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Biomedical subjects

H Kaneda

Publications and source records attributed to H Kaneda.

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

Transradial coronary intervention in Japanese patients.

The objectives of this study was to test the feasibility and safety of transradial coronary intervention (TRI) in Japanese patients. We compared the results of TRI in 1,791 lesions (1,360 patients) between November 1995 and December 1997 with those of transfemoral coronary intervention (TFI) in 966 lesions (793 patients) between April and October 1995. We also examined the radial artery pulse in 294 patients 1-2 weeks after TRI by palpation and Doppler examination. Arterial puncture, coronary artery cannulation, lesion, and patient success rates were similar in both groups. No significant difference was noted in the major complication rate. Local complications were significantly lower in the TRI group (0.3% vs. 3.3%, P < 0.001). Doppler studies of the radial artery were performed in 294 patients chosen at random. In the first 234 patients, the sheath was pulled out 3 hr after the procedure, and in the last 60 patients, immediately after the procedure; radial artery occlusion rates were 5% and 0%, respectively. In conclusion, TRI seems safe and feasible in Japanese patients.

Aged↗
PubMed1999

Spatio-temporal analysis of cortical activity evoked by gustatory stimulation in humans.

Gustatory activated regions in the cerebral cortex have not been identified precisely in humans. In this study we recorded the magnetic fields from the brain in response to two tastants, 1 M NaCl and 3 mM saccharin. We estimated the location of areas activated sequentially after the onset of stimulation with magnetic source imaging. We investigated the primary gustatory area (area G) precisely, and found it at the transition between the parietal operculum and the insular cortex. The central sulcus was activated less frequently than area G but with almost the same latency in cases of NaCl stimulation. Following area G, we found activation in several cortical regions, e.g. both the frontal operculum and the anterior part of the insula, the hippocampus, the parahippocampal gyrus and the superior temporal sulcus.

Adult↗
PubMed1999

Oxidative stress causes enhanced endothelial cell injury in human heme oxygenase-1 deficiency.

The first known human case of heme oxygenase-1 (HO-1) deficiency is presented in this report. The patient is a six-year-old boy with severe growth retardation. He has been suffering from persistent hemolytic anemia characterized by marked erythrocyte fragmentation and intravascular hemolysis, with paradoxical increase of serum haptoglobin and low bilirubin. An abnormal coagulation/fibrinolysis system, associated with elevated thrombomodulin and von Willebrand factor, indicated the presence of severe, persistent endothelial damage. Electron microscopy of renal glomeruli revealed detachment of endothelium, with subendothelial deposition of an unidentified material. Iron deposition was noted in renal and hepatic tissue. Immunohistochemistry of hepatic tissue and immunoblotting of a cadmium-stimulated Epstein-Barr virus-transformed lymphoblastoid cell line (LCL) revealed complete absence of HO-1 production. An LCL derived from the patient was extremely sensitive to hemin-induced cell injury. Sequence analysis of the patient's HO-1 gene revealed complete loss of exon-2 of the maternal allele and a two-nucleotide deletion within exon3 of the paternal allele. Growth retardation, anemia, iron deposition, and vulnerability to stressful injury are all characteristics observed in recently described HO-1 targeted mice. This study presents not only the first human case of HO-1 deficiency but may also provide clues to the key roles played by this important enzyme in vivo.

Animals↗
PubMed1998

Developmental changes and functional properties of human memory T cell subpopulations defined by CD60 expression.

The present study was undertaken to examine developmental changes of T cells expressing CD60 and their functional properties. Three-color immunofluorescence analysis revealed that the CD60 antigen was preferentially expressed on a proportion of memory (CD45RO+) CD4+ T cells, but less on memory CD8+ T cells, while this antigen is undetectable in naive (CD45RO-) T cells. A frequency of memory CD4+ T cells expressing CD60 in the peripheral blood was negligible in newborns and gradually increased with advancing age. CD60+ memory CD4+ T cells showed stronger proliferative responses to PPD and produced higher levels of IL-4 and IL-10 than CD60- ones, whereas production of IL-2 and IFN-gamma was similarly found in both cell subpopulations. In addition, it was shown that efficient helper activity for Ig production by B cells was predominated in CD60+ memory CD4+ T cells. These results suggest that CD60 may be primarily expressed on the functionally differentiated memory effector cells among circulating CD45RO+ CD4+ T cells.

