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Biomedical subjects

F Yamaguchi

Publications and source records attributed to F Yamaguchi.

At least 37 records · Page 2Linked to original sources
PubMed1999

The expression of Ca2+/calmodulin-dependent protein kinase I in rat retina is regulated by light stimulation.

Ca2+/calmodulin-dependent protein kinase I (CaM-kinase I) in rat retina was analyzed by immunohistochemical analysis, Western blot analysis and kinase activity assay. Western blot analysis revealed two immunoreactive bands similar to those detected in the brain. Developmental studies revealed that CaM-kinase I expression increased in accordance with postnatal development. Expression of CaM-kinase I in the retinas of rats raised in the complete darkness markedly decreased. CaM-kinase I activity assay supported these findings. Synapsin I was shown to be a possible intrinsic substrate of CaM-kinase I in rat retina. These results elucidated that CaM-kinase I is expressed in the retina and may play an important role in the retinal functions and that the expression of CaM-kinase I is regulated by light stimulation.

Animals↗
PubMed1999

Free radical scavenging activity of grape seed extract and antioxidants by electron spin resonance spectrometry in an H(2)O(2)/NaOH/DMSO system.

The scavenging effects of grape seed extract (GSE) on free radicals formed in an H(2)O(2)/NaOH/DMSO system were examined using a spin-trapping electron spin resonance (ESR) method and compared with other natural antioxidants, ascorbic acid, dl-alpha-tocopherol, and beta-carotene. GSE reduced greatly the ESR signal intensity of superoxide radical-5,5-dimethyl-1-pyrroline-N-oxide (DMPO) adducts. GSE also exhibited weak scavenging activity on hydroxyl radical and a little scavenging activity on methyl radical. Ascorbic acid exhibited strong superoxide and hydroxyl radical scavenging activities, but it increased the amount of methyl radical at high concentration. dl-alpha-Tocopherol reduced the amount of superoxide anion, especially the amount of methyl radical. However, it slightly reduced the amount of hydroxyl radical. beta-Carotene reduced the amount of hydroxyl radical and methyl radical, but it also slightly reduced superoxide anion. In the case of combination use of beta-carotene and dl-alpha-tocopherol, all radical species were suppressed. Combination of GSE and dl-alpha-tocopherol also could reduce all radical species. beta-Carotene and dl-alpha-tocopherol could reduce the methyl radical formation induced by ascorbic acid.

Dimethyl Sulfoxide↗
PubMed1999

Evaluation of free radical scavenging activities of antioxidants with an H(2)O(2)/NaOH/DMSO system by electron spin resonance.

An H(2)O(2)/NaOH/DMSO system has been developed for the formation of three free radicals, and the application of the system was examined with the antioxidants ascorbic acid and tocopherol. Superoxide anion, hydroxyl radical,and methyl radical are simultaneously generated in this system. The scavenging activity of ascorbic acid and tocopherol for these radicals was estimated by 5, 5'-dimethyl-1-pyrroline-N-oxide spin trapping electron spin resonance. Both water-soluble and oil-soluble antioxidants could be evaluated by using this system. Ascorbic acid specifically inhibited the superoxide anion and hydroxyl radical, whereas tocopherol suppressed the methyl radical.

Antioxidants↗
PubMed1999

Improvement of exercise capacity of rats with chronic heart failure by long-term treatment with trandolapril.

