Search PubMed⌕ Search

Biomedical subjects

T Adachi

Publications and source records attributed to T Adachi.

At least 253 records · Page 14Linked to original sources
PubMed1997

[A study of gastroesophageal reflux by 24-hour esophageal pH monitoring in patients with bronchial asthma].

To evaluate the incidence of abnormal gastroesophageal reflux in patients with bronchial asthma and the influence of drug therapy on the gastroesophageal reflux, we investigated the gastroesophageal reflux patterns using an ambulatory 24-hour esophageal monitoring in 25 healthy volunteers and 58 asthmatics. All the patients were stable conditions at the time of the study. Bronchodilator therapy was continued, if necessary along with steroid inhalation and xanthines. Compared with healthy volunteers, the asthmatics had significantly greater esophageal acid exposure time, more frequent reflux episode, and longer single reflux time. About 70% of asthmatics had abnormal gastroesophageal reflux. Asthma medications were not associated with the incidence of abnormal gastroesophageal reflux. However, asthmatics receiving beta(2)-stimulants therapy (n = 27) had significantly greater esophageal reflux exposure time than those not receiving (n = 31). Our study suggested that most asthmatics have abnormal gastroesophageal reflux unrelated to asthma attack or asthma medications and that beta(2)-stimulants used in asthmatics may worsen gastroesophageal reflux.

Adult↗
PubMed1997

[Results of a survey of Japanese cedar pollinosis in Hachijyojima].

We performed a questionnaire survey of Japanese cedar pollinosis among 7,946 residents of the Sakashita region (Mitsune, Ogago) and Sakaue region (Kashidate, Sueyoshi, Nakanogo) of Hachijyojima who were at least 15 years of age. The response rate was 21.3%. The percentage of respondents who reported three or more nasal symptoms concurrentry with two ocular symptoms in early spring (from the end of February to the end of March) was 1.8% in the Sakashita region and 0.3% in the Sakaue region. About 1.5% of Hachijyojima residents were suspected to have Japanese cedar pollinosis. On scratch tests of symptomatic subjects, 9.2% showed positive reactions for Japanese cedar antigen, and 12.1% had an IgE RAST score of 2 or more. The peak Japanese cedar pollen concentration between February 11 and March 31, 1992 was 74/cm2 on March 6 in the Sakashita region and 127/cm2 on the same day in the Sakaue region. This survey confirmed the presence of a low incidence of Japanese cedar pollinosis in Hachijyojima, an isolated island 290 km from Tokyo.

Adolescent↗
PubMed1996

The crystal structure of hepatitis C virus NS3 proteinase reveals a trypsin-like fold and a structural zinc binding site.

During replication of hepatitis C virus (HCV), the final steps of polyprotein processing are performed by a viral proteinase located in the N-terminal one-third of nonstructural protein 3. The structure of NS3 proteinase from HCV BK strain was determined by X-ray crystallography at 2.4 angstrom resolution. NS3P folds as a trypsin-like proteinase with two beta barrels and a catalytic triad of His-57, Asp-81, Ser-139. The structure has a substrate-binding site consistent with the cleavage specificity of the enzyme. Novel features include a structural zinc-binding site and a long N-terminus that interacts with neighboring molecules by binding to a hydrophobic surface patch.

Amino Acid Sequence↗
PubMed1996

Reduction of 14-16 kDa allergenic proteins in transgenic rice plants by antisense gene.

An antisense gene strategy was applied to suppress the 14-16 kDa allergen gene expression in maturing rice seeds. Gene constructs producing antisense RNAs of the 16 kDa allergen under the control of some rice seed-specific promoters were introduced into rice by electroporation. Immunoblot and RNA blot analyses of the seeds from the transgenic rice plants using the allergen-specific monoclonal antibody and a sequence-specific antisense RNA probe demonstrated that the 14-16 kDa allergen proteins and their transcripts of the seeds from several transgenic lines were present in much lower in amounts than those of the seeds from parental wild-type rice. The high levels of reduction observed were stably inherited in at least three generations.

