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Biomedical subjects

Y Sato

Publications and source records attributed to Y Sato.

At least 163 records · Page 9Linked to original sources

Deficiency of a cytosolic ascorbate peroxidase associated with chilling tolerance in soybean.

We investigated the isozyme profiles of antioxidant enzymes in cultivars and lines with different seed productivity in cool climate conditions as a step towards understanding the physiological and genetical mechanisms underlying chilling tolerance in soybean. While no difference in superoxide dismutase, or catalase isozyme profiles was observed among the cultivars and lines tested, we found polymorphism in the ascorbate peroxidase isozyme profile; there were two types, with or without a cytosolic isoform (APX1). The cultivars and lines lacking APX1 proved more tolerant to chilling temperatures, as evaluated by yielding ability. The genotype-dependent deficiency of APX1 was consistent in plants and tissues under various oxidative stress conditions including the exposure to low-temperatures. In addition, the genetic analysis of progeny derived from crossing between cultivars differing in the isozyme profile indicated that the APX1 deficiency is controlled by a single recessive gene (apx1), and is inherited independently of the genes that have previously been identified for their association with chilling tolerance. Molecular and linkage analyses suggested that the variant gene of the APX1-absent genotype coding for a cytosolic APX, which contained a single nucleotide substitution and a single nucleotide deletion in the coding region, is responsible for the genotype-dependent deficiency of APX1. The association of APX1 deficiency with chilling tolerance is discussed in detail.

Amino Acid Sequence↗

Detection of peptide-specific CTL-precursors in peripheral blood lymphocytes of cancer patients.

Development of therapeutic vaccines is one of the major areas of tumour immunotherapy today. However, clinical trials of peptide-based cancer vaccines have rarely resulted in tumour regression. This failure might be due to an insufficient induction of cytotoxic T lymphocytes in the current regimes, in which cytotoxic T lymphocytes-precursors in pre-vaccination peripheral blood mononuclear cells are not measured. Initiation of immune-boosting through vaccination could be better than that of immune-priming with regard to induction of prompt and strong immunity. If this is also the case for therapeutic vaccines, pre-vaccination measurement of peptide-specific cytotoxic T lymphocytes-precursors will be important. In the present study, we investigated whether cytotoxic T lymphocytes-precursors reacting to 28 kinds of peptides of vaccine candidates (13 and 15 peptides for HLA-A24(+) and HLA-A2(+) patients, respectively) were detectable in pre-vaccination peripheral blood mononuclear cells of 80 cancer patients. Peptide-specific cytotoxic T lymphocytes-precursors were found to be detectable in peripheral blood mononuclear cells of the majority of cancer patients (57 out of 80 cases, 71%). The mean numbers of positive peptides were 2.0 peptides per positive case. Peripheral blood mononuclear cells incubated with positive peptides, not with negative peptides, showed significant levels of HLA-class-I-restricted cytotoxicity to cancer cells. The profiles of positive peptides entirely varied among patients, and were not influenced by the cancer origin. These results may provide a scientific basis for the development of a new approach to cancer immunotherapy, e.g.) cytotoxic T lymphocytes-precursor-oriented peptide vaccine.

Antigens, Neoplasm↗

Sigma-nucleus potential in A=28.

We have studied the (pi(-),K+) reaction on a silicon target to investigate the sigma-nucleus potential. The inclusive spectrum was measured at a beam momentum of 1.2 GeV/c with an energy resolution of 3.3 MeV (FWHM) by employing the superconducting kaon spectrometer system. The spectrum was compared with theoretical calculations within the framework of the distorted-wave impulse approximation, which demonstrates that a strongly repulsive sigma-nucleus potential with a nonzero size of the imaginary part reproduces the observed spectrum.

Journal Article↗

Symmetry-dependent multielectron excitations near the C 1s ionization threshold and distortion of the shape resonance in CO(2).

Satellite bands accompanying the C 1s photoline for the CO2 molecule parallel to the electric vector of the incident radiation E are found to be more intense than those for CO2 perpendicular to E in the shape resonance region. This indicates that multielectron excitations are caused in part by the interaction of the outgoing C 1s photoelectron with the valence electrons. The photoelectron-impact valence excitations couple with the C 1s single-hole ionization and distort the shape resonance significantly. We assign the broad resonance at approximately 312 eV to a distorted Sigma(u) shape resonance.

