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Biomedical subjects

A Hirata

Publications and source records attributed to A Hirata.

At least 145 records · Page 8Linked to original sources
PubMed1996

Antitussive effect of herbal medicine bakumondo-to: a case report.

A 50 year-old woman with progressive systemic sclerosis accompanied by interstitial pneumonia complained of a dry cough. A variety of antitussive agents were given for the dry cough over a one year period, but her symptoms continued. However, when a herbal medicine Bakumondo-to was administered, her intractable dry cough subsided dramatically within 10 days. Bakumondo-to may be a good antitussive agent for interstitial pneumonia associated with a dry cough that is resistant to other antitussives.

Adrenergic beta-Agonists↗
PubMed1996

Clockwise whirlpool sign at color Doppler US: an objective and definite sign of midgut volvulus.

PURPOSE: To evaluate the clockwise whirlpool sign at color Doppler ultrasound (US) in the diagnosis of midgut volvulus. MATERIALS AND METHODS: Pediatric patients (160 boys, 76 girls; age range, 0 day to 14 years) with possible midgut volvulus underwent abdominal gray-scale US and color Doppler US. Midgut volvulus was diagnosed by recognition of the whirlpool sign (wrapping of the superior mesenteric vein and the mesentery around the superior mesenteric artery). If the whirlpool rotated clockwise with caudal movement of the transducer, the direction of the whirlpool was defined as clockwise. RESULTS: Color Doppler US showed a whirlpool sign that was clockwise in 12 of 13 patients with surgically confirmed midgut volvulus and counterclockwise in three patients without midgut volvulus. Sensitivity, specificity, and positive predictive value of clockwise whirlpool sign for midgut volvulus were 92%, 100%, and 100%. CONCLUSION: The clockwise whirlpool sign is diagnostic of midgut volvulus. Color Doppler US should be performed as an initial imaging study in children suspected of having midgut volvulus.

Adolescent↗
PubMed1996

Permeability-related changes revealed at endothelial cell borders in inflamed venules by lectin binding.

Plasma leakage in inflammation results from intercellular gaps that form in the endothelium of venules. These gaps and related morphological changes in endothelial cells are not readily seen by light microscopy. In this study we sought to visualize such changes by using the selective binding properties of plant lectins. Acute inflammation was induced in the trachea of pathogen-free F344 rats by injecting substance P intravenously, and 1, 3, or 10 min later the vasculature was perfused with fixative followed by a biotinylated lectin. Lectin binding was localized by avidinbiotin complex-peroxidase histochemistry and viewed in tracheal whole mounts by differential-interference contrast microscopy. The binding patterns of the 20 lectins tested fell into 4 groups. Most of the lectins either bound uniformly to the endothelium of normal and inflamed venules (group 1, e.g., Lycopersicon esculentum lectin) or bound weakly or not at all to venules (group 2, e.g., Maackia amurensis I lectin). The uniform binding of group 1 lectins not only revealed the overall vascular architecture but also made visible intercellular gaps and fingerlike processes at endothelial cell borders in inflamed venules. In postcapillary venules after substance P, the fingerlike processes were present along an average of 32% of the endothelial cell perimeter at 1 min, 25% at 3 min, and 7% at 10 min, compared with a baseline value of 2%. A third group of lectins (group 3, e.g., concanavalin A) bound selectively to focal patches of inflamed venules but bound weakly to normal venules. The fourth group (group 4, e.g., Ricinus communis I lectin) bound preferentially to focal patches in inflamed venules and also bound uniformly to normal venules. The focal binding of group 3 and 4 lectins coincided with sites of plasma leakage marked by extravasation of the particulate tracer monastral blue and was associated with subendothelial components of the vessel wall. We conclude that selected lectins reveal novel features of focal sites of plasma leakage, endothelial gaps, and fingerlike processes at endothelial cell borders in inflamed venules.

Animals↗
PubMed1996

The mechanisms of the improvement of insulin sensitivity by angiotensin converting enzyme inhibitor.