Allergens↗
PubMed1996

Influence of dietary protein levels on the acute toxicity of methylmercury in mice.

The influence of dietary protein levels on the acute toxicity of methylmercury (MeHg) was investigated using C57BL/6N male mice fed either a 24.8% protein diet (normal protein diet, NPD) or a 7.5% protein diet (low protein diet, LPD). When MeHg was administered to each group of mice, all mice died at a medium or high dose (80 or 120 mumol/kg, respectively) within 16 or 7 days, respectively, but not at a low dose (40 mumol/kg) in both dietary groups. Although no difference was observed in the survival rate at a medium dose, NPD-fed mice died earlier despite lower brain Hg than LPD-fed mice at a high dose. Accordingly, death, in our observations, could not be due to neural damage by MeHg. When a high dose of MeHg was administered to mice, plasma aspartate aminotransferase and alanine aminotransferase activities increased in NPD-fed mice but not in LPD-fed mice in spite of similar hepatic Hg levels. Therefore, the higher susceptibility of the liver could be reason for the shorter survival period in NPD-fed mice. Since plasma creatinine increased within 24 h after MeHg administration at a medium or high dose, renal dysfunction could be a major factor in death. The present results suggest that susceptibility to acute MeHg toxicity was higher in NPD-fed mice than in LPD-fed mice, possibly due to the difference in hepatic susceptibility.

Alanine Transaminase↗
PubMed1996

Nitrous oxide depresses somatocardiac sympathetic A- and C-reflexes in anesthetized rats.

Effect of nitrous oxide (N2O) on the somatosympathetic A- and C-reflexes was investigated using artificially ventilated rats anesthetized with alpha-chloralose and urethane. Somatocardiac sympathetic A- and C-reflexes were elicited in the inferior cardiac nerve by electrical stimulation of A and C afferent fibers of the tibial nerve, respectively. Both reflexes were depressed by inhalation of N2O for 20 min. The depression was greater in the C-reflex than in the A-reflex. The depressive effects of N2O on both reflexes were unchanged after pretreatment with intravenous naloxone (0.2 or 2.0 mg/kg) or by prolongation of the inhalation of N2O for 2 h. These results suggest that the opioid receptor is not involved and that acute tolerance is not developed in the depressive action of N2O on the somatosympathetic A- and C-reflexes.

Anesthetics, Inhalation↗
PubMed1996

Selective removal of human serum amyloid P component from rat blood by use of an immunoaffinity membrane in an extracorporeal circulation system.

We examined the suitability of an immunoaffinity membrane (IAM) bearing specific antibody as a ligand for removing human serum amyloid P component (hSAP) from blood passed through a simple extracorporeal circulation system established in rats. The specific antibody was the most effective of the various ligands tested for removing hSAP from human blood. To determine the value of the hSAP in human or rat plasma, we also developed a simple ELISA. In the rat extracorporeal circulation system, the hSAP level in the inlet blood to the IAM module decreased to 49% of the initial concentration within 60 min. In contrast, the hSAP remained at the initial concentration throughout the study in the module without the IAM. The use of this extracorporeal circulation system in this case allows preclinical evaluation of the ex vivo removal of a human plasma component in an animal model. Biocompatibility of the IAM was also examined. No change in blood cell counts or activation of the coagulation system occurred after contact with the IAM. Non-specific adsorption was not observed, since there was no statistically significant difference in IgG, complement C3, or albumin level between the pre- and post-treatment with this module. The immunological effects of the IAM were also examined using this system. Four weeks after the termination of the extracorporeal circulation, the rats examined showed no detectable antibody titer to the ligand.

Adsorption↗
PubMed1996

Cloning of the rice seed alpha-globulin-encoding gene: sequence similarity of the 5'-flanking region to those of the genes encoding wheat high-molecular-weight glutenin and barley D hordein.

