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H Sato

Publications and source records attributed to H Sato.

At least 217 records · Page 12Linked to original sources
PubMed2001

Conformation and recognition control of peptide ribonucleic acid containing pyrimidine/purine mixed sequence.

Peptide ribonucleic acids (PRNA), tethering 5'-amino-5'-deoxyribonucleoside as a recognition moiety for RNA/DNA, have been designed and synthesized, as a novel nucleic acid model. External switching of the recognition behavior of PRNA containing not only pyrimidine nucleobase but also purine nucleobase, with complementary oligomeric DNA/RNA has been demonstrated for the first time through both the orientational switching of the nucleobase of PRNA and electrostatic repulsion between borate ester anion of PRNA and phosphodiester anion of DNA/RNA, induced by added borates.

Base Sequence↗
PubMed2001

Epidermal growth factor enhances lipopolysaccharide-induced procoagulant activity on the cell surface of endothelial cells.

Endotoxin [lipopolysaccharide (LPS)] and some cytokines are known to induce tissue factors with the expression of procoagulant activity (PCA) on the cell surface of endothelial cells. We established a modified quantitative procedure for PCA expressed on the cell surface, and studied the effects of serum and epidermal growth factor (EGF) on the LPS-induced activation of PCA on cultured human umbilical vein endothelial cells. Meanwhile, human umbilical cord serum elevated PCA more than either fetal bovine serum (FBS) or human adult serum. Generally, the existence of LPS raises the concentration of EGF in the blood, since monocytes and other types of cells express EGF and release it into the vessel by LPS stimulation. Although 10 ng/ml EGF did not induce PCA even in the presence of 10% FBS, it enhanced LPS-induced PCA under the same conditions. In the presence of 10% FBS, PCA induced both by LPS alone and by LPS + EGF was reduced the same amount by the protein kinase C (PKC) inhibitors H7 and H8. These results suggest that the serum contains some cofactor other than EGF, and that EGF enhanced this LPS-induced PCA independent of the cofactor through PKC-involved signaling.

Blood Coagulation↗
PubMed2001

Effects of gadolinium on the retention and translocation of 239Pu-hydroxide.

The effect of gadolinium on the lung retention, excretion, and translocation of plutonium was studied in rats instilled intratracheally with plutonium hydroxide with and without gadolinium. Three types of plutonium hydroxide were prepared: pure 239Pu-hydroxide colloid, that containing a high concentration of gadolinium, and that containing a low concentration of gadolinium. The lung retention of 239Pu was higher and the fecal excretion was lower in the rats administered 239Pu-hydroxide containing a high concentration of gadolinium than those administered pure 239Pu-hydroxide colloid. The translocation of 239Pu from lung to other organs including the liver, spleen, femur, and kidney was not affected by gadolinium. The cytological examination of bronchoalveolar lavage cells showed that the administration of 239Pu-hydroxide containing a high concentration of gadolinium induced the inflammatory reactions in the lung. The delayed alveolar clearance of plutonium in the rats administered 239Pu-hydroxide colloid containing a high concentration of gadolinium may be attributable to the change in physicochemical characteristics of colloid and the inflammation induced in the lung by gadolinium.

Animals↗
PubMed2001

Guanabenz, an antihypertensive centrally acting alpha2-agonist, suppresses morning elevations in aggregation of human platelets.

