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Biomedical subjects

H Saito

Publications and source records attributed to H Saito.

At least 37 records · Page 2Linked to original sources
PubMed2005

Origin of the tunnel anisotropic magnetoresistance in Ga(1-x)Mn(x)As/ZnSe/Ga(1-x)Mn(x)As magnetic tunnel junctions of II-VI/III-V heterostructures.

We investigated spin-dependent transport in magnetic tunnel junctions made of III-V Ga(1-x)Mn(x)As electrodes and II-VI ZnSe tunnel barriers. The high tunnel magnetoresistance (TMR) ratio up to 100% we observed indicates high spin polarization at the barrier/electrodes interfaces. We found anisotropic tunneling conductance having a magnitude of 10% with respect to the direction of magnetization to linearly depend on the magnetic anisotropy energy of Ga(1-x)Mn(x)As. This proves that the spin-orbit interactions in the valence band of Ga(1-x)M(x)As are responsible for the tunnel anisotropic magnetoresistance (TAMR) effect.

Journal Article↗
PubMed2005

Detection of needle puncture to blood vessel using puncture force measurement.

Although blood sampling is frequently performed, a system to take blood samples automatically has not yet been developed. In the paper, as a first step towards automatic blood sampling, an examination of an automatic method for puncturing blood vessels is described. The force waveforms produced by puncturing rabbit ear veins were measured. A characteristic peak, possibly associated with the needle piercing the vessel wall, was observed in each waveform of ten successful cases of 14 trials. An algorithm that allowed the detection of this peak was developed, and parameters of a filter to improve the accuracy of the algorithm were determined. Using this algorithm, automatic needle punctures were performed in a rabbit ear vein and then were simulated using the data derived from manual needle puncture on four other rabbits. The results gave 30 fully successful cases of 33 trials of needle puncture and showed that measurement of the puncture force may be important for automatic needle puncture of blood vessels.

Animals↗
PubMed2005

Enzyme replacement therapy in Japanese Fabry disease patients: the results of a phase 2 bridging study.

Fabry Disease (alpha-galactosidase A deficiency) is an X-linked hereditary disorder leading to the pathological accumulation of globotriaosylceramide (GL-3) in lysosomes, particularly in the vascular endothelium of the kidney, heart and brain. We report the results of an open-label phase 2 study that was undertaken to evaluate whether ethnic differences exist that would affect agalsidase beta (Fabrazyme) treatment of Fabry patients in the Japanese population, relative to safety and efficacy. The study design mirrored the design of the completed phase 3 clinical trial that led to approval of the product agalsidase beta. The 13 Japanese, male Fabry patients enrolled in the study received the enzyme replacement therapy over a period of 20 weeks as biweekly infusions. All selected efficacy end points showed improvements that were comparable with findings from the phase 3 study. These improvements included reductions of GL-3 accumulation in both kidney and skin capillary endothelial cells to (near) normal levels (92% of patients). Kidney and plasma GL-3 levels decreased by 51.9% and 100%, respectively, by ELISA. Renal function remained normal. Fabry-associated pain, and quality of life, showed improvement over baseline in multiple categories. Related adverse events were mild or moderate in intensity and mostly infusion-associated (fever and rigors). As expected, IgG antibody formation was observed in 85% of the patients, but had no effect on treatment response. These results suggest that treatment with agalsidase beta is safe and effective in Japanese patients with Fabry disease. With regard to safety and efficacy, no differences were observed as compared to the caucasian population.

Adult↗
PubMed2005

Antigenicity of sulfanilamide and its metabolites using fluorescent-labelled compounds.