A genomic clone encoding the rice endosperm major globulin (alpha-globulin) with an apparent molecular mass of 26 kDa was isolated, and its nucleotide (nt) sequence and transcription start point (tsp) were determined. The tsp was identical to that of the gene encoding the wheat high-molecular-weight (HMW) glutenin subunit. The consensus '-300 element' and an A + T-rich sequence exist upstream from the TATA box in the 5'-flanking region. A nt sequence of about 130 bp in the 5'-flanking region was found to be markedly homologous to those of the genes encoding the wheat HMW glutenin subunit and barley D hordein.

Alpha-Globulins↗
PubMed1996

The specificity of association of the IgD molecule with the accessory proteins BAP31/BAP29 lies in the IgD transmembrane sequence.

Mature B cells co-express on their cell surface two classes of antigen receptor, the IgM and IgD immunoglobulins. The structural and functional differences between the two receptor classes are poorly understood. Recently two proteins of 29 and 31 kDa (BAP29 and BAP31) have been described that are preferentially associated with membrane IgD but only weakly with membrane IgM. We describe here the cloning of full-length murine and human BAP31 cDNAs encoding proteins of 245 and 246 amino acids respectively. The two BAP31 proteins are 95% identical. The BAP31 gene is ubiquitously expressed in murine tissues and is located on the X chromosome in both mouse and man. The murine BAP31 protein has 43% sequence identity to murine BAP29. Both proteins have a hydrophobic N-terminus and an alpha-helical C-terminus which ends with a KKXX motif implicated in vesicular transport. By a mutational analysis we have identified amino acids in the transmembrane sequence of the delta m chain that are critical for binding to BAP31/BAP29. A structural model of the BAPs and their potential functions are discussed.

Amino Acid Sequence↗
PubMed1996

Substitution of glycine for arginine-213 in extracellular-superoxide dismutase impairs affinity for heparin and endothelial cell surface.

Extracellular-superoxide dismutase (EC-SOD) levels in sera divide into two discontinuous groups: a low-level group below 400 ng/ml and a high-level group above 400 ng/ml [Adachi, Nakamura, Yamada, Futenma, Kato and Hirano (1994) Clin. Chim. Acta 229, 123-131]. Molecular genetic studies have shown that the donors in the high-level group have a single base substitution generating the exchange of glycine for arginine-213 (R213G) in the heparin-binding domain of EC-SOD [Sandström, Nilsson, Karlsson and Marklund (1994) J. Biol. Chem. 269, 19163-19166; Yamada, Yamada, Adachi, Goto, Ogasawara, Futenma, Kitano, Hirano and Kato (1995) Jpn. J. Hum. Genet. 40, 177-184]. The serum EC-SOD level in homozygote subjects was significantly higher than that in heterozygotes and in normal subjects. Serum EC-SOD from heterozygotes and homozygotes had equally decreased affinity for heparin, as judged by heparin-HPLC, as compared with that from normal donors. This result suggests that the serum EC-SOD in heterozygotes was mainly composed of the mutant form which has reduced heparin affinity. On the other hand, fibroblast cells derived from heterozygote subjects generated mRNA of both normal and mutant EC-SOD (m-EC-SOD), and expressed the corresponding proteins. EC-SOD is a tetrameric enzyme, and in heterozygote donors would be heterogeneous with regard to the constitution of normal and mutant subunits. The enzyme form consisting of only mutant subunits, the form with the weakest heparin affinity, can be preferentially driven out to the plasma phase, because EC-SOD in the vasculature exists in equilibrium between plasma and the endothelial cell surface. The binding of m-EC-SOD to bovine aortic endothelial cells was about 50-fold less than that of normal EC-SOD. This result suggests that the binding of m-EC-SOD to vascular endothelial cells is much decreased in vivo, which causes a high level of serum EC-SOD.

Animals↗
PubMed1996

The same nuclear proteins bind to the 5'-flanking regions of genes for the rice seed storage protein: 16 kDa albumin, 13 kDa prolamin and type II glutelin.