1. The effects of long-term treatment with trandolapril, an angiotensin I-converting enzyme inhibitor, on exercise capacity of rats with chronic heart failure (CHF) following coronary artery ligation were examined. CHF was developed by 8 weeks after the coronary artery ligation. 2. The running time of rats with CHF in the treadmill test was shortened to approximately 65% of that of sham-operated rats (16.3+/-1.2 vs. 25.1+/-1.6 min, n = 7; P<0.05). ATP, creatine phosphate (CP), and lactate contents of the gracilis muscle of rats with CHF were similar to those of sham-operated rats before running. After running, ATP and CP were decreased and lactate was increased in both rats with CHF and sham-operated rats. There were no significant differences in the levels of energy metabolites between rats with CHF and sham-operated rats. The rates of decrease in ATP and CP and rate of increase in lactate in the gracilis muscle of rats with CHF during exercise were greater than those of sham operated rats (2.5, 2.0 and 1.5 fold high, respectively), suggesting wastage of energy during exercise in the animals with CHF. 3. Myofibrillar Ca2+ -stimulated ATPase (Ca-ATPase) activity of skeletal muscle of rats with CHF was increased over that of the sham-operated control (62.03+/-1.88 vs. 52.34+/-1.19 micromol Pi mg(-1) protein h(-1) n = 7; P<0.05). The compositions of myosin heavy chain (MHC) isoforms of gracilis muscle were altered by CHF; decreases in MHC types I and IIb and an increase in MHC type IIa were found (P<0.05). 4. Rats with CHF were treated with 1 mg kg(-1) day(-1) trandolapril from the 2nd to 8th week after surgery. Treatment with trandolapril prolonged the running time, reversed the rates of decrease in ATP and CP and the rate of increase in lactate, and restored the Ca-ATPase activity (51.11+/-0.56 micromol Pi mg(-1) protein h(-1), n = 7; P<0.05) and composition ratio of MHC isoforms in the gracilis muscle. 5. The results suggest that long-term trandolapril treatment of rats with CHF may restore their ability to utilize energy without wastage and thus improve exercise capacity.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

The reversible change of GluR2 RNA editing in gerbil hippocampus in course of ischemic tolerance.

The ischemic tolerance is known to show protective effects on the neurons and the restricted Ca2+ influx through Ca2+ channels might be involved. In alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor, ribonucleic acid (RNA) editing of the GluR2 subunit determines receptor desensitization and Ca2+ permeability. The authors investigated the effect of ischemic tolerance on the messenger RNA editing of Q/R and R/G sites of GluR2 subunit in hippocampus. It was found that the rate of RNA editing in Q/R site showed no change (100% edited), whereas that in R/G site decreased significantly (83.3% normal editing level to 60.4%) at day 3 (preconditioning period) and returned to normal level at day 14 (after preconditioning period). Further investigation revealed that the decrease of editing rate in ischemic tolerance resulted mainly from the decrease of editing in CA1 area.

Animals↗
PubMed1998

Bisphenol-A induces cellular transformation, aneuploidy and DNA adduct formation in cultured Syrian hamster embryo cells.

Bisphenol-A (BP-A) is a major component of epoxy, polycarbonate and other resins. For an assessment of in vitro carcinogenicity and related activity of BP-A, the abilities of this compound to induce cellular transformation and genetic effects were examined simultaneously using the Syrian hamster embryo (SHE) cell model. Cellular growth was reduced by continuous treatment with BP-A at doses > or = 100 microM. However, colony-forming efficiencies were not decreased significantly following treatment with up to 200 microM BP-A for 48 hr. Morphological transformation of SHE cells was induced by treatment of cells with BP-A at 50 to 200 microM for 48 hr. BP-A exhibited transforming activity at doses > or = 50 microM but was less active than the benzo[alpha]pyrene used as a positive control. Over the dose range that resulted in cellular transformation, treatment of SHE cells with BP-A failed to induce gene mutations at the Na+/K+ ATPase locus or the hprt locus. No statistically significant numbers of chromosomal aberrations were detected in SHE cells treated with BP-A. However, treatment of cells with BP-A induced numerical chromosomal changes in the near diploid range at doses that induced cellular transformation. 32P-Postlabeling analysis revealed that exposure of cells to BP-A also elicited DNA adduct formation in a dose-dependent fashion. Our results indicate that BP-A has cell-transforming and genotoxic activities in cultured mammalian cells and potential carcinogenic activity.

Aneuploidy↗
PubMed1998

Effects of long-term treatment with trandolapril on sarcoplasmic reticulum function of cardiac muscle in rats with chronic heart failure following myocardial infarction.