To determine whether the antihypertensive agent guanabenz affects the circadian rhythm in the hemorheologic properties of the platelet, we evaluated the aggregability of platelets collected from 11 healthy subjects in the morning and the evening after the oral administration of this agent, daily for 2 weeks. We analyzed platelet aggregation by the turbidimetric method. In an in vitro study, guanabenz, 10 nM-100 microM, did not affect platelet aggregation, whereas epinephrine induced platelet aggregation at an EC50 of 1.5 microM. The healthy volunteers demonstrated a diurnal variation in platelet aggregability that was high in the morning and low in the evening (66 +/- 10% and 56 +/- 11% respectively, of the percent platelet aggregation induced by epinephrine). The same variation was seen with the platelet aggregation induced by adenosine diphosphate (ADP) (62 +/- 8% [morning] vs. 51 +/- 7% [evening]). After the administration of guanabenz, platelet aggregability was significantly reduced in the morning compared with that before drug administration, when platelet aggregation was induced by epinephrine (49 +/- 9%, p < 0.05) or ADP (48 +/- 7%, p < 0.05), although the plasma levels of catecholamine were unchanged. A suppressive effect of guanabenz on platelet aggregability was observed in the evening, as the platelets were stimulated by epinephrine (38 +/- 9%, p < 0.05), but not by ADP (49 +/- 5%). Findings suggest that guanabenz mainly suppressed the morning enhancement in platelet aggregability, which contributes to the formation of intravascular thrombi. Thus, in addition to its antihypertensive actions, guanabenz may help to reduce the risk of vascular accidents, which frequently occur in the morning.

Adenosine Diphosphate↗
PubMed2001

Clinical significance of urinary interleukin-6 in children with reflux nephropathy.

PURPOSE: We determined urinary interleukin-6 (IL-6) in children with reflux nephropathy to evaluate the clinical significance of this cytokine in the progression of renal injury. MATERIALS AND METHODS: Enrolled in this study were 34 boys and 32 girls in whom 99mtechnetium dimercapto-succinic acid renal scan showed renal scarring. Vesicoureteral reflux had been corrected surgically at least 3 years before study entry. Urinary IL-6 was determined by enzyme-linked immunosorbent assay using spot urine samples. Simultaneously we measured serum creatinine, beta2-microglobulin, alpha1-microglobulin, urinary alpha1-microglobulin and albumin. In addition, IL-6 expression was assessed by immunohistochemical study in the scarred kidneys of 3 boys and 1 girl who underwent nephrectomy due to severe reflux nephropathy with little function on renal scan. RESULTS: Urinary IL-6 was significantly higher in children with severe bilateral renal scarring than in those with mild scarring and normal controls. Urinary IL-6 correlated significantly with serum alpha1-microglobulin (Spearman test p <0. 03), beta2-microglobulin (p <0.003), creatinine (p <0.02) and urinary albumin (p <0.0001). Histological evaluation revealed that IL-6 was predominantly expressed in the tubules in and adjacent to fibrotic areas. CONCLUSIONS: Our observations indicate that tubular IL-6 may be involved in the pathogenesis of tubulointerstitial injury in reflux nephropathy and urinary IL-6 may be a useful tool for monitoring the progression of reflux nephropathy.

Adolescent↗
PubMed2001

Implications of excessive fibrinolysis and alpha(2)-plasmin inhibitor deficiency in patients with severe head injury.

OBJECTIVE: To evaluate the involvement of the fibrinolytic system, especially focused on alpha(2)-plasmin inhibitor, in patients with head injury. METHODS: This study consisted of 47 patients with isolated blunt head trauma in whom blood sampling could be initiated within 3 hours after injury. Patients were divided into two groups according to Glasgow Outcome Scale score status at 3 months after injury. In Group 1 patients (n = 26), the outcome was characterized as good recovery or moderate disability; in Group 2 patients (n = 21), the outcome was characterized as severe disability, vegetative state, or death. RESULTS: Concentrations of thrombin-antithrombin III complex were greater than 100 microg/L in 39 of 47 patients, and concentrations in Group 2 patients were elevated significantly beyond the concentrations in Group 1 patients. Activities of alpha(2)-plasmin inhibitor in Group 2 were significantly lower than in Group 1 (P < 0.0001). In Group 1 patients, alpha(2)-plasmin inhibitor activity was greater than 60%, while in all but four Group 2 patients, the inhibitor was reduced to less than 60% of normal activity within 3 hours of injury. All patients with alpha(2)-plasmin inhibitor activity less than 60% showed a marked bleeding tendency and/or severe brain edema. Using sandwich enzyme-linked immunosorbent assay, fibrinogen degradation product and fibrin degradation product were measured separately. A significant correlation was apparent between thrombin-antithrombin III complex and fibrinogen degradation product, as well as between the complex and fibrin degradation product. Marked decreases in alpha(2)-plasmin inhibitor were noted only in patients with thrombin-antithrombin III complex concentrations exceeding 500 microg/L. CONCLUSION: Fibrinolysis and fibrinogenolysis may be involved according to the degree of coagulation activation in the pathophysiology of severe head injury. Decreased activity of alpha(2)-plasmin inhibitor indicated poor prognosis and may be an exacerbating factor in the acute phase of head trauma.