Expression of rice seed storage-protein genes is dramatically regulated over a short period of seed maturation. To characterize the expression mechanism of the rice seed storage protein genes, their expression of major storage protein genes (16 kDa albumin, 13 kDa prolamin and type II glutelin) were compared by RNA blot analysis. Their coordinate expression suggests that the transcriptional regulatory machinery is shared among the glutelin, prolamin and albumin-genes. We isolated two novel genomic genes for prolamins (PG5a and PG5b) and obtained the promoter region of the glutelin gene by PCR. The 5'-flanking regions of these three rice seed storage protein genes were found to contain some similar conserved sequences. Nuclear extract partially purified from maturing rice seeds was used for the gel shift assay of the 5' region of the RA gene. We identified two DNA sequences of RA gene which were recognized by independent DNA-binding proteins. The complexes of these DNA sequences and DNA-binding proteins were inhibited by the fragments containing the 5' regions of the prolamin and glutelin genes, suggesting that these three genes share transcription factors.

Albumins↗
PubMed1996

Is the presence of hyperlipidemia associated with impairment of endothelium-dependent neointimal relaxation after percutaneous transluminal coronary angioplasty?

To determine whether hyperlipidemia affects the endothelium-dependent vasomotor response along the dilated vessel after percutaneous transluminal coronary angioplasty (PTCA), we evaluated 32 patients with one-vessel disease, 3-6 months after successful PTCA without restenosis. Fourteen patients had mild stenotic lesions not subjected to PTCA (non-PTCA sites) in addition to the PTCA sites. Vessel diameter changes at 32 PTCA and 36 non-PTCA sites were assessed by quantitative angiography, before and after intracoronary injection of acetylcholine (20 micrograms to the right and 50 micrograms to the left coronary artery) and of nitroglycerin (0.1-0.3 mg). The acetylcholine response ranged from 46% (dilation) to -100% (constriction). All coronary arteries were dilated in response to nitroglycerin, which suggested preservation of the function of vascular smooth muscle, and the presence of an abnormality in endothelial function in those patients with a constrictor response to acetylcholine. There was a negative correlation between the acetylcholine response and the serum total cholesterol level at PTCA sites (r = -0.37; P = 0.038) and at non-PTCA sites (r = -0.46; P = 0.005). These findings indicate that hyperlipidemia is associated with a loss of endothelium-dependent vasodilation, not only at non-PTCA but also at PTCA sites, at which restoration of endothelial function might have occurred. They also suggest that hyperlipidemia may be related to the functional state of the regenerated endothelium at sites where PTCA had been previously performed.

Acetylcholine↗
PubMed1996

Methylmercury transport across the placenta via neutral amino acid carrier.

Methylmercury (MeHg) penetrates the placental barrier to affect developing fetuses in the uterus. However, the mechanism of placental MeHg transport is not well defined. To clarify the MeHg transport system that functions in the placenta, pregnant rats were intravenously administered MeHg on day 18 of gestation. The fetal blood was collected from the umbilical cord at 30 and 60 min after the administration, and its mercury concentration was measured. MeHg was found to be rapidly transported to the fetal blood in a time- and dose-dependent manner, and predominantly distributed in the blood cells there. MeHg transport was effectively suppressed by the co-injection of neutral amino acids, i.e., L-methionine and L-phenylalanine, suggesting that MeHg is actively transported as its cysteine conjugate via the neutral amino acid carrier system. The suppression by methionine was not so marked as by phenylalanine. Since methionine administration caused a rapid increase of the cysteine, which functioned as a predominant carrier in MeHg transport, in the maternal plasma, newly synthesized cysteine seemed to accelerate the mercury uptake. Accordingly, the acceleration by the extra cysteine would compensate partly the competitive effect of methionine as a neutral amino acid.