Adolescent↗
PubMed1998

A syndrome of peripheral blood T-cell infection with Epstein-Barr virus (EBV) followed by EBV-positive T-cell lymphoma.

The role of Epstein-Barr virus (EBV) in the pathogenesis of severe, chronic active EBV infection and its complications is unclear. We investigated two Japanese patients diagnosed with severe, chronic active EBV infection who subsequently developed EBV-positive T-cell lymphoma. The patients displayed abnormally high antibody titers to EBV antigens, and had evidence of peripheral blood CD4(+) T-cell infection with EBV, 19 months and 3 months, respectively, before the diagnosis of EBV-positive T-cell lymphoma. The lymphomas were infected with monoclonal EBV and expressed the EBV latency genes EBNA-1, LMP-1, and LMP-2. Genetic studies showed that the virus detected in the T-cell lymphoma was indistinguishable, with respect to type and previously defined LMP-1 and EBNA-1 gene variations, from virus detected in the peripheral blood T cells 19 months earlier. These studies support an important pathogenetic role of T-cell infection with EBV in chronic active EBV infection and in the EBV-positive T-cell lymphoma that followed.

Antibodies, Viral↗
PubMed1998

Oxidation of lipids in low density lipoprotein particles.

This study was undertaken to understand further the mechanisms and dynamics of the oxidation of lipids in low density lipoprotein (LDL) particles, aiming specifically at elucidating the material balance between oxygen uptake and products found and also the relative susceptibilities to oxidation of cholesteryl ester in the core and phosphatidylcholine in the outer monolayer in the LDL particles. It was found that considerable amount of oxygen uptake could not be accounted for by conjugated diene or total peroxides. Total peroxide was measured from the phosphine oxide formed from triphenylphosphine or diphenyl-pyrenylphosphine by reduction of peroxides. Cholesteryl ester hydroperoxides and phosphatidylcholine hydroperoxides were the major peroxides formed in LDL oxidation, but they accounted for about 60% of total peroxide. Cholesterol was also oxidized, but its oxidation was significant only at the later stages of the reaction. It was also found that the oxidizability of cholesteryl ester relative to phosphatidylcholine was larger within the LDL particle than in homogeneous solution and this was interpreted in the context of the physical properties of LDL particle.

Cholesterol↗
PubMed1998

Maternal inheritance of mouse mtDNA in interspecific hybrids: segregation of the leaked paternal mtDNA followed by the prevention of subsequent paternal leakage.

The transmission profiles of sperm mtDNA introduced into fertilized eggs were examined in detail in F1 hybrids of mouse interspecific crosses by addressing three aspects. The first is whether the leaked paternal mtDNA in fertilized eggs produced by interspecific crosses was distributed stably to all tissues after the eggs' development to adults. The second is whether the leaked paternal mtDNA was transmitted to the subsequent generations. The third is whether paternal mtDNA continuously leaks in subsequent backcrosses. For identification of the leaked paternal mtDNA, we prepared total DNA samples directly from tissues or embryos and used PCR techniques that can detect a few molecules of paternal mtDNA even in the presence of 10(8)-fold excess of maternal mtDNA. The results showed that the leaked paternal mtDNA was not distributed to all tissues in the F1 hybrids or transmitted to the following generations through the female germ line. Moreover, the paternal mtDNA leakage was limited to the first generation of an interspecific cross and did not occur in progeny from subsequent backcrosses. These observations suggest that species-specific exclusion of sperm mtDNA in mammalian fertilized eggs is extremely stringent, ensuring strictly maternal inheritance of mtDNA.

Animals↗
PubMed1998

Patients' views on residual blood use for research purposes.

In order to document patients' views on residual blood use for research purposes, a questionnaire survey was conducted at Aichi Cancer Center Hospital in October 1997. Subjects were patients who had undergone blood tests at a central blood sampling room in the morning during the week of the study enrollment. The questionnaire was handed out and collected at a waiting area in front of the blood sampling room. Of the 583 patients to whom we tried to hand out the questionnaire, 558 participated (258 males, 294 females, and 6 of sex unknown) and 25 refused. Those who regarded research to improve health care as important were 76.7% of those sampled. Only 28 patients (5.0%) answered that they would not permit the use of their residual blood for research purposes. Although logistic analysis did not detect significant factors influencing the giving of permission, the percentage who would not permit the use of their residual blood for research purposes was significantly higher in cancer outpatients (6.7%) than in inpatients (1.0%). It seems desirable for hospitals to establish an open policy concerning residual blood use for research purposes.