Antithrombin III↗
PubMed2001

Allelotype frequency of the thiopurine methyltransferase (TPMT) gene in Japanese.

Polymorphisms at three loci in the thiopurine methyltransferase (TPMT) gene are known to be responsible for azathioprine and 6-mercaptopurine (6MP) toxicity. Among them, only TPMT*3C variant allele with A719G mutation was found in 15/522 (2.9%; 17/1044 alleles; 1.6%) Japanese individuals including two homozygotes. The allele frequency was different from that in Caucasians, and investigation of TPMT polymorphisms with consideration of ethnic differences before administration of azathioprine or 6MP may provide clinically useful information.

Alleles↗
PubMed2001

Chemotherapy-induced unconjugated hyperbilirubinemia caused by a mutation of the bilirubin uridine-5'-diphosphate-glucuronosyltransferase gene.

Chemotherapy for malignant neoplasms sometimes causes unconjugated hyperbilirubinemia in the absence of liver dysfunction. We analyzed the association of chemotherapy-induced hyperbilirubinemia with mutations of the bilirubin uridine-5'-diphosphate (UDP)-glucuronosyltransferase gene (UGT1A1) from two leukemic patients in whom chemotherapy resulted in a hyperbilirubinemic response. We isolated genomic DNA from peripheral blood samples and amplified UGT1A1 by polymerase chain reaction. The amplified DNA fragments were analyzed by direct sequencing. The genes of the two patients revealed an identical heterozygous missense mutation in exon 1 (211G-->A: G71R). This UGT1A1 mutation may be the basis of chemotherapy-induced unconjugated hyperbilirubinemia.

Adolescent↗
PubMed2001

Epithelial expression of caveolin-2, but not caveolin-1, is enhanced in the inflamed mucosa of patients with ulcerative colitis.

Caveolae are vesicular invaginations of the plasma membrane that act as a scaffold of the assembly of many classes of signaling molecules. Caveolins are the principal structural component of caveolae membranes, and three distinct forms of caveolins have been identified: caveolin-1, caveolin-2, and caveolin-3. In this study, we evaluated the changes in the caveolin-1 and caveolin-2 expression in the inflamed mucosa of patients with IBD. Tissue samples were obtained endoscopically from patients with ulcerative colitis (UC) (n = 18), Crohn's disease (n = 10) and ischemic colitis (n = 8). Normal colorectal tissues were also obtained (n = 15). The caveolin expression was evaluated by standard immunohistochemical procedure. In normal colonic mucosa, caveolin-1 expression was detected in the smooth-muscle cells of the muscularis mucosae and the endothelial cells, but caveolin-2 expression was not detected. In the inflamed mucosa of patients with active UC, caveolin-2 expression was clearly detectable as small scattered foci on the luminal surfaces of epithelial cells, but caveolin-1 expression was similar to that in normal mucosa. Caveolin-2 expression increased in accordance with the disease activity of UC. This enhanced caveolin-2 expression was not detected in active Crohn's disease or ischemic colitis. In conclusion, we demonstrated that the epithelial expression of caveolin-2 is markedly enhanced in the inflamed mucosa of patients with UC. It is likely that the enhanced caveolin-2 expression in patients with UC was associated with the altered signal transductions in the intestinal epithelial cells. Furthermore, our results suggest that there are differences in the phenotypic features of epithelial cells between UC and Crohn's disease.