To investigate the role of kinins in augmentation of insulin sensitivity by angiotensin converting enzyme inhibitor (ACEI), the effects of ACEI (delapril) on the insulin resistance in fructose-fed rats (FFR) were evaluated with or without the administration of bradykinin receptor antagonist (Hoe 140). Male Sprague-Dawley rats were fed on fructose rich chow (FFR) or standard chow (control) for 4 weeks and treated with 10 mg/kg/day of delapril with or without Hoe 140 (0.5 mg/kg/day) for an additional 2 weeks. Steady state plasma glucose (SSPG) and steady state plasma insulin (SSPI) were determined while the rats were conscious. Insulin (2.5 mU/kg/min) and glucose (8 mg/kg/min) were simultaneously infused to determine insulin sensitivity in each group. Mean blood pressure (MBP), SSPG and SSPI were significantly higher in FFR than in control, and were significantly lower in the FFR+delapril than in FFR+vehicle. There were no difference in MBP, SSPG and SSPI between FFR+delapril+vehicle and FFR+delapril+Hoe 140. We concluded that the main mechanisms of improving the insulin sensitivity by ACEI may not be the enhancement of kinins but the suppression of angiotensin II in FFR.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Detection of transforming growth factor-beta in sputum from patients with bronchial asthma by eosinophil survival assay and enzyme-linked immunosorbent assay.

BACKGROUND: We have shown that interleukin-5 (IL-5) and granulocyte-macrophage colony-stimulating factor (GM-CSF) are present in sputum from patients experiencing acute asthma attacks, by eosinophil survival assay. The viability of guinea-pig eosinophils was significantly increased in the presence of such sputum extracts after 3 days' culture, and it was inhibited by the addition of anti-IL-5 and anti-GM-CSF antibodies. However, the contribution of IL-5 to the increase in eosinophil viability was less than expected from the values of IL-5 measured by enzyme-linked immunosorbent assay (ELISA). Therefore, we speculated that something in sputum inhibited the function of IL-5. OBJECTIVE: Transforming growth factor-beta (TGF-beta) was the only cytokine we tested that inhibited the prolongation of survival of guinea-pig eosinophils induced by IL-5. The objective of this study is to detect TGF-beta in the same sputum. METHODS: Guinea-pig eosinophils were cultured with or without anti-TGF-beta antibody in the presence of sputum extracts, and the eosinophil viability was counted after 3 days. Measurement of TGF-beta 1 in sputum was performed by ELISA. RESULTS: Eosinophil viabilities with and without anti-TGF-beta antibody were 79.7 +/- 2.9% and 69.0 +/- 2.7%, respectively, and the difference between them was statistically significant (P < 0.05, n = 9). The concentration of TGF-beta 1 in the sputum was 21.7 +/- 3.3 ng/mL (n = 9). CONCLUSION: These observations suggest that TGF-beta is present in sputum from patients with bronchial asthma.

Adult↗
PubMed1996

Damage to respiratory epithelium by guinea-pig eosinophils stimulated with IgG-coated Sepharose beads.

BACKGROUND: There are no reports of respiratory epithelial damage induced by immunoglobulin-stimulated eosinophils. OBJECTIVE: We tried to induce damage to respiratory epithelium by guinea-pig (GP) eosinophils stimulated with guinea-pig IgG (GP-IgG)-coated Sepharose 4B beads. METHODS: GP tracheal epithelium was cultured together with GP eosinophils that had been collected from the peritoneal cavity, purified on a Percoll gradient, and stimulated with GP-IgG-coated beads (GP eosinophils:beads = 20:1). Damage to the epithelium was observed with an inverted microscope. RESULTS: After 24 h of culture with three 10(6) eosinophils, irregularity of the surface of the epithelium, desquamation, shedding of cilia, and abnormal beating of cilia were observed. This damage was first observed after 12 h of incubation, and was more severe at 24 h. No damage was found when beads coated with human serum albumin (HSA) were used. GP eosinophils stimulated with GP-IgG released significantly more EPO than those stimulated with HSA, at 6 and 24 h. Heparin and catalase partially inhibited the epithelial damage. O2-production by eosinophils was also enhanced with GP-IgG-coated beads. CONCLUSION: Both granule basic proteins and reactive oxygen radical may be responsible for epithelial damage, probably via an EPO + H2O2 + halide system. These results confirmed that stimulated eosinophils can damage respiratory epithelium.