1 Calcium transport activity of isolated cardiac sarcoplasmic reticulum (SR) including Ca2+ uptake and release is decreased in animals with chronic heart failure (CHF) following myocardial infarction. The present study was undertaken to determine whether an angiotensin converting enzyme (ACE) inhibitor, trandolapril, improves cardiac sarcoplasmic reticular function in animals with CHF following myocardial infarction. 2 CHF was induced by left coronary artery ligation in rats, which resulted in an infarction of approximately 45% of the left ventricle. Aortic flow and cardiac output index were decreased, and left ventricular end-diastolic pressure was increased 8 weeks after the operation, suggesting the development of CHF. 3 The developed force transients of cardiac skinned fibres of the rats with CHF were decreased when the skinned fibre was preloaded for 0.25-1 min with 10(-5) M Ca2+ (48-88%) and when preloaded with 10(-6) M Ca2+ and then exposed to 0.1-1 mM caffeine (45-93%). 4 The [3H]-ryanodine-binding activity in SR-enriched fractions was reduced by 23% in the CHF group. These results suggest that the amount of Ca2+ released from SR is decreased due to a reduced rate of SR Ca2+ uptake and a downregulation of the SR Ca2+-release channel. 5 Rats were treated orally with 3 mg kg(-1) day(-1) trandolapril from the 2nd to the 8th week after the coronary artery ligation. Treatment with trandolapril attenuated the reduction in aortic flow and cardiac output index and the increase in left ventricular end-diastolic pressure, and improved the developed force transients of the skinned fibre of the animal with CHF without causing a reduction of infarct size. Treatment with trandolapril also attenuated the reduction in ryanodine receptor density in the viable left ventricle of the rat with CHF. 6 It is concluded that long-term treatment with trandolapril attenuates cardiac SR dysfunction in rats with CHF and that the mechanism underlying this effect is, at least in part, attributed to prevention of downregulation of Ca2+ release channel.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

The effect of chronic treatment with trandolapril on cyclic AMP-and cyclic GMP-dependent relaxations in aortic segments of rats with chronic heart failure.

1 Characteristics of cyclic GMP- and cyclic AMP-mediated relaxation in aortic segments of rats with chronic heart failure (CHF) and the effects of chronic treatment with an angiotensin I converting enzyme (ACE) inhibitor, trandolapril, were examined 8 weeks after coronary artery ligation. 2 Cardiac output indices of coronary artery-ligated and sham-operated rats were 125+/-8 and 189+/-10 ml min(-1) kg(-1), respectively (P<0.05), indicating the development of CHF at this period. 3 The maximal relaxant response of aortic segments to 10 microM acetylcholine in rats with CHF and sham-operated rats was 64.0+/-5.7 and 86.9+/-1.9%, respectively (P<0.05), whereas the relaxant response to sodium nitroprusside (SNP) remained unchanged. Tissue cyclic GMP content in rats with CHF was lower than that of sham-operated rats. 4 In endothelium-intact segments of rats with CHF, the maximal relaxant response to 10 microM isoprenaline (44.5+/-6.7%) was lower that sham-operated rats (81.3+/-2.5%, P<0.05) and the concentration-response curve for NKH477, a water-soluble forskolin, was shifted to the right without a reduction in the maximal response. Isoprenaline-induced relaxation of aortic segments was attenuated by NG-nitro-L-arginine methyl ester (L-NAME) in sham-operated rats, but not in rats with CHF. Relaxation to 30 microM dibutyryl cyclic AMP in rats with CHF (26.8+/-2.7%) was lower than that in sham-operated rats (63.4+/-11.8%, P<0.05). 5 Trandolapril (3 mg kg(-1) day(-1)) was orally administered from the 2nd to 8th week after the operation. Aortic blood flow of rats with CHF (38.5+/-3.6 ml min(-1)) was lower than that of sham-operated rats (55.0+/-3.0 ml min(-1)), and this reduction was reversed (54.1+/-3.4 ml min(-1)) by treatment with trandolapril. The diminished responsiveness described above was normalized in the trandolapril-treated rat with CHF (i.e., the maximal relaxation to acetylcholine, 94.7+/-1.0%; that to isoprenaline, 80.5+/-2.8%; that to dibutyryl cyclic AMP, 54.7+/-6.2%). However, aortic segments of trandolapril-treated rats with CHF, L-NAME did not attenuate isoprenaline-induced relaxation and the tissue cyclic GMP level was not fully restored, suggesting that the ability of the endothelium to produce NO was still partially damaged. 6 The results suggest that vasorelaxation in CHF, diminished mainly due to dysfunction in endothelial nitric oxide (NO) production and cyclic AMP-mediated signal transduction, was partially restored by long-term treatment with trandolapril. The mechanism underlying the restoration may be attributed in part to prevention of CHF-induced endothelial dysfunction.