Blood↗
PubMed1998

Evolutionary relationships among Japanese pond frogs inferred from mitochondrial DNA sequences of cytochrome b and 12S ribosomal RNA genes.

The evolutionary relationships among Japanese pond frogs (Rana nigromaculata, R.porosa porosa, and R. p. brevipoda) were investigated by analyzing nucleotide sequences of mitochondrial cytochrome b (cyt b) and 12S rRNA genes. The nucleotide sequences of 444-bp segment of the cyt b gene and 410-bp segment of 12S rRNA gene were determined by the PCR-direct sequencing method using 18 frogs from 13 populations of Japanese pond frogs, and phylogenetic trees were constructed by the neighbor-joining and maximum likelihood methods using R. catesbeiana as an outgroup. The sequenced 444-bp segment of cyt b gene provided 69 variables sites, and the sequenced 410-bp segment of 12S rRNA gene provided 21 variables sites. The numbers of nucleotide substitutions per site of the cyt b gene within ingroup were 0.0022-0.0205 at the populational level, 0.0368-0.0462 at the racial or subspecific level, and 0.1038-0.1244 at the specific level, whereas those of the 12S rRNA gene were 0-0.0074 at the populational or subspecific level, and 0.0378-0.0456 at the specific level. Most nucleotide substitutions within ingroup occurred at the third codon position of the cyt b gene and were silent mutations. High frequencies of transitions relative to transversions were shown at cyt b and 12S rRNA genes within ingroup. The phylogenetic trees constructed from the nucleotide sequences of the cyt b gene showed that after outgroup R. catesbeiana separated from ingroup frogs, ingroup Japanese pond frogs diverged into R.nigromaculata and R.porosa, then the latter diverged into R.p. porosa, R.p. brevipoda (the typical Okayama race), and the Nagoya race of R.p.porosa. The phylogenetic trees constructed from the nucleotide sequences of the 12S rRNA gene also showed distinct divergence between two species, but not any divergence within species.

Amino Acid Sequence↗
PubMed1998

Decreased physical performance of congenic mice with mismatch between the nuclear and the mitochondrial genome.

Maternal transmission of mitochondrial DNA (mtDNA) allows us to generate mtDNA congenic strain by repeating backcrosses of female mice to male mice of an inbred strain, which carries different mtDNA haplotype from that of the female progenitor. Since genetic backgrounds of inbred strains commonly used (e.g., C57BL/6J [B6] and BALB/c) are mainly derived from an European subspecies of Mus musculus domesticus, congenic strains, in which mtDNA originated from an Asian subspecies M. musculus musculus or an European species M. spretus, give in vivo condition that mismatch occurs between the mitochondrial and the nuclear genome. So far, little has been known how the mismatch condition affects the physiological phenotype of the mice. To address this question, we established two mtDNA congenic strains, C57BL/6J(B6)-mtSPR and BALB/c-mtSHH, which carry M. spretus- and M. m. musculus-derived mtDNAs, representing the conditions of interspecific and intersubspecific mitochondrial-nuclear genome mismatch, respectively. Using these congenic strains, we examined their physical performance by measuring their running time on a treadmill belt until exhaustion. The result clearly showed that the mtDNA congenic strains manifested a significant decrease in the level of physical performance, when compared with their progenitor strains. It also appeared that the congenic mice manifested growth rate. Thus, all results indicated that mismatch between the mitochondrial and the nuclear genome causes phenotypic changes in individuals of mice.

Animals↗
PubMed1997

Genetic polymorphism of 5,10-methylenetetrahydrofolate reductase (MTHFR) as a risk factor for coronary artery disease.