Animals↗
PubMed1995

Down-regulation of bcl-xs gene expression in rat thymocytes by dexamethasone.

In order to test a hypothesis that the expression of bcl-x gene promotes apoptosis by antagonizing the function of bcl-2 gene product, time course of the expression of bcl-x was investigated using the dexamethasone-treated rat thymocytes which were undergoing apoptosis. Unexpectedly, dexamethasone suppressed the expression of bcl-x in a dose- and time-dependent manner. Such decrease was detected even in the presence of cycloheximide, suggesting that the suppression is due to the genomic (primary) effect of dexamethasone. Since the expression of bcl-xL, as measured by a specific nucleotide probe, was not detected at a quantifiable level, the decrease was apparently attributed to that in bcl-xS. Our present observations propose a new role of the bcl-xS gene product, in which the bcl-x gene product may be necessary for survival of immature thymocytes rather than for their apoptosis.

Animals↗
PubMed1995

Ontogeny of neuropsin mRNA expression in the mouse brain.

In our previous study, we found a novel gene encoding a serine protease termed neuropsin (NP) which exhibited activity-dependent gene expression or repression in the mouse hippocampus (Chen et al., 1995). In the present study, we examined the ontogeny of NP mRNA expression by in situ hybridization in the brain. Weak hybridization signals were also observed in the choroid plexus at this stage in addition to neuronal labeling. The signals continued to show this localization pattern until postnatal day 12. After embryonic day 18, the number of hybridization signals localized in the neurons of the forebrain limbic area were more predominant than those in the lower brainstem. NP gene expression spread in the anterior olfactory nucleus, hippocampus, septal nuclei, diagonal band of Broca, amygdala and limbic cortex successively from early embryonic to adult stage, though signals in the other brain regions were gradually decreased after birth. Thus, the widespread localization and two types of expression pattern, constitutive or transient, suggest that NP is a multiple functional protein involved in development, neuronal plasticity and cerebrospinal fluid production.

Animals↗
PubMed1995

Effects of angiotensin receptor antagonist and angiotensin converting enzyme inhibitor on insulin sensitivity in fructose-fed hypertensive rats and essential hypertensives.

This study was designed to investigate the effects of angiotensin II (AII) receptor antagonist and angiotensin converting enzyme (ACE) inhibitor on insulin resistance, and the mechanism by which ACE inhibitor improves insulin-dependent glucose uptake (insulin sensitivity) in an insulin-resistant hypertensive rat model (fructose-fed rats, FFR) and in essential hypertensives (EHT). Male Sprague-Dawley rats were fed on fructose-rich or standard chow for 4 weeks and treated either with 10 mg/kg/day of delapril (n = 8), 1 mg/kg/day of TCV-116 (AII receptor antagonist; n = 13), or vehicle (n = 9) for the latter 2 weeks. Steady-state plasma glucose (SSPG) was measured with the subjects in the conscious state; simultaneously, we infused insulin (2.5 mU/kg/min) and glucose (8 mg/kg/min) to determine insulin sensitivity in each group. Thirteen EHT were hospitalized and the 2-h euglycemic hyperinsulinemic glucose clamp (GC) method was performed in a fasting condition before and after 2 weeks' administration of TCV-116 (8 mg/day) in 7 EHT and of delapril (120 mg/day) in 6 EHT. Insulin sensitivity was evaluated as M-value calculated from the infusion rate of glucose. Mean blood pressure (MBP) was higher in FFR (137.7 +/- 73.8 mm Hg, P < .05) compared to controls (120.8 +/- 2.7 mm Hg), and was lower in both the delapril (108.1 +/- 6.3 mm Hg, P < .05) and TCV-116 (112.8 +/- 4.3 mm Hg, P < .05) groups than in FFR.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1995

Epitope analysis using anti-oligosaccharide (G4) monoclonal antibody.

A murine monoclonal antibody recognizing (1-->6)-beta-D-glucopyranosyl laminaritriose (G4) was prepared by immunizing BALB/c mice with G4-bovine serum albumin conjugate and fusing the splenocytes with mouse myeloma cells. The monoclonal antibody (IgM) provoked by the cloned cells showed low reactivity with schizophyllan, an antitumor polysaccharide, but notable reactivity with some low-molecular-weight schizophyllans. This antibody was useful for determination of the epitope of several polysaccharides. The extent of reactivity of this monoclonal antibody was related only to the molecular weight of schizophyllan.