Journal Article↗

A case of true malignant histiocytosis: identification of histiocytic origin with use of immunohistochemical and immunocytogenetic methods.

We report here an autopsy case of true malignant histiocytosis. The patient was a 67-year-old woman who exhibited fever, wasting, hepatosplenomegaly, and progressive pancytopenia. The bone marrow aspiration disclosed hemophagocytosing cells, which resembled histiocytes. The molecular analysis did not show the clonal gene rearrangement of T-cell receptor or immunoglobulin heavy chain. Although the patient had been started on methylprednisolone pulse therapy and chemotherapy with etoposide, she died from cerebral hemorrhage. The autopsy specimens of spleen and liver showed extensive infiltration of atypical cells, for which histiocytic origin was identified with an immunohistochemical method using monoclonal antibodies against CD11c, CD68, macrophage colony-stimulating factor (M-CSF), M-CSF receptor, lysozyme, antitrypsin and alpha1-antichymotrypsin. Recent investigations have disclosed that in most cases diagnosed as malignant histiocytosis, hemophagocytosis was reactive and not evoked by histiocytic malignancy. True malignant histiocytosis, for which histiocytic origin is confirmed, is extremely rare.

Aged↗

Proton energy spectra in the nonmesonic weak decay of 12lambdaC and 28lambdaSi hypernuclei.

Numbers of protons per Gamma hypernuclear weak decay were measured as a function of proton energy above 40 MeV, explicitly identifying production of Gamma hypernuclei by the (pi+,K+) reaction. The ratios between the neutron-stimulated to proton-stimulated nonmesonic decay widths, Gamma((Lambda)n-->nn)/Gamma((Lambda)p-->np) ( = Gamma(n)/Gamma(p)) were extracted by fitting the proton energy spectra. The present result claims that the proton yields are suppressed and the Gamma(n)/Gamma(p) ratios are close to 1 both for 12LambdaC and 28LambdaSi in contradiction to theoretical expectations based on meson exchange models.

Journal Article↗

Selective nitration of mitochondrial complex I by peroxynitrite: involvement in mitochondria dysfunction and cell death of dopaminergic SH-SY5Y cells.

3-Nitrotyrosine (3-NT) is a specific marker of protein nitration by peroxynitrite (ONOO-) produced from nitric oxide and superoxide. Increase in 3-NT containing protein (3-NT protein) was reported in brains from patients with some neurodegenerative disorders and aging. In this paper, intracellular localization of 3-NT protein was examined in dopaminergic SH-SY5Y cells using the selective antibody against protein-bound 3-NT. 3-NT protein was detected in plasma membrane/nucleus and mitochondria fractions, and interestingly in polypeptide composition of mitochondrial complex I. ONOO--generating SIN-1 induced apoptotic cell death with concomitant increase in 3-NT protein and reduction in mitochondrial ATP synthesis. In addition, an inhibitor of proteasomes, carbobenzoxy-L-isoleucyl-gamma-t-butyl-L-glutamyl-L-alanyl-L-leucinal, enhanced the effects of ONOO-. These results suggest that ONOO- may induce mitochondrial dysfunction and cell death in neurons through nitration of mitochondrial complex I subunits.

Adenosine Triphosphate↗

Effects of mechanical properties of adhesive resins on bond strength to dentin.