Amino Acid Transport Systems↗
PubMed1996

Collateral channels that develop after an acute myocardial infarction prevent subsequent left ventricular dilation.

OBJECTIVES: We sought to evaluate the effect of collateral channels that develop late after a first anterior myocardial infarction on left ventricular dilation and function. BACKGROUND: Collateral channels in an infarct-related artery may develop long after occlusion of the artery. Well visualized collateral channels that appear immediately after a myocardial infarction reduce infarct size and preserve left ventricular function. However, the functional significance of collateral channels that develop late after myocardial infarction has not been evaluated in terms of left ventricular function. METHODS: We studied 21 patients with a first anterior myocardial infarction and an infarct-related artery that remained totally occluded after reperfusion therapy and did not reopen within 1 month of infarction. No collateral channels were observed during the acute period. Patients were classified into two groups according to the extend of collateral formation 1 month after infarction: group C, patients with well developed collateral channels (n = 11), and group NC, patients with absent or poorly developed collateral channels (n = 10). Infarct size was determined by peak creatine kinase activity and thallium-201 single-photon emission computed tomography. Global and regional left ventricular function and left ventricular volumes were assessed by left ventriculography. These measurements were identical in both groups 1 month after infarction. Left ventricular function was reevaluated after 2.12 +/- 0.79 years (mean +/- SD). RESULTS: There were no significant changes in global and regional left ventricular function between the two groups during the long-term follow-up period. However, the end-diastolic volume index of group NC increased from 71 +/- 14 to 85 +/- 19 ml/m2, whereas that of group C decreased from 64 +/- 18 to 59 +/- 12 ml/m2. This important change during the long-term follow-up period resulted in a significant difference (p = 0.0006) in the end-diastolic volume index between the groups 2 years after onset (p = 0.002), whereas 1 month after infarction the difference was not significant (p = 0.36). A similar pattern was observed for the end-systolic volume index (group C: 38 +/- 16 to 35 +/- 14 ml/m2; group NC: 45 +/- 12 to 58 +/- 18 ml/m2, p = 0.018). The power of the tests to detect the observed differences showing nonsignificant results ranged from 0.05 to 0.38, whereas the power of the tests indicating a significant difference in end-diastolic and end-systolic volume indexes was >0.88. CONCLUSIONS: Collateral channels that develop after a myocardial infarction do not reduce the infarct size or prevent left ventricular dilation within 1 month of infarction. In contrast, such collateral channels prevent subsequent ventricular dilation and the deterioration of left ventricular function over 2 years. However, our results may have been biased because of the small number of patients.

Aged↗
PubMed1996

Eosinophil apoptosis caused by theophylline, glucocorticoids, and macrolides after stimulation with IL-5.

BACKGROUND: Glucocorticoids have long been used as the most potent drugs in the treatment of bronchial asthma. Data reported recently have led to the proposal that theophylline and macrolides have antiinflammatory effects. OBJECTIVE: We examined the abilities of theophylline, glucocorticoids, and macrolides to counteract the prolongation of eosinophil survival caused by IL-5. METHODS: Purified guinea pig eosinophils were cultured in the presence or absence of human IL-5 and with or without the aforementioned drugs at various concentrations. The percentage of cells alive after 3 days in culture was determined. RESULTS: Aminophylline (AM), methylprednisolone (MP), erythromycin (EM), and clarithromycin (CAM) suppressed the IL-5 induced prolongation of eosinophil survival in a dose-dependent manner. The effects of these drugs on eosinophil survival were significantly greater at low concentrations of IL-5 than at high concentrations of IL-5. When eosinophils were cultured in the presence of IL-5 (1 ng/ml) with physiologic concentrations of MP (10(-6) mol/L), AM (10(-4) mol/L), and either EM or CAM (both 10 micrograms/ml), the effect of IL-5 was almost completely abolished, and the morphologic changes in eosinophils observed by electron microscopy were consistent with apoptosis. DNA extracted from eosinophils cultured with IL-5 and each of the drugs was definitely fragmented. CONCLUSIONS: One mechanism of the effectiveness of these drugs is induction of eosinophil apoptosis. Some combination of these drugs may be useful in the treatment of bronchial asthma.