Acetylcholine↗
PubMed1998

Identification of Bombyx mori midgut receptor for Bacillus thuringiensis insecticidal CryIA(a) toxin.

As part of a study of the mechanism by which Bacillus thuringiensis insecticidal crystal protein acts, a Bombyx mori receptor to the CryIA(a) toxin specific for lepidopterans was examined. Histological examination showed that the toxin acted on the brush-border membrane of the midgut columnar cells and broke its infolding structure, causing cell lysis. The membrane vesicles were purified, and a 175-kDa protein binding the toxin was found that accounted for some 0.015% of membrane proteins. The protein, designated BtR175, was a glycoprotein that reacted with concanavalin A. Anti-BtR antibodies inhibited the binding of toxin to membrane vesicles in vitro and decreased the effect of the toxin to silkworms in vivo. BtR175, although found in the gut, was not found in fat bodies, integument, or silk glands. These results indicated that BtR175 was the receptor protein for the insecticidal toxin. Proteins (137 and 107 kDa) binding the CryIA(a) toxin also were found in the gut membranes of Tenebrio moritor larvae, a coleopteran not sensitive to the toxin. The specificity of the toxin could not be explained only in term of the existence of its binding protein.

Animals↗
PubMed1998

[Inhibition of fibroblast growth factor receptor 1 expression in human glioblastoma cell contributes to the cell growth suppression].

Although normal human astrocytes rarely express fibroblast growth factor receptor 1 (FGFR 1) mRNA, expression of FGFR 1 mRNA in astrocytomas increases as malignancy progresses. This result suggests that FGFR 1 can be one of important factors for glioblastoma cell growth. In our study, specific antisense oligonucleotides for FGFR 1 mRNA inhibited cell growth of SNB 19, human glioblastoma cell line, while sense oligonucleotides showed no cell reduction. And Southern blot analysis demonstrated decreased expression of FGFR 1 mRNA in only antisense group. Furthermore, cross-linking analysis revealed decreased number of FGFR 1 in antisense-treated SNB 19 in protein level. These results conclude that cell growth inhibition was caused by suppression of both transcription and translation of FGFR 1 mRNA. Interestingly, alpha-specific antisense also inhibited expression of beta-, and gamma-type of FGFR 1 mRNA which had no binding sites for the oligonucleotides. This fact indicates that antisense oligonucleotides binds to premature mRNA, which is previous form of mature mRNA before splicing, in nucleus. It is previously reported that basic fibroblast growth factor (bFGF), major ligand to FGFR 1, was overly expressed in human malignant astrocytomas. Thus, increased number of FGFR 1 may contribute to the acceleration of bFGF autocrine or paracrine mechanism in glioblastoma.

Brain Neoplasms↗
PubMed1997

An assessment of antigenic potential of beta-lactam antibiotics, low molecular weight drugs, using guinea pig models.

Allergic reactions are among the common adverse effects in humans. However, it is widely assumed that there are practically no reliable animal models for preclinical tests of low-molecular weight drugs that are available to predict such reactions. This study was designed to compare the detecting ability of test methods for antigenic potential of eight beta-lactam antibiotics with which allergic outcome has been reported in humans. The tests included active systemic anaphylaxis (ASA), delayed type skin reaction (DSR), maximization test (GPMT) in guinea pigs sensitized with antibiotics emulsified with Freund's complete adjuvant, passive cutaneous anaphylaxis (PCA) and enzyme-linked immunosorbent assay (ELISA) as serological tests. PCA and ELISA though using protein-conjugates as detecting antigens, especially ELISA, showed positive reactions with relatively high incidence. On the other hand, GPMT was the most sensitive method to detect antigenic potential of antibiotics despite the use of antibiotics alone for sensitizing and challenging phases. It is suggested that GPMT can be considered the most reliable method in preclinical testing.