In order to clarify the onset mechanisms of drug-induced allergies, three fluorescent-labelled compounds were synthesized by subjecting sulfanilamide (SA), a base compound for sulfonamides, and its active metabolites, i.e. sulfanilamide hydroxylamine and sulfanilamide nitroso, to dansylation using dansylchloride. In other words, 5-dimethylamino-N-(4-aminobenzyl)-naphthalenesulfonamide (DNS-4ABA), 5-dimethylamino-N-(4-hydroxylaminobenzyl)-1-naphthalenesulfonamide (DNS-4HABA) and 5-dimethylamino-N-(4-nitrosobenzyl)-1-naphthalenesulfonamide (DNS-4NSBA) were synthesized as model haptens. When analysed by HPLC, a conjugate of DNS-4HABA and glutathione (GSH) with nucleophilic amino acids had two peaks (P-1 and P-2). FAB-MS and 1H-NMR revealed that the DNS-4HABA-GSH conjugate consisted of sulphinamide and semimercaptal. The reactivity of GSH to DNS-4ABA, DNS-4HABA and DNS-4NSBA was quantified by HPLC using an oxidization system (horseradish peroxidase/H2O2). The results show that production of DNS-4NSBA-GSH-conjugate was four to eight times higher than that of DNS-4HABA-GSH conjugate, but that DNS-4ABA did not bind with GSH. Skin reactions were assessed using guinea pigs, and strong delayed erythema was seen with DNS-4NSBA, which bound most strongly with GSH, whereas weak delayed erythema was seen with DNS-4ABA, which did not bind with GSH. This suggests a correlation between GSH conjugate production and skin reactions. DNS-4HABA enzymatically bound with proteins in rat and guinea pig liver cytosol and microsomal fractions. The proteins that bound to DNS-4HABA were purified by HPLC and then subjected to N-terminal amino acid analysis. Ubiquitin (10 kDa) and fatty acid binding protein (30 kDa) were detected in the rat liver cytosol fraction; retinol-dehydrogenase (35 kDa) in the rat microsomal fraction; and glutathione-S-transferase B (mmu) (25 kDa) in the guinea pig liver cytosol fraction. When DNS-4HABA or DNS-4NSBA binds to proteins that play important roles in the body, unexpected adverse reactions may occur. Furthermore, by utilizing our technique using model compounds, it may be possible to identify the carrier proteins of various compounds, including pharmaceutical agents.

Animals↗
PubMed2005

FFT analysis of the X-ray tube voltage waveforms of high-frequency generators for radiographic systems.

PURPOSE: To present a novel method for analyzing the voltage waveform from high-frequency X-ray generators for radiographic systems. MATERIAL AND METHODS: The output signal of the actual voltage across the tube of a high-frequency generator was measured using the built-in voltage sense taps that are used for voltage regulation feedback in X-ray generators. The output signal was stored in an analyzing recorder, and the waveforms were analyzed using FFT analysis. The FFT analysis of high-frequency generators consisted of obtaining the power spectrum, comparing the major frequency components in the tube voltage waveforms, and examining the intensity of each frequency component. RESULTS: FFT analysis enables an objective comparison of the complex tube voltage waveforms in high-frequency X-ray generators. FFT analysis detected the change in the X-ray tube voltage waveform that occurred when there were problems with the high-frequency generator. CONCLUSION: High-frequency X-ray generators are becoming the universal choice for radiographic systems. The X-ray tube voltage and its waveform are important features of an X-ray generator, and quality assurance (QA) is important, too. As a tool for engineers involved in the design and development of X-ray generators, we can see that our methods (FFT analysis) might have some value as a means of describing generator performance under varying conditions. Furthermore, since the X-ray tube voltage waveform of a high-frequency generator is complex, FFT analysis may be useful for QA of the waveform.

Algorithms↗
PubMed2005

Feasibility of rapid-sequence 31P magnetic resonance spectroscopy in cardiac patients.

PURPOSE: To determine the clinical feasibility of rapid-sequence phosphorus-31 magnetic resonance spectroscopy (31P-MRS) of the heart with cardiac patients using a 1.5T clinical MR system. MATERIAL AND METHODS: Twenty cardiac patients, i.e. dilated cardiomyopathy (DCM) 13 cases, hypertrophic cardiomyopathy (HCM) 3 cases, hypertensive heart diseases (HHD) 3 cases, and aortic regurgitation (AR) 1 case were examined using rapid cardiac 31P-MRS. Complete three-dimensional localization was performed using a two-dimensional phosphorus chemical-shift imaging sequence in combination with 30-mm axial slice-selective excitation. The rapid-sequence 31P-MRS procedure was phase encoded in arrays of 8 x 8 steps with an average of 4 acquisitions. The total examination time, including proton imaging and shimming, for the rapid cardiac 31P-MRS procedure, ranged from 10 to 15 min, depending on the heart rate. Student's t test was used to compare creatine phosphate (PCr)/adenosine triphosphate (ATP) ratios from the cardiac patients with those of the control subjects (n = 13). RESULTS: The myocardial PCr/ATP ratio obtained by rapid 31P-MRS was significantly lower (P < 0.001) in DCM patients (1.82 +/- 0.33, mean +/- SD), and in patients with global myocardial dysfunction (combined data for 20 patients: 1.89 +/- 0.32) than in normal volunteers (2.96 +/- 0.59). These results are similar to previous studies. CONCLUSION: Rapid-sequence 31P-MRS may be a valid diagnostic tool for patients with cardiac disease.