Caveolin 1↗
PubMed2001

New fabrication system for dental implant surgical stents: time-saving laboratory technique using a light-curing resin and transparent artificial teeth.

BACKGROUND: Surgical stents are a prerequisite for dental implant diagnosis. However, the traditional fabrication method including wax-up, investment, and resin polymerization is time consuming. PURPOSE: This article introduces a new fabrication system using a light-curing resin and transparent artificial teeth to reduce time spent in the laboratory. MATERIALS AND METHOD: The process of this system includes placing the light-curing resin and the artificial teeth on the partially edentulous dentition and alveolar ridge, making an appropriate pattern for the stent, light-curing for 5 minutes, briefly polishing, and making holes for titanium guide pins. RESULTS: This system requires only 30 to 40 minutes in the laboratory to complete a stent after mounting the casts on the articulator. Owing to the elasticity of the light-curing resin, this system eliminates the need for a blockout procedure on the undercuts of existing teeth on the casts, protects the casts from breakage, and provides the appropriate retention intraorally without any retainers. As well, titanium guide pins embedded in the stent were clearly identified by panoramic and computed tomographies. CONCLUSIONS: The new fabrication system proposed here can be time saving and, further, serve benefits for radiographic diagnosis.

Dental Implantation, Endosseous↗
PubMed2001

Excitation wavelength-dependent changes in Raman spectra of whole blood and hemoglobin: comparison of the spectra with 514.5-, 720-, and 1064-nm excitation.

Raman spectra of whole blood and oxy-hemoglobin (Hb) were measured under the same conditions with visible (514.5 nm) and near-infrared (NIR; 720 and 1064 nm) excitation, and the obtained spectra were compared in detail. The Raman spectrum of blood excited with visible light is dominated by very intense bands due to carotenoids, so that it was difficult to obtain information about Hb from the spectrum. The Raman spectra of whole blood and oxy-Hb excited with 720 nm light are very close to each other; both spectra are essentially Raman spectra of the heme chromophore that is preresonant with Q bands. Qualitative spectral analysis including band assignment and investigation of nature of resonance effect were carried out for the Raman spectra with 720 nm excitation. The spectra of whole blood and oxy-Hb excited with 1064 nm light contain contributions from nonresonance Raman spectra of the heme chromophore and Raman spectra of proteins. The 1064 nm excited spectra of blood and oxy-Hb are similar to each other but different in some features. For example, bands due to protein appear stronger in the spectrum of whole blood than in that of oxy-Hb which does not contain protein except globin part. The comparison between the 514.5, 720, and 1064 nm excited Raman spectra reveal that the excitation wavelength of 720 nm is more practical than that of visible light and 1064 nm in the Raman analysis of Hb, such as oxygenation, specially in situ measurement.

Adult↗
PubMed2001

Augmentation of human immunodeficiency virus type 1 subtype E (CRF01_AE) multiple-drug resistance by insertion of a foreign 11-amino-acid fragment into the reverse transcriptase.

A human immunodeficiency virus type 1 (HIV-1) subtype E (CRF01_AE) variant (99JP-NH3-II) possessing an in-frame 33-nucleotide insertion mutation in the beta3-beta4 loop coding region of the reverse transcriptase (RT) gene was isolated from a patient who had not responded to nucleoside analogue RT inhibitors. This virus exhibited an extremely high level of multiple nucleoside analog resistance (MNR). Neighbor-joining tree analysis of the pol sequences indicated that the 99JP-NH3-II variant had originated from the swarm of drug-sensitive predecessors in the patient. Population-based sequence analyses of 82 independently cloned RT segments from the patient suggested that the variants with the insertion, three or four 3'-azido-3'-deoxythymidine resistance mutations, and a T69I mutation in combination had strong selective advantages during chemotherapy. Consistently, in vitro mutagenesis of a drug-sensitive predecessor virus clone demonstrated that this mutation set functions cooperatively to confer a high level of MNR without deleterious effects on viral replication capability. Homology modeling of the parental RT and its MNR mutant showed that extension of the beta3-beta4 loop by an insertion caused reductions in the distances between the loop and the other subdomains, narrowing the template-primer binding cleft and deoxynucleoside triphosphate-binding pocket in a highly flexible manner. The origin of the insert is elusive, as every effort to find a homologue has been unsuccessful. Taken together, these data suggest that (i) HIV-1 tolerates in vivo insertions as long as 33 nucleotides into the highly conserved enzyme gene to survive multiple anti-HIV-1 inhibitors and (ii) the insertion mutation augments multiple-drug resistance, possibly by reducing the biochemical inaccuracy of substrate-enzyme interactions in the active center.