Anaphylaxis↗
PubMed1997

Molecular cloning of 5-hydroxytryptamine (5-HT) type 1 receptor genes from the Japanese puffer fish, Fugu rubripes.

To characterize the structure of Fugu G-protein coupled receptor family and its evolutionary divergence, we have cloned and sequenced the Fugu 5-HT type 1 receptor genes by Polymerase Chain Reaction (PCR) with degenerate primers followed by phage library screening. The analysis of the deduced amino acid sequences showed that F1A alpha and F1A beta have the highest homology to the human 5-HT1A receptor (71.5% and 63.7%, respectively). Another clone, F1D, showed highest (70.5%) homology to the human type 1D receptor. The amino acid residues that are important for ligand binding have been conserved in these Fugu genes. The phylogenetic tree analysis suggests that the duplication event of the Fugu type 1A receptor may have occurred after the divergence of Fugu and the tetrapod lineage.

Amino Acid Sequence↗
PubMed1997

Involvement of calmodulin-dependent protein kinases-I and -IV in long-term potentiation.

Multifunctional Ca2+/calmodulin-dependent protein kinases (CaMKs) are thought to be involved in the induction of long-term potentiation (LTP). In the present study, LTP was induced by theta burst stimulation in the Schaffer collateral area of the stratum radiatum in the hippocampal CA1 region of the rat hippocampus. LTP-induced and control hippocampal slices were studied by Western blot and immunohistochemical analyses using CaMK-I, -II and -IV antibodies. Increased amounts of all three CaMKs were found in LTP-induced hippocampal slices as indicated by Western blot as well as by the density of their immunoreactivity. Our data clearly shows that not only CaMK-II but also CaMK-I and -IV contribute to synaptic plasticity formed in LTP.

Animals↗
PubMed1997

Cardiac sarcoplasmic reticular function in rats with chronic heart failure following myocardial infarction.

Sarcoplasmic reticular function of rats with chronic heart failure (CHF) following coronary artery ligation was examined. The coronary artery ligation produced 43% infarction of the left ventricle and increased left ventricular end-diastolic pressure 8 weeks after the operation, suggesting the development of CHF by this period. The developed force transients of the skinned fiber of coronary artery-ligated rats were decreased when the skinned fiber was preloaded for 0.25-0.5 min with 10(-5)M Ca2+ (53-70%) and when preloaded with 10(-6)M Ca2+ and then exposed to 0.1-1 mM caffeine (39-87%). The results suggest that the rate of Ca2+ uptake by the sarcoplasmic reticulum (SR) and its ability to release Ca2+ were reduced in the failing heart. [3H]Ryanodine binding activities in homogenates and SR-enriched fractions were significantly reduced in the coronary artery-ligated group (32% and 21%, respectively). The results suggest that the amount of Ca2+ released from SR decreased due to decreased Ca2+ uptake rate of SR and down-regulation of the SR Ca(2+)-release channel, which contributes to cardiac dysfunction in failing hearts following acute myocardial infarction.

Animals↗
PubMed1997

Activation of cardiac muscarinic receptor and ischemic preconditioning effects in in situ rat heart.