BACKGROUND: Epidemiological studies have identified hyperhomocyst(e)inemia as an independent risk factor for coronary artery disease (CAD). Recently, the alanine/valine (A/V) polymorphism of the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene, one of the key enzymes catalyzing remethylation of homocysteine, has been reported. The VV genotype correlates with increased plasma homocyst(e)ine levels as a result of the reduced activity and increased thermolability of this enzyme. In this study, we examined the distribution of the MTHFR genotypes in Japanese men and the association between the VV genotype and CAD. METHODS AND RESULTS: The diagnoses of CAD of all the studied patients were confirmed by coronary angiography. The MTHFR genotype was analyzed by PCR followed by HinfI digestion. In 778 healthy male subjects, the frequency of the V allele was 0.33, comparable to that in a French Canadian population. In 362 patients with CAD, the VV genotype was significantly more frequent than in control subjects (16% versus 10%, P=.0067). The association of the VV genotype with CAD was further increased in patients with > or = 99% stenotic lesions (18%, P=.0010), whereas no significant association with the VV genotype was observed in patients without a > or = 99% stenosis. When the genotype frequency was compared among patients with different numbers of stenotic coronary arteries, the frequency of the VV genotype was significantly higher in patients with triple-vessel disease (26%) than in patients with single- or double-vessel disease (15% and 14%, respectively). CONCLUSIONS: The VV genotype of MTHFR was also common in the Japanese population and was significantly associated with CAD. The frequency of this genotype in particular was correlated with the severity of disease. The VV genotype associated with a predisposition to increased plasma homocyst(e)ine levels may represent a genetic risk factor for CAD.

5,10-Methylenetetrahydrofolate Reductase (FADH2)↗
PubMed1997

Neurochemical and metabolic consequences of elevated cerebrospinal fluid quinolinic acid concentrations in rat brain.

Quinolinic acid (QUIN) is an endogenous excitatory amino acid, which is elevated in brain tissues or cerebrospinal fluid (CSF) in several acute and chronic inflammatory central nervous system (CNS) diseases. The functional significance of this elevation is unknown but speculations of excitotoxicity have been raised. We have begun to address the pathologic consequences of elevated CSF QUIN by studying the effects of intracerebroventricular (i.cv) administration of QUIN on regional choline acetyltransferase (ChAT) activity, somatostatin content and glucose metabolism in the rat brain. QUIN (12 and 60 nmol) i.cv administration once a day for 7 days (total dose; 84 and 420 nmol, respectively) had minimal effect on somatostatin content and no effect on ChAT activity. In contrast, following continuous i.cv infusion of QUIN for 14 days using an osmotic minipump (480 nmol), ChAT activity dropped in the hippocampus and the striatum and somatostatin content was reduced in the frontal cortex, hippocampus, striatum and amygdala. Moreover, following the QUIN infusion, glucose utilization decreased in the basal nucleus of Meynert, frontal cortex, and portions of the basal ganglia and the limbic system. These results indicate that subchronic i.cv infusion of QUIN to rats results in selective regional neurochemical and metabolic changes distributed throughout the CNS. These results suggest target brain areas and transmitter systems which may be associated with neurologic syndromes characterized by elevated CSF QUIN levels.

Animals↗
PubMed1997

[Gene Polymorphism of 5, 10-methylenetetrahydrofolate reductase as a coronary risk factor].

Hyperhomocysteinemia has been identified as a possible risk factor for coronary artery disease. The association of the alanine/valine (A/V) polymorphism of 5, 10-methylenetetrahydrofolate reductase (MTHFR), one of the key enzymes catalyzing re-methylation of homocysteine, with coronary artery disease was examined in 362 Japanese males with a diagnosis of coronary artery disease confirmed with coronary angiography. The A/V polymorphism was analyzed with PCR followed by Hinf I digestion. The screening of 778 male volunteer controls revealed that the frequency of V allele in Japanese was 0.33, comparable to that in the French Canadian population. The VV genotype, which correlates with increased plasma homocysteine levels due to reduced activity and increased thermolability of this enzyme, was significantly more frequent in patients with coronary artery disease (15.7%, n = 362) than in controls (10.2%, n = 778; p = 0.0067). The association of the VV genotype with coronary artery disease was further increased in patients with > or = 99% stenotic lesion (p = 0.0010). In these patients, the frequency of the VV genotype was significantly higher in patients with triple-vessel disease (26%) than in patients with single- or double-vessel disease (15% and 14%, respectively). The fasting plasma homocysteine levels in VV subjects were higher than those in AV or AA subjects. The VV genotype of MTHFR associated with increased plasma homocysteine levels may represent an important genetic risk factor for coronary artery disease, especially with the occurrence of myocardial infarction.