Adenosine Triphosphate↗
PubMed2005

Insulin sensitivity independently influences brachial-ankle pulse-wave velocity in non-diabetic subjects.

AIMS: Measurement of pulse-wave velocity (PWV) is a non-invasive technique for assessing arterial stiffness. Although insulin resistance is associated with intimal-medial thickness of the carotid artery evaluated by B-mode ultrasonography, it is not known whether it is related to PWV. The aim of this study was to determine the relationship between homeostasis model assessment insulin sensitivity index (HOMA-%S) and PWV in non-diabetic subjects. We also examined the effects of oral glucose tolerance test (OGTT) 2-h glucose and plasma high-sensitivity C-reactive protein (CRP) on PWV, as these two parameters are associated with atherosclerosis. METHODS: A 75-g oral glucose tolerance test was performed in 1934 Japanese subjects who were undergoing health examinations. Of these subjects, we recruited 1541 non-diabetic subjects without chronic or acute inflammation, malignant diseases, autoimmune disorders, elevated serum creatinine levels, and abnormal hepatic function tests. Subjects who had an abnormal ankle/brachial blood pressure index of less than 0.9 were also excluded. Brachial-ankle PWV and plasma high-sensitivity CRP were measured on 1541 subjects who satisfied the admission criteria. RESULTS: PWV was 12.55+/-1.61 (mean+/-sd) m/s and plasma CRP concentration was 0.4 mg/l (median, range, 0.1-5.8 mg/l) in the study subjects. By multivariate regression analysis, HOMA-%S was found to be an independent negative risk factor for PWV, while systolic blood pressure, age and triglycerides were positively associated with PWV. OGTT 2-h glucose was weakly and independently related to PWV in male subjects. Plasma CRP was not independently associated with PWV. CONCLUSIONS: Insulin resistance is independently associated with PWV in non-diabetic subjects.

Adult↗
PubMed2005

Carbon dioxide increases acid resistance in Escherichia coli.

AIMS: To investigate how carbon dioxide affects the acid resistance of Escherichia coli. METHODS AND RESULTS: Escherichia coli W3110 was grown in minimal EG medium at pH 7.5, and cells were adapted at pH 5.5 at 37 degrees C with and without supply of carbon dioxide and nitrogen gases. The number of colonies grown on LB medium was measured after cells were challenged in minimal EG medium of pH 2.5 at 37 degrees C under various conditions. When carbon dioxide was supplied at both the acid adaptation and challenge stages, 94% of cells survived after the acid challenge for 1 h, while the survival rates were 50 and 67% when nitrogen gas and glutamate were supplied respectively. After the acid challenge for 3 h, the survival rate observed with the carbon dioxide gas supply was again 2.5-fold higher than those with the nitrogen gas supply. CONCLUSION: Carbon dioxide was shown to participate in the maintenance of high viability under acidic conditions. SIGNIFICANCE AND IMPACT OF THE STUDY: This study provides useful information for research into bacterial pathogenesis, fermentation and food preservation.

Adaptation, Physiological↗
PubMed2005

Obesity enhances the induction of plasminogen activator inhibitor-1 by restraint stress: a possible mechanism of stress-induced renal fibrin deposition in obese mice.

BACKGROUND AND OBJECTIVES: Cardiovascular/thrombotic diseases are frequently induced by a variety of stressors. Obese patients are susceptible to thrombotic diseases associated with stress, but the underlying mechanism is still unknown. We have begun to investigate the expression of a primary inhibitor of fibrinolysis, plasminogen activator inhibitor-1 (PAI-1), in association with tissue thrombosis, using restraint-stressed obese mice. METHODS AND RESULTS: We analyzed the expression of PAI-1 after restraint (immobilization) stress in genetically obese mice in comparison with their lean counterparts. Dramatic increases in PAI-1 antigen in plasma and in tissue extracts were observed in the obese mice exposed to restraint stress. The induction of PAI-1 mRNA by stress in the tissues was also pronounced in the stressed obese mice as compared with the lean mice, especially in the hearts and adipose tissues. In situ hybridization analysis revealed that strong signals for PAI-1 mRNA were localized in the adipocytes, cardiovascular endothelial cells, and renal glomerular cells of the stressed obese mice. Histological examination revealed that renal glomerular fibrin deposition was detected only in the obese mice after 2 h of restraint stress. CONCLUSIONS: Obesity enhances the stress-mediated PAI-1 induction in the blood and tissues. This phenomenon may be associated with the increased risk of stress-induced renal fibrin deposition in obese subjects.

