Biomedical subjects

M Shigyo

Publications and source records attributed to M Shigyo.

31 records · Page 2Linked to original sources

PubMed1996

Establishment of a series of alien monosomic addition lines of Japanese bunching onion (Allium fistulosum L.) with extra chromosomes from shallot (A. cepa L. aggregatum group).

Forty one plants of alien monosomic addition lines of Allium fistulosum L. with extra chromosomes from A. cepa L. Aggregatum group (FF + nA) were produced through the second backcross of amphidiploids between these two species to A. fistulosum. Identification of the extra chromosomes in the 16 plants by elaborate karyotype analyses indicate that a complete series (eight different types) of the alien monosomic addition lines was established in Allium for the first time in this study. Chromosomal locations of malate dehydrogenase (MDH) gene, triosephosphate isomerase (TPI) gene and 5S rDNA of A. cepa Aggregatum group were determined using the series; The gene locus Mdh-1 was located on 4A, Tpi-1 on 3A and a 5S rDNA locus on 7A. Our previous and present studies using the alien monosomic addition lines revealed 11 genetic markers (isozyme and 5S rDNA) assigned to all eight chromosomes of A. cepa Aggregatum group, and these markers reconfirmed the completion of the series. Extra chromosomes of 25 other plants were examined by means of simple analyses of the chromosome markers and karyotypes. Of the total 41 plants, frequencies of the alien monosomic addition lines with extra chromosomes 1A to 8A were as follows: 1A, 5 plants; 2A, 3; 3A, 5; 4A, 9; 5A, 4; 6A, 2; 7A, 11; and 8A, 