Adult↗
PubMed1995

Contribution of hydrophobic residues to the stability of human lysozyme: calorimetric studies and X-ray structural analysis of the five isoleucine to valine mutants.

In order to understand the contribution of hydrophobic residues to the conformational stability of human lysozyme, five Ile mutants (Ile --> Val) in the interior of the protein were constructed. The thermodynamic parameters characterizing the denaturation of these mutant proteins were determined by scanning calorimetry, and the three-dimensional structure of each mutant protein was solved at high resolution by X-ray crystallography. The thermodynamic analyses at 64.9 degrees C and at pH 2.7 revealed the following. (1) The stabilities of all the mutant proteins were decreased as compared with that of the wild-type protein. (2) The changes in the calorimetric enthalpies were larger than those in the Gibbs energies, and were compensated by entropy changes. (3) The destabilization mechanism of the mutant proteins differs, depending on the location of the mutation sites. X-ray analyses showed that the overall structures of all the mutant human lysozymes examined were identical to that of the wild-type protein, and only small structural rearrangements were observed locally around some of the mutation sites. The most striking change among the mutant proteins was found in the mutant protein, 159V, which contains a new water molecule in the cavity created by the mutation. The thermodynamic stabilities of the mutant proteins are discussed in light of the high-resolution X-ray structures of the wild-type and five mutant human lysozymes examined.

Calorimetry, Differential Scanning↗
PubMed1995

Elimination of paternal mitochondrial DNA in intraspecific crosses during early mouse embryogenesis.

To examine whether mtDNA is uni- or biparentally transmitted in mice, we developed an assay that can detect sperm mtDNA in a single mouse embryo. In intraspecific hybrids of Mus musculus, paternal mtDNA was detected only through the early pronucleus stage, and its disappearance co-incided with loss of membrane potential in sperm-derived mitochondria. By contrast, in interspecific hybrids between M. musculus and Mus spretus, paternal mtDNA was detected throughout development from pronucleus stage to neonates. We propose that oocyte cytoplasm has a species-specific mechanism that recognizes and eliminates sperm mitochondria and mtDNA. This mechanism must recognize nuclearly encoded proteins in the sperm midpiece, and not the mtDNA or the proteins it encodes, because sperm mitochondria from the congenic strain B6.mtspr, which carries M. spretus mtDNA on background of M. musculus (B6) nuclear genes, were eliminated early by B6 oocytes as in intraspecific crosses. We conclude that cytoplasmic genomes are transmitted uniparentally in intraspecific crosses in mammals as in Chlamydomonas and that leakage of parental mtDNA is limited to interspecific crosses, which rarely occur in nature.

Animals↗
PubMed1995

Increases in cortical neuropeptide Y and somatostatin concentrations following haloperidol-depot treatment in rats.

The concentrations of neuropeptide Y (NPY) and somatostatin (SS) have been said to be altered in the brain and cerebrospinal fluid of schizophrenic patients. This alteration could result from the neuroleptic treatment. Therefore, it is of interest to evaluate effects of long-term treatment with neuroleptics on the peptide concentrations in the brain. Haloperidol (HPD) is one of the most frequently used neuroleptics for the treatment of schizophrenia. We determined regional brain levels of NPY and SS following HPD administration in the rat. A single intraperitoneal injection of HPD, at a dose of 1 mg/kg, did not affect peptide levels in the brain regions studied. Four weeks after an intramuscular deposit injection of HPD decanoate, 50 mg/kg, NPY concentrations were increased in a number of areas of the cerebral cortex. SS content was also significantly increased in the lateral prefrontal cortex and anterior cingulate cortex. Both peptide levels were decreased in the striatum. These results suggest that the reduction found in these peptides' levels in the cerebral cortex of the brain from schizophrenic patients may not be the consequence of HPD treatment and that these peptides' levels might be increased in the cerebral cortex of the brain of schizophrenic patients following the treatment with HPD.

Animals↗