Activation of cardiac muscarinic receptors by vagal stimulation decreases cardiac work, which may have a protective effect against ischemic injury. To determine whether cardiac muscarinic receptors contribute to the mechanisms of preconditioning effects, we examined the effect of carbachol on ischemia/reperfusion damage and the effect of vagotomy on cardioprotection induced by ischemic preconditioning. Rats were subjected to 30 min of left coronary artery occlusion followed by 30-min reperfusion in situ. Pre-conditioning was induced by three cycles of 2-min coronary artery occlusion and, subsequently by 5 min of reperfusion. The incidence of ischemic arrhythmias, such as ventricular tachycardia (VT) and ventricular fibrillation (VF), and the development of myocardial infarction were markedly reduced by the preconditioning. Carbachol infusion (4 micrograms/kg per min) delayed the occurrence of VT and VF during ischemia and reduced the infarct size. Compared with non-ischemic left ventricle, the cyclic guanosine monophosphate (GMP) content in the ischemic region of the left ventricle was decreased by ischemia/reperfusion, whereas the cyclic adenosine monophosphate (AMP) content of this region was increased. These changes were reversed by preconditioning. Similar changes in cyclic GMP and AMP content in the ischemic region were seen in rats undergoing carbachol treatment. These results suggest the possible contribution of muscarinic receptor stimulation to preconditioning. Vagotomy prior to preconditioning diminished the antiarrhythmic effects, whereas it did not block the anti-infarct effect afforded by pre-conditioning. Vagotomy abolished the preconditioning effect on the tissue cyclic GMP, but it did not attenuate the decrease in tissue cyclic AMP. The results suggest that muscarinic stimulation exerts preconditioning-mimetic protective effects in ischemic/reperfused hearts, but that a contribution of reflective vagal activity to the mechanism for preconditioning is unlikely.

Animals↗
PubMed1997

Changes in fatty acid compositions of myocardial lipids in rats with heart failure following myocardial infarction.

Changes in fatty acid composition of myocardial lipids were examined in rats with heart failure following myocardial infarction. Left ventricular systolic pressure (LVSP) was decreased and left ventricular end-diastolic pressure (LVEDP) was elevated 24 h, 1 and 12 weeks after left coronary artery ligation (CAL), suggesting the development of heart failure at these periods in this model. Hearts were isolated 24 h, 1 week and 12 weeks after the operation. Myocardial lipids in the infarcted scar tissue, non-infarcted remaining left ventricle including interseptum and right ventricle were separated into phospholipid (PL), triacylglycerol (TG), diacylglycerol (DAG) and free fatty acid (FFA) fractions. In the scar tissue PL content markedly decreased whereas TG, DAG and FFA contents increased 24 h after CAL. Despite a marked decrease in constituted fatty acids of PL fraction in the scar tissue the percentage of arachidonic acid in PL was elevated 12 weeks after CAL, suggesting that release of arachidonic acid during PL degradation was suppressed. In the non-infarcted viable left ventricle PL content remained unchanged throughout the experiment whereas TG, DAG and FFA contents were elevated 24 h after CAL. Despite no changes in PL and other lipid contents in the non-infarcted tissue the percentage of linoleic acid in PL was reduced and that of docosahexaenoic acid in PL was elevated 12 weeks after CAL. Our findings showed that myocardial lipid composition of the non-infarcted left ventricle was altered only in an early stage of the development of heart failure and fatty acid compositions of PL was exchanged in a late stage of the development of heart failure. The exchange may be related to cardiac dysfunction or myocardial remodelling in the rat with heart failure.

Animals↗
PubMed1996

Molecular cloning of the novel human G protein-coupled receptor (GPCR) gene mapped on chromosome 9.

A novel human GPCR gene was cloned by PCR with degenerate primers designed from cannabinoid type 1 receptor (CB1) sequences and a full-length clone was isolated by screening of a human genomic DNA library. This gene, termed EDG-3, is highly homologous (51.9 % overall and 69.2 % in seven transmembrane regions) to human EDG-1, 47.9 % to rat AGR16 but only 28.0 % to human CB1 receptor. The Northern hybridization analysis showed that a 2.8 kb transcript of EDG-3 is abundantly expressed in the heart followed by placenta, kidney and liver. The EDG-3 gene was mapped on the human chromosome 9q22.1-q22.2 by fluorescence in situ hybridization analysis. Although the ligand and physiological role of this receptor is unknown, this gene may be a new member of the EDG family.

Amino Acid Sequence↗