Aminophylline↗
PubMed1996

Eosinophil peroxidase stimulates the release of granulocyte-macrophage colony-stimulating factor from bronchial epithelial cells.

BACKGROUND: Asthma is characterized by an accumulation of activated eosinophils in the airway. Eosinophil viability-enhancing activity is present in the sputum of patients with asthma, largely because of granulocyte-macrophage colony-stimulating factor (GM-CSF). Bronchial epithelial cells have been shown to release cytokines including GM-CSF when stimulated with IL-1 beta or tumor necrosis factor-alpha. OBJECTIVE: The study was designed to determine whether eosinophil peroxidase (EPO) stimulates the release of GM-CSF from bronchial epithelial cells. METHODS: Epithelial cells (BEAS-2B) were cultured in serum free HD-F12 medium in a 24-well tissue culture plate until they became confluent. The cells were then exposed to EPO (5.9 x 10(-8) to 5.9 x 10(-7) mol/L) for 15 minutes, washed twice, and cultured in 1 ml of HD-F12. The supernatants were harvested at 3, 6, or 24 hours, and GM-CSF concentration was measured by ELISA. BEAS-2B cells were also treated with a system comprising EPO (1.9 x 10(-9) to 5.9 x 10(-8) mol/L) + 10(-5) mol/L H2O2 + 10(-4) mol/L Br for 24 hours. RESULTS: The GM-CSF concentration in the supernatant pretreated with EPO increased in a time- and concentration-dependent manner compared with control. The release of GM-CSF was not inhibited by catalase but was inhibited by cyclohexamide and by mixing of EPO with heparin, suggesting that the action is due to the cationic property of EPO. When EPO was combined with H2O2 and Br, 5.9 x 10(-9) mol/L EPO + 10(-5) mol/L H2O2 released two times more GM-CSF into the supernatants compared with control. CONCLUSION: These results suggest that EPO stimulates epithelial cells to release GM-CSF and forms a self-stimulatory cycle.

Asthma↗
PubMed1996

Purification and partial characterization of an indomethacin hydrolyzing enzyme from pig liver.

PURPOSE: Indomethacin is well known to be metabolized via O-demethylation and N-deacylation. In this paper we found an enzyme involved in the hydrolysis of amide-linkage of indomethacin and partially characterized it as well as its substrate specificity. METHODS: An indomethacin hydrolyzing enzyme was purified to homogeneity from pig liver microsomes using columns of Q-Sepharose, Red-Sepharose and Blue-Sepharose. The enzyme activity was assayed by measuring of rho-chlorobenzoic acid liberated from indomethacin by HPLC. RESULTS: The purified enzyme effectively hydrolyzed the amide linkage in indomethacin but not those in alpha-naphthylacetate and rho-nitrophenylacetate, which are typical substates for carboxylesterase. The subunit molecular mass of the enzyme was 65 kDa according SDS-polyacrylamide gel electrophoresis. The Michaelis constant (K(m)) and maximum velocity (Vmax) values for indomethacin were 67.8 microM and 9.02 nmol/min/mg protein, respectively. The amino acid sequence analysis of the enzyme after cyanogen bromide cleavage showed high homology with a mouse carboxylesterase isozyme designated as ES-male. The activity of indomethacin hydrolysis was relatively high in the pig, rabbit and human liver homogenate, but not in those from rat and mouse. On the other hand, purified human liver carboxylesterases pl 5.3 and 4.5, and pig liver carboxylesterases have no catalytic activity for indomethacin. CONCLUSIONS: These results indicate that the hydrolysis of amide-linkage of indomethacin in humans would be associated with an enzyme similar to the indomethacin hydrolyzing enzyme from pig liver microsomes described here.

Animals↗