Animals↗
PubMed1995

Location of focal silver staining at endothelial gaps in inflamed venules examined by scanning electron microscopy.

The century-old histological technique of silver nitrate staining has proven to be extremely useful for visualizing endothelial cell borders and localizing endothelial gaps, but the significance of the staining is still not fully understood. To gain some insight into what silver nitrate stains, we developed a method that enabled us to use scanning electron microscopy with backscattered and secondary electron imaging to examine silver staining at endothelial cell borders of venules of the rat tracheal mucosa. We found that in normal venules, silver lines followed the smooth contour of cell borders. However, 1 min after endothelial permeability was increased by substance P, cell borders were irregular and displaced from the silver lines by as much as 4.3 microns, and the lines were accompanied by three types of silver deposits. Most common (46% of total) were annulus-shaped silver deposits that surrounded endothelial gaps. These deposits averaged 1.5 microns in width, were positioned symmetrically across cell borders, and were located at a depth of 0.3 micron beneath the luminal surface. Many endothelial gaps were partitioned into multiple pores (mean, 2.4) by fingerlike processes of endothelial cells. Surprisingly, the gaps occupied only 5.4% of the total area of the silver deposits and constituted 0.15% of the luminal surface of the leaky postcapillary venules. A second type of silver deposit (19% of total) was positioned asymmetrically with respect to the cell border and marked sites where endothelial cell margins still overlapped but appeared to be vertically separated by obliquely oriented gaps. A third type marked gaps at three-cell junctions; these were no more abundant than deposits elsewhere around the cell perimeter, suggesting that three-cell junctions were not unusually leaky sites. We conclude that silver nitrate marks endothelial cell borders and outlines endothelial cell gaps by staining an element of intercellular junctions. The annular shape of many silver deposits around gaps suggests that junctional elements in the apposing cells are separated during gap formation but are still present at the gap perimeter.

Animals↗
PubMed1995

Eosinophil viability-enhancing activity in sputum from patients with bronchial asthma, Contributions of interleukin-5 and granulocyte/macrophage colony-stimulating factor.

To investigate the mechanisms of eosinophil activation in the airways of patients with asthma, we attempted to detect eosinophil-activating cytokines in sputum extracts obtained from asthmatic patients during acute attacks or in remission by eosinophil survival assay. Purified guinea pig eosinophils were cultured in the presence or absence of sputum extracts, and the eosinophil viability was measured on Day 4. Eosinophil viability in the presence of sputum extracts derived from patients during moderate or severe attacks was significantly higher than that for sputum obtained from patients in remission or during mild attacks or from those with other respiratory diseases, including bronchiectasis and diffuse panbronchiolitis (p < 0.05). The total symptom score during the week prior to sputum collection correlated with the eosinophil viability (rs = 0.79, p < 0.01). Eosinophil viability-enhancing activity (EVEA) in the sputum of asthmatic patients with moderate or severe attacks was neutralized by anti-IL-5 antibody and by anti-GM-CSF antibody by 19.9 +/- 13.7% and 76.9 +/- 8.2% (mean +/- SEM, n = 7), respectively. EVEA was completely neutralized by a combination of anti-IL-5 and anti-GM-CSF antibodies. There was a significant correlation between the concentration of eosinophil cationic protein (ECP) in sputum extracts and the eosinophil viability (rs = 0.54, p < 0.05). These findings suggest that IL-5 and GM-CSF are present in the sputum during asthma attacks and that these cytokines are at least partially responsible for eosinophil activation in asthma.

Animals↗
PubMed1995

Influence of aging on insulin sensitivity in essential hypertensives and normotensives.