Adipocytes↗
PubMed2005

Roles of virD4 and cagG genes in the cag pathogenicity island of Helicobacter pylori using a Mongolian gerbil model.

BACKGROUND AND AIMS: The roles of the virD4 and the cagG genes in the cag pathogenicity island of Helicobacter pylori for gastroduodenal pathogenesis are unclear and their roles in vivo have not been examined. METHODS: Seven week old male Mongolian gerbils were inoculated with the wild type H pylori TN2GF4, its isogenic virD4, or cagG mutants. Animals were sacrificed at 4, 12, and 24 weeks after inoculation. Gastric inflammation and H pylori density were evaluated by histology, inflammatory response (as measured by interleukin (IL)-1beta mRNA levels), proliferative activity (as assessed by 5'-bromo-2'deoxyuridine labelling indices), and host systemic reaction (as measured by anti-H pylori IgG antibody). RESULTS: Degree of gastric inflammation, proliferative activity, and mucosal IL-1beta mRNA levels remained low throughout the first 12 weeks in gerbils infected with the virD4 mutants. Degree of gastric inflammation and proliferative activity increased at 24 weeks with the virD4 mutants reaching levels comparative with those seen at four weeks with the wild-type strains. Mucosal IL-1beta mRNA levels were also increased at 24 weeks with the virD4 mutants and levels at 24 weeks were similar between the wild-type and virD4 mutants. In contrast, gerbils infected with the cagG mutants had reduced ability to colonise gerbils, and no or little gastric inflammation or proliferative activity was observed. CONCLUSIONS: Loss of the virD4 gene temporally retarded but did not abrogate gastric inflammation. Loss of the cagG gene abolished gastric inflammation partially via reduced ability to colonise gerbils. Unknown factors related to the type IV secretion system other than CagA may influence gastric inflammation.

Animals↗
PubMed2005

[Surgical treatment for postinfarction ventricular septal perforation].

Between November 1985 and April 2003, surgical treatment for ventricular septal perforation (VSP) after acute myocardial infarction was performed in 16 patients. Patients were divided into 2 groups by method of operation. One group is infarct exclusion technique (n = 10). The other group is trans right ventricular (RV) approach (n = 6). No significant differences were observed between 2 groups in preoperative states. Operative death rate was high in both groups. Five patients (50%) were died in infarct exclusion group, 4 patients (67%) in trans RV group. Infarct exclusion technique needed longer extracorporeal circulation time (201 +/- 33 min) than trans RV approach (170 +/- 32 min). Although trans RV approach is attractive for its simplicity, 3 cases died of rupture of remained left ventricle infarction area. On the other hand, there were no mortality cases caused by left ventricle rupture in infarct exclusion technique group. As this result, we select infarct exclusion technique as a surgical correction for VSP.

Aged↗
PubMed2005

[Successful repair of supravalvular aortic stenosis using Steinberg 3 sinuses reconstruction; report of a case].

Steinberg method is a modification of Doty extended aortoplasty for supravalvular aortic stenosis (SAS). This modification entails placement of an additional patch in the left coronary sinus. A 3-year-old boy was diagnosed as SAS with aortic valvular stenosis. He was noticed a systolic murmur from 1 month after his birth. Echocardiography showed left ventricular hypertrophy, and pressure gradient of 80 mmHg was measured between the ascending aorta and the left ventricle. Cardiac catheterization revealed severe aortic stenosis at the sino-tubular (ST) junction. We adopted Steinberg 3 sinuses reconstruction. After this operation, there was no pressure gradient at ST junction although aortic valvular stenosis remained and mild aortic valve regurgitation newly developed. As this method can produce a symmetric aortic root, it may reduce aortic valve deformity especially on the left coronary cusp.

Aorta↗
PubMed2005

[Surgical treatment for the patient with atrial septal defect and Andersen syndrome].

An 18-year-old girl with atrial septal defect and Andersen syndrome is reported. Andersen syndrome was described as a hereditary disease characterized by periodic paralysis, prolongation of the QT interval with ventricular arrhythmia and characteristic physical features including low set ear and micrognathia. We successfully performed cardiac operation for this rare associated malformation.

