytes) and Escherichia coli cells released from a biofilm model formed in vitro on the surface of cotton threads in an artificial medium were compared with those of phagocytes and bacteria released from a newly developed in-vitro biofilm model. This new model of bacterial biofilm on the surface of cotton threads was developed by soaking cotton threads in rat carboxymethylcellulose pouch exudate and culturing E. coli in the exudate. The structure of the biofilm model and the surface structure of the bacteria in the biofilm resembled those observed in vivo in infected pouches, and they were quite different from those observed with the biofilm model in artificial medium. Both bacteria released from biofilm models in an artificial medium and those from biofilms in rat carboxymethylcellulose pouch exudate, in vitro, were almost equally resistant to killing by phagocytes. The sensitivity of these bacteria to phagocytosis was no different from that of normal bacteria grown in artificial medium. Bacteria from both models were also less sensitive to the killing activity of H2O2. Electronmicroscopy showed that bacteria from both models had some products that interacted with ruthenium red on their surfaces, but the respective quantities of these products differed.

Animals↗
PubMed1994

Interaction between clarithromycin and biofilms formed by Staphylococcus epidermidis.

Interactions between clarithromycin and biofilms formed by Staphylococcus epidermidis were investigated by using a clarithromycin-resistant strain. Treatment of the colonization with a relatively low concentration of clarithromycin resulted in the eradication of slime-like structure and a decrease in the quantity of hexose. Another result was increased penetration of antibiotics through the biofilm of S. epidermidis.

Clarithromycin↗
PubMed1994

ATBF1, a multiple-homeodomain zinc finger protein, selectively down-regulates AT-rich elements of the human alpha-fetoprotein gene.

ATBF1 is a 306-kDa protein containing four homeodomains, 17 zinc finger motifs, and several segments potentially involved in transcriptional regulation (T. Morinaga, H. Yasuda, T. Hashimoto, K. Higashio, and T. Tamaoki, Mol. Cell. Biol. 11:6041-6049, 1991). At least one of the homeodomains of ATBF1 binds to an AT-rich element in the human alpha-fetoprotein (AFP) enhancer (enhancer AT motif). In the present work, we analyzed the transcriptional regulatory activity of ATBF1 with respect to the enhancer AT motif and similar AT-rich elements in the human AFP promoter and the human albumin promoter and enhancer. Gel retardation assays showed that ATBF1 binds to the AFP enhancer AT motif efficiently; however, it binds weakly or not at all to other AT-rich elements in the AFP and albumin regulatory regions studied. Alterations of the enhancer AT motif by site-specific mutagenesis resulted in the loss of binding of ATBF1. Cotransfection experiments with an ATBF1 expression plasmid and the chloramphenicol acetyltransferase (CAT) gene fused to AFP promoter or enhancer fragments showed that ATBF1 suppressed the activity of AFP enhancer and promoter regions containing AT-rich elements. This suppression was reduced when the mutated AT motifs with low affinity to ATBF1 were linked to the CAT gene. The ATBF1 suppression of AFP promoter and enhancer activities appeared to be due, at least in part, to competition between ATBF1 and HNF1 for the same binding site. In contrast to the AFP promoter and enhancer, the albumin promoter and enhancer were not affected by ATBF1, although they contain homologous AT-rich elements. These results show that ATBF1 is able to distinguish AFP and albumin AT-rich elements, leading to selective suppression of the AFP promoter and enhancer activities.

Animals↗
PubMed1994

Activin A: negative regulator of amylase secretion and cell proliferation in rat pancreatic acinar AR42J cells.

Activin A, a member of the transforming growth factor-beta supergene family, exists in secretory granules of non-B-cells of rat pancreatic islet (H. Yasuda, K. Inoue, H. Shibata, T. Takeuchi, Y. Eto, Y. Hasegawa, N. Sekine, Y. Totsuka, T. Mine, E. Ogata, and I. Kojima. Endocrinology 133: 624-630, 1993). Because functions of exocrine pancreas are influenced by hormones in pancreatic islet, it is possible that activin A affects the function of pancreatic acinar cells. To examine this possibility, we studied the effects of activin A on amylase secretion and DNA synthesis in AR42J cells. In these cells, dexamethasone (Dx) induces increases in secretory organelles and secretion of amylase (C. D. Logsdon, J. Moessner, J. A. Williams, and I. D. Goldfine. J. Cell Biol. 100: 1200-1208 1985). Activin A did not change the rate of amylase release by itself nor affect the cholecystokinin-stimulated amylase release from Dx-treated differentiated AR42J cells. However, when activin A was added together with Dx, activin A inhibited Dx-induced increase in amylase content in a dose-dependent manner. In the presence of 1 nM activin A, the effect of Dx was abolished. In the absence of Dx, amylase content of the cells was also reduced by activin A in a dose-dependent manner. The maximum inhibitory effect was obtained by 10 nM activin A, and at this concentration amylase content became undetectable. In addition, activin A potently inhibited DNA synthesis as assessed by [3H]thymidine incorporation.(ABSTRACT TRUNCATED AT 250 WORDS)

Activins↗
PubMed1994

An investigation of diterpenes from the leaves of Rabdosia trichocarpa and their antibacterial activity against oral microorganisms.

The ethanolic extract of Rabdosia trichocarpa leaves showed antibacterial activity against cariogenic mutans streptococci and periodontopathic Porphyromonas gingivalis. Chromatographic separation and purification of the extract afforded ten diterpenes, including one novel ent-kauren type compound named trichoranin. Some of these compounds possess potent antibacterial activity against these oral micro-organisms, indicating that these diterpenes may be useful natural substances for the maintenance of oral health.

Anti-Bacterial Agents↗
PubMed1994

Homocysteine induces iron-catalyzed lipid peroxidation of low-density lipoprotein that is prevented by alpha-tocopherol.

Homocystinuria is an inborn error of methionine metabolism that is characterized by the premature development of arteriosclerosis. As one of the major factors in the pathogenesis of arteriosclerosis, modification of low-density lipoprotein (LDL) has received widespread attention by many investigators. In this study, to elucidate the relationship between elevated homocysteine levels and premature arteriosclerosis, we investigated the role of homocysteine in the iron-catalyzed oxidative modification of LDL. When LDL isolated from a healthy subject was incubated with homocysteine and ferric ion, a gradual decrease of polyunsaturated fatty acids (PUFA), formation of thiobarbituric acid-reactive substances (TBARS) and fluorescent substances, and the fragmentation of apoprotein B (apoB) were observed. The extent of oxidative modification was dependent on the concentration of homocysteine. Modification of LDL was suppressed until the remaining alpha-tocopherol concentration reached a critical level. When the alpha-tocopherol content of LDL was increased by 2.6-fold, both the formation of TBARS and the fragmentation of apoB were suppressed. These results suggest that homocysteine might promote iron-catalyzed oxidation of LDL and imply its role for the development of premature arteriosclerosis.

Adult↗