Insulin resistance and hyperinsulinemia have been linked with essential hypertension. Age-associated increases in glucose intolerance and hypertension are also well established. To clarify the influence of aging on the insulin sensitivity, euglycemic hyperinsulinemic glucose clamp technique was carried out in 41 normotensive subjects and 42 patients with essential hypertension. The subjects of these groups were divided into two subgroups: young (< 40 years old) and middle-elderly (> or = 40 years old). Insulin sensitivity was assessed as M-value, the rate at which glucose must be infused to maintain a basal blood glucose level. In normotensive subjects, the young subgroup had a significantly higher M-value than did the middle-elderly subgroup. There was a significant negative correlation between age and M-value in normotensive subjects. On the other hand, there was no significant difference in M-value between the young and middle-elderly subgroups in the patients with essential hypertension. The age did not correlate with M-value in the hypertensive group. The normotensive subjects showed a significantly lower M-value than the hypertensive patients in the young group, but not in the middle-elderly group. These results indicate that 1) insulin sensitivity declines with age in normotensive subjects and that 2) insulin sensitivity is already diminished in the early stage of hypertension, and no further decrease in insulin sensitivity occurs with aging in essential hypertensive patients.

Adult↗
PubMed1995

Effects of hyperinsulinemia under the euglycemic condition on calcium and phosphate metabolism in non-obese normotensive subjects.

The effect of acute insulin infusion on the metabolism of calcium (Ca) and phosphate (P) was examined in 17 healthy subjects. They were hospitalized and kept on a constant diet for 5 days, and an euglycemic hyperinsulinemic glucose clamp was applied. Synthetic human insulin was infused at the rate of 40 mU/m2/min for 2 hr, and glucose was also infused to maintain basal glucose levels of each subject. The control study was performed in 8 of the 17 subjects, into whom 10% xylitol was infused for 2 hr at the rate of 100 ml/hr. The plasma insulin concentrations were 7.94 +/- 0.35 and 62.3 +/- 14.3 mU/liter before and after the glucose clamp technique, but serum free Ca ion was increased significantly (p < 0.05), and serum P and serum parathyroid hormone (PTH) were decreased significantly (p < 0.001). Creatinine clearance did not change during the glucose clamp technique. Urinary excretion of Ca (UCaV) was significantly higher after the glucose clamp than the control study. Fractional excretion of Ca (FECa) was increased significantly (p < 0.05), and urinary excretion of P (UPV) and fractional excretion of P (FEP) were decreased significantly (p < 0.05) under the hyperinsulinemic condition. The results suggested that, under the conditions of euglycemic hyperinsulinemia by glucose clamp technique, insulin increased the serum free Ca ion, and as a result, PTH was suppressed. Decreased PTH might induce calciuresis and enhance tubular P reabsorption under hyperinsulinemia. Insulin increased serum free Ca ion might relate to the vasodilating action of insulin by its decrease of intracellular free Ca ion in vascular smooth muscle.

Adult↗
PubMed1995

Serum levels of soluble interleukin-2 receptor in asthma patients.

We measured the serum concentration of soluble interleukin-2 receptor (sIL-2R) in asthma patients and healthy controls to evaluate T-lymphocyte activation in this disease. The SIL-2R concentrations in patients with asthma irrespective of presence of acute attacks were significantly higher than those of the controls (p < 0.001). Although the sIL-2R concentrations were similar in the patients with acute asthma and those in remission, levels in patients with moderate and severe asthma attacks were significantly higher than levels for patients in remission (p < 0.001). These results suggest that T-lymphocyte activation occurs in asthma patients and becomes more prominent during moderate and severe acute attacks.

Adolescent↗
PubMed1994

IL-1 beta regulates the expression of the Gi2 alpha gene via lipid mediators in guinea pig tracheal muscle.

When isolated guinea pig muscle preparations were incubated with human recombinant IL-1 beta, mRNA level of Gi2 alpha but not of Gs alpha increased in a time and dose dependent manner. The increase was partially blocked by inhibitors of lipoxygenase (NDGA) and cyclooxygenase (indomethacin) and PAF antagonist (SC47014A), while U46619 (thromboxane A2 mimetic), LTD4, 15-HETE and PAF partially mimicked it. The IL-1 beta induced Gi2 alpha expression was almost completely inhibited by anti-phospholipase A2 antiserum, whereas preimmune serum had no apparent effects. From these observations, we suggest that IL-1 beta first induces the synthesis and release of Type II inflammatory phospholipase A2, which in turn stimulates the expression of Gi2 alpha gene via production of various lipid mediators.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