Adolescent↗
PubMed2004

Randomised phase II study of docetaxel/cisplatin vs docetaxel/irinotecan in advanced non-small-cell lung cancer: a West Japan Thoracic Oncology Group Study (WJTOG9803).

Docetaxel plus cisplatin and docetaxel plus irinotecan are active and well-tolerated chemotherapy regimens for advanced non-small-cell lung cancer (NSCLC). A randomised phase II study compared their efficacy and toxicity in 108 patients with stage IIIb/IV NSCLC, who were randomised to receive docetaxel 60 mg m(-2) and cisplatin 80 mg m(-2) on day 1 (DC; n=51), or docetaxel 60 mg m(-2) on day 8 and irinotecan 60 mg m(-2) on day 1 and 8 (DI; n=57) every 3 weeks. Response rates were 37% for DC and 32% for DI patients. Median survival times and 1- and 2-year survival rates were 50 weeks (95% confidence interval: 34-78 weeks), 47 and 25% for DC, and 46 weeks (95% confidence interval: 37-54 weeks), 40 and 18% for DI, respectively. The progression-free survival time was 20 weeks (95% confidence interval: 14-25 weeks) with DC and 18 (95% confidence interval: 12-22 weeks) with DI. Significantly more DI than DC patients had grade 4 leucopenia and neutropenia (P<0.01); more DC patients had grade >/=2 thrombocytopenia (P<0.01). Nausea and vomiting was more pronounced with DC (P<0.01); diarrhoea was more common with DI (P=0.01). Three treatment-related deaths occurred in DC patients. In conclusion, although the DI and DC regimens had different toxicity profiles, there was no significant difference in survival.

Adult↗
PubMed2004

The deficiency of immunoregulatory receptor PD-1 causes mild osteopetrosis.

Recently, the involvement of immune responses in metabolic bone disease and/or local bone destruction has received much attention. Cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), a member of the immunoglobulin (Ig) superfamily, negatively regulates T cell activation. The deficiency of CTLA-4 induces profound osteopenia with an increase in osteoclastogenesis, suggesting the important role of activated T cells in osteoclastogenesis. Programmed death-1 (PD-1) is the newly identified immunoregulatory receptor, which also belongs to the Ig superfamily. Both CTLA-4 and PD-1 are induced on activated T cells, however, there are no reports linking PD-1 with osteoclasts. In the present study, we have examined the bone phenotype in PD-1-deficient mice PD-1-/- and the role of PD-1 in osteoclastogenesis and osteoclast function. Both trabecular and cortical bone mineral densities of tibia were significantly increased, as observed in peripheral quantitative computed tomography (pQCT), at 12 weeks of age in PD-1-/- mice. Histomorphometric analysis of the PD-1-/- mice and the age-matched controls at 12 weeks of age showed a 2-fold increase in bone volume (BV/TV) with a 55% decrease in osteoclast number (N.Oc/BS). Bone formation indices were similar in both groups. The number of soluble receptor activator of nuclear factor kappaB ligand (sRANKL)-induced osteoclast-like cells (OCLs) derived from the PD-1-deficient splenocytes was significantly decreased (by 25%). On the other hand, PD-1 deficiency did not affect the bone-resorbing activity of mature osteoclasts. Our results suggest that PD-1 deficiency reduces osteoclastogenesis resulting in an osteopetrotic phenotype. Identical members of the Ig superfamily, CTLA-4 and PD-1, which negatively regulate immune responses, may differentially affect osteoclastogenesis and bone remodeling.

Animals↗
PubMed2004

Malignant transformation of endometriosis and genetic alterations of K-ras and microsatellite instability.

OBJECTIVES: To clarify the role of specific genetic alterations in the multi-step process of malignant transformation of endometriosis. METHODS: In cases of ovarian endometrioid carcinoma, we separated regions of normal endometriosis, atypical endometriosis and ovarian endometrioid carcinoma by laser microdissection, and examined K-ras mutation and microsatellite instability in each separated tissue sample. RESULTS: We detected K-ras mutation and microsatellite instability in endometrioid carcinoma tissue, but not in normal or atypical endometriosis bordering the cancerous region. CONCLUSIONS: The present findings suggest that K-ras mutation and microsatellite instability are associated with malignant transformation from atypical endometriosis to ovarian endometrioid carcinoma.

Adult↗