Adult↗
PubMed2001

Human parvovirus B19 induces cell cycle arrest at G(2) phase with accumulation of mitotic cyclins.

Human parvovirus B19 infects specifically erythroid progenitor cells, which causes transient aplastic crises and hemolytic anemias. Here, we demonstrate that erythroblastoid UT7/Epo cells infected with B19 virus fall into growth arrest with 4N DNA, indicating G(2)/M arrest. These B19 virus-infected cells displayed accumulation of cyclin A, cyclin B1, and phosphorylated cdc2 and were accompanied by an up-regulation in the kinase activity of the cdc2-cyclin B1 complex, similar to that in cells treated with the mitotic inhibitor. However, degradation of nuclear lamina and phosphorylation of histone H3 and H1 were not seen in B19 virus-infected cells, indicating that the infected cells do not enter the M phase. Accumulation of cyclin B1 was persistently localized in the cytoplasm, but not in the nucleus, suggesting that B19 virus infection of erythroid cells raises suppression of nuclear import of cyclin B1, resulting in cell cycle arrest at the G(2) phase. The B19 virus-induced G(2)/M arrest may be the critical event in the damage of erythroid progenitor cells seen in patients with B19 virus infection.

CDC2 Protein Kinase↗
PubMed2001

Impact of diabetes mellitus on long term survival after acute myocardial infarction in patients with single vessel disease.

OBJECTIVE: To assess the influence of diabetes on long term prognosis after reperfusion treatment and its interaction with multivessel disease. DESIGN: A retrospective observational study. SETTING: Hiroshima City Hospital. PATIENTS: 1660 consecutive patients with acute myocardial infarction who underwent coronary angiography within 24 hours after the onset of chest pain. MAIN OUTCOME MEASURES: Influence of diabetes on 10 year survival after infarction was assessed using the generalised Wilcoxon test and Cox's proportional hazards regression. Follow up was completed in 1622 patients (98%). RESULTS: Diabetic patients had more multivessel disease than non-diabetic patients (53% v 34%, p < 0.001). When only patients with single vessel disease were compared, diabetes was associated with a reduced 10 year survival after infarction (p = 0.002). On the other hand, in patients with multivessel disease there was no significant difference in survival between diabetic and non-diabetic patients (p = 0.70). Multivariate analysis also showed that diabetes was an independent risk factor related to 10 year mortality after infarction in patients with single vessel disease (odds ratio (OR) 1.81, 95% confidence interval (CI) 1.27 to 2.54; p = 0.001) and not in patients with multivessel disease (OR 1.17, 95% CI 0.85 to 1.60; p = 0.34). CONCLUSIONS: Diabetes is an independent predictor of long term mortality after infarction in patients with single vessel disease. However, in the presence of multivessel disease, prognosis after infarction is impaired regardless of diabetes, and the influence of diabetes is less obvious.

Catheterization, Central Venous↗
PubMed2001

Bronchial sleeve resection with complete preservation of the lung for carcinoma.

Conservative sleeve resection with complete preservation of the lung parenchyma is very rarely applicable for the treatment of bronchial carcinomas. We used this surgical procedure in four patients with bronchial carcinoma in various sites of the central airway, and we obtained successful results. The pathological types were two squamous cell carcinomas and two low-grade malignant tumors (mucoepidermoid carcinoma and adenoid cystic carcinoma). If patients are properly selected, this operative procedure appears to be a safe and radical therapeutic option for the treatment of bronchial neoplasms arising from major bronchi.