OBJECTIVES: The purpose of this study was to evaluate the relationship between the micro-tensile bond strength to dentin and mechanical properties of the cured adhesive resins. METHODS: Coronal dentin surfaces of extracted human teeth were treated with four commercial self-etching priming systems (Clearfil SE Bond; UniFil Bond; Tokuso Mac-Bond II; and Imperva Fluoro Bond) and bonded with a resin composite. After 24h storage in water at 37 degrees C, the bonded specimens were trimmed and subjected to micro-tensile bond strength testing at a cross-head speed of 1mm/min. Debonded surfaces were observed under a FE-SEM. For testing mechanical properties, 0.7-mm thick slabs of each adhesive resin were prepared, light-cured, and stored dry at the room temperature for 24h. After trimming, ultimate micro-tensile strength was measured. The nano-hardness and Young's modulus were also evaluated using cured adhesives that were prepared in the same manner as described above. RESULTS: The micro-tensile bond strengths to dentin and ultimate micro-tensile strengths of the resins were not significantly different among all systems (P>0.05). However, the nano-hardness and Young's modulus of Clearfil SE Bond and Imperva Fluoro Bond adhesive resins were significantly higher than those of UniFil Bond and Tokuso Mac-Bond II resins (P<0.05). The micro-tensile bond strength significantly correlated with the ultimate micro-tensile strength of the resins (r(2)=0.77; P<0.05), but was not correlated with the nano-hardness or Young's modulus (P>0.05). SEM observation of the debonded surfaces revealed a mixed type of fracture with a combination of interfacial and cohesive failure within the adhesive resin. SIGNIFICANCE: The four self-etching priming systems exhibited similar dentin bond strengths, which also correlates with the ultimate strength of the adhesive resins.

Acid Etching, Dental↗

Effect of gender differences and voluntary exercise on antioxidant capacity in rats.

The effects of gender difference and voluntary exercise on antioxidant capacity in rats were evaluated. The subjects were divided into two groups, physically active and sedentary. In the sedentary group, the level of hydroxyl radical in the liver was higher (P<0.001) in male rats than in female rats, however, in the physically active group, the level in male rats was lower (P<0.05) than in female rats. The levels of reduced glutathione (GSH) in physically active males and females were higher compared to those in the sedentary group. The physically active group also showed an increase in antioxidant enzymes, such as glutathione peroxidase (GPx), glutathione reductase (GR) and superoxide dismutase activities. The level of liver GSH was higher in physically active females than in physically active males. For both groups, GPx and GR activities in females were significantly higher than in males. These results indicate that female rats have an intrinsically higher antioxidant capacity, which resulted in increased levels of GSH via the glutathione redox cycle and gamma-glutamyl cycle enzymes. The adaptation to altered antioxidant capacity, induced by physical activity, appeared to be affected by gender differences.

Animals↗

RETRACTED: Changes in the supporting muscles of the fractured hip in elderly women.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief. The Journal has been made aware of concerns regarding the ethical approval for this study, and the study protocol and data were disputed. Since Dr Sato passed away, the co-authors were contacted about the complaint. Dr Izumi Kondo confirmed that the T score for sufficient 25OHD group in Table 2 was out of range and this was overlooked at the time of writing. He was unable to confirm whether the proper ethical approval was obtained or comment on the study protocol as his role was to advise on the statistical methodology of the revised paper. The other two co-authors did not respond, and one could not be located. This constitutes a violation of our publishing policies and publishing ethics standards.

Adenosine Triphosphatases↗

Amelioration of osteoporosis by menatetrenone in elderly female Parkinson's disease patients with vitamin D deficiency.

Significant reduction in bone mineral density (BMD) occurs in patients with Parkinson's disease (PD), correlating with immobilization and with vitamin D deficiency, and increasing the risk of hip fracture, especially in elderly women. As a biological indicator of compromised vitamin K status, an increased serum concentration of undercarboxylated osteocalcin (Oc) has been associated with reduced BMD in the hip and an increased risk of fracture in otherwise healthy elderly women. We evaluated treatment with vitamin K(2) (menatetrenone; MK-4) in maintaining BMD and reducing the incidence of nonvertebral fractures in elderly female patients with PD. In a random and prospective study of PD patients, 60 received 45 mg of MK-4 daily for 12 months, and the remaining 60 (untreated group) did not. At baseline, patients of both groups showed vitamin D and K(1) deficiencies, high serum levels of ionized calcium, and glutaminic residue (Glu) Oc, and low levels of parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1,25-(OH)(2)D], indicating that immobilization-induced hypercalcemia inhibits renal synthesis of 1,25-(OH)(2)D and compensatory PTH secretion. BMD in the second metacarpals increased by 0.9% in the treated group and decreased by 4.3% in the untreated group (p < 0.0001). Vitamin K(2) level increased by 259.8% in the treated group. Correspondingly, significant decreases in Glu Oc and calcium were observed in the treated group, in association with an increase in both PTH and 1,25-(OH)(2)D. Ten patients sustained fractures (eight at the hip and two at other sites) in the untreated group, and one hip fracture occurred among treated patients (p = 0.0082; odds ratio = 11.5). The treatment with MK-4 can increase the BMD of vitamin D- and K-deficient bone by increasing vitamin K concentration, and it can also decrease calcium levels through inhibition of bone resorption, resulting in an increase in 1,25-(OH)(2)D concentration.

Aged↗

Phylogenetic analysis of field isolates of feline calcivirus (FCV) in Japan by sequencing part of its capsid gene.

The molecular epidemiology of the infectious disease caused by feline calcivirus (FCV) in Japan was investigated by analysing the phylogenetic relationship among 21 Japanese field isolates, including the F4 strain, and 30 global isolates. Parts of the capsid gene (B-F) of the isolates were amplified by RT-PCR, and the amino acid sequences were compared with those from the global isolates. Thirty-seven and 14 out of a total of 51 isolates were clustered into two distinct genogroups, I and II respectively, by UPGMA and NJ analysis. Seven of the 21 Japanese isolates (33%) fell into group I together with 30 global isolates, while the other 14 Japanese isolates (67%) belonged to group II. The bootstrap repetition analysis of groups I and II formed by the NJ method gave a value of 99.00%. The 14 latter Japanese isolates were clearly separated from the isolates in group I, and they were different from any previously known FCV, forming a new genogroup, which implies that this lineage has been confined to Japan. Comparing the amino acid sequences shared by groups I and II, the amino acid at position 377 in B region was asparagine (Asn or Asp (NH2)) in group I, while it was lysine (Lys) in all the strains in group II. Similarly, the amino acid at position 539 in the F region was alanine (Ala) or proline (Pro) in group I, while it was valine (Val) in group II; glycine (Gly) at position 557 in group I was serine (Ser) in Group II; and phenylalanine (Phe) or leucine (Leu) at position 566 in genogroup I was tyrosine (Tyr) in group II.

Amino Acid Sequence↗

Streptococcus mutans binding to solid phase dextran mediated by the glucan-binding protein C.

Streptococcus mutans GbpC is a wall-anchored surface protein which is involved in dextran-dependent aggregation. The GbpC phenotype is observed only in cells grown under stress conditions. In order to detect the GbpC protein of S. mutans, we isolated the wall fraction following digestion of the cell wall of this organism by N-acetylmuramidase, and detected the GbpC protein from S. mutans cells by western analysis with anti-GbpC serum. Interestingly, S. mutans cells exhibiting the negative dextran(alpha-1,6 glucan)-dependent aggregation (ddag) phenotype expressed the protein and could bind to immobilized dextran.

Bacterial Adhesion↗

gbpC and pac gene mutations detected in Streptococcus mutans strain GS-5.

The Streptococcus mutans gbpC gene encoding cell wall-anchoring glucan-binding protein C is involved in the dextran(alpha-1,6 glucan)-dependent aggregation (ddag) of this organism. Unlike cells of other strains of S. mutans, strain GS-5 cells did not exhibit dextran(alpha-1,6 glucan)-dependent aggregation under any conditions. We therefore hypothesized that the gbpC gene may be mutated in strain GS-5. Sequencing analysis of the 1752-nucleotide GS-5 gbpC gene revealed a point mutation that switched codon 65 to a TAA termination codon. Strain GS-5 was previously reported also to have a mutation in the pac gene encoding the cell wall-anchored major protein antigen. The laboratory-maintained strain GS-5 is regarded as having lower cariogenicity than the original isolate. The decreased cariogenicity developed during the laboratory culture of strain GS-5 may have been caused by mutations in an environment lacking appropriate selective pressures.

Antigens, Bacterial↗

Phenotypes and mitochondrial DNA substitutions in families with A3243G mutation.

OBJECTIVE: To clarify the relationship between mitochondrial DNA (mtDNA) sequence variations and phenotypes in patients with A3243G mutation. MATERIALS AND METHODS: We studied whole mtDNA sequences in two families with A3243G mutation and characteristic clinical features. Two brothers in Family 1 had shown thiamine deficiency and mitochondrial myopathy without central nervous system involvement. In Family 2, a 16-year-old woman showed the symptoms of mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). Her mother had had diabetes mellitus and died at the age of 42. The proportion of A3243G mtDNA in blood was 87 and 89% in the patients of Family 1, and 25% in the patient and less than 5% in the mother of Family 2. RESULTS: The mtDNA analysis revealed the following homoplasmic substitutions: T1520C and C12153T found only in Family 1, and A15954G found only in Family 2. These substitutions were not detected in seven other MELAS patients or in 50 controls. CONCLUSION: These substitutions might be specific to these families and could be one of the factors that modulate their clinical features together with the A3243G mutation.

Adolescent↗

Reduced efficacy of treatment of strongyloidiasis in HTLV-I carriers related to enhanced expression of IFN-gamma and TGF-beta1.

Strongyloidiasis, a human intestinal infection caused by Strongyloides stercoralis (S. stercoralis), is difficult to cure with drugs. In particular, a decrease of the efficacy of treatment has been reported in patients dually infected with S. stercoralis and human T-cell leukaemia virus type I (HTLV-I), both of which are endemic in Okinawa, Japan. However, the factors influencing this resistance remain unclear. In the present study, patients infected with S. stercoralis, with or without HTLV-I infection, were treated with albendazole, followed up for one year and separated into two groups, cured and non-cured. The cure rate of S. stercoralis was lower in HTLV-I carriers (P < 0.05). Serum levels of S. stercoralis-specific IgA, IgE, IgG, IgG1 and IgG4 antibodies were estimated, and a decrease of IgE (P < 0.05) and an increase of IgG4 (P < 0.05) were observed in the non-cured group, especially in HTLV-I carriers. RT-PCR of cytokines using peripheral blood mononuclear cells revealed that S. stercoralis patients with HTLV-I showed a high frequency of expression of IFN-gamma and TGF-beta1, whereas those without HTLV-I showed no expression of these cytokines. IFN-gamma- and TGF-beta1-positive HTLV-I carriers showed a decrease of IgE (P < 0.05), an increase of IgG4 (P < 0.01) and a lower cure rate (P < 0.01) compared with those who were negative for both cytokines. These results suggest that persistent infection with HTLV-I affected S. stercoralis-specific immunity and reduced therapeutic efficacy.

Aged↗

Diminution of early insulin response to glucose in subjects with normal but minimally elevated fasting plasma glucose. Evidence for early beta-cell dysfunction.

AIM: Systematic analysis of beta-cell function in Japanese health examinees. METHODS: In 938 Japanese health examinees (627 men and 311 women, mean age and body mass index, 54.0 years and 23.6 kg/m2, respectively), plasma specific insulin was measured at fasting and during a 75-g oral glucose tolerance test. The subjects were stratified into six groups based on fasting plasma glucose < or = 5.1 mmol/l, 5.2-6.0 mmol/l, 6.1-6.9 mmol/l, 7.0-7.8 mmol/l, 7.9-8.7 mmol/l, and > or = 8.8 mmol/l as the 1st, 2nd, 3rd, 4th, 5th and 6th groups, respectively. RESULTS: Distribution of fasting insulin showed a very modest 'inverted U' shape, with the peak in the 5th group. Progressive increase from the 1st toward the 5th group was significant. In contrast, the ratio of change in insulin to change in glucose from 0 to 30 min during the glucose tolerance test was greatest in the 1st group and progressively declined in the groups with higher fasting glycaemia. Difference in the ratio was most striking and highly significant between the 1st and 2nd groups. Distribution of the insulin to glucose ratio of subjects with normal glucose tolerance significantly overlapped with that of untreated patients with diabetes. CONCLUSIONS: In a Japanese population, (i) beta-cell starts to deteriorate during normoglycaemia with a minimal elevation of fasting plasma glucose, and (ii) there are glucose-tolerant subjects with beta-cell dysfunction.

Adolescent↗