Adult↗
PubMed2001

FcgammaRIIa polymorphism in Japanese patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is an immune complex-mediated disease and organ damage is caused by the deposition of immune complex. Receptors which recognize the Fc portion of immunoglobulin G (FcgammaR) play a key role in the phagocytosis of immune complexes. As the gene encoding for FcgammaR of class IIa (FcgammaRIIa) has two allelic forms, H131 and R131, which differ in their affinity to IgG2, this polymorphism might have implications in handling immune complex. We studied the distribution of the FcgammaRIIa polymorphism in 90 Japanese patients with SLE. We also examined the association between FcgammaRIIa polymorphism and the disease activity of SLE and the histopathological findings of lupus nephritis. FcgammaRIIa polymorphism was determined by PCR and dot blot analysis. The allelic frequency of H131 in patients with SLE was significantly lower (H131/R131 = 0.44/0.56) than that of normal controls (H131/R131 = 0.62/0.38; P < 0.05). No significant association was observed between FcgammaRIIa polymorphism and the clinical parameters for the activity of SLE. There was no association between FcgammaRIIa polymorphism and the histological findings in lupus nephritis. The difference in the distribution of FcgammaRIIa alleles between patients with SLE and normal subjects indicates that this polymorphism is a candidate of susceptibility gene for SLE in Japanese.

Adolescent↗
PubMed2001

Comparison of suppressive potency between prednisolone and prednisolone sodium succinate against mitogen-induced blastogenesis of human peripheral blood mononuclear cells in-vitro.

Clinically, both prednisolone and prednisolone sodium succinate are widely used as immunosuppressive agents for the treatment of various allergic disorders. However, whether prednisolone sodium succinate itself has immunosuppressive or anti-inflammatory effects is unclear, and prednisolone sodium succinate may exhibit its efficacy only after hydrolytic conversion to prednisolone in-vivo. If this is the case, the impairment of prednisolone sodium succinate conversion to prednisolone in some clinical conditions may attenuate the efficacy of prednisolone sodium succinate. We therefore compared the pharmacological efficacy of prednisolone with that of prednisolone sodium succinate in-vitro using human peripheral blood mononuclear cells (PBMCs). PBMCs were obtained from 5 healthy subjects and 1 patient with pneumonia. The cells were incubated in the presence of concanavalin A and the cell growth was estimated by 3-(4,5-dimethyl thiazo-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Both prednisolone and prednisolone sodium succinate dose-dependently suppressed PBMC blastogenesis. Mean (s.d.) prednisolone and prednisolone sodium succinate IC50 (concentration of drug that gave 50% inhibition of cell growth) values were 580.0 (1037.9) and 3237.1 (4627.3) nM, respectively. The ratio of prednisolone IC50/prednisolone sodium succinate IC50 ranged from 0.005 to 0.230. Thus, prednisolone sodium succinate potency was markedly lower than that of prednisolone. After incubation of PBMCs with 100 microM prednisolone sodium succinate, 22.7-42.9 microM prednisolone was liberated into the culture medium, as determined by HPLC. The ratio of prednisolone liberation from prednisolone sodium succinate was not affected by the presence of fetal bovine serum or PBMC, or both, in the culture medium. These results suggested that the PBMC-suppressive effects of prednisolone sodium succinate might be due, at least partially, to prednisolone liberated from prednisolone sodium succinate into the culture medium. Prednisolone sodium succinate can be converted to prednisolone in the absence of serum or PBMCs, but the ratio of this conversion was very slow (t(1/2) > 4 days). Therefore, impairment of the enzymatic conversion of prednisolone sodium succinate to prednisolone in some pathological conditions such as liver diseases may result in attenuation of the clinical efficacy of prednisolone sodium succinate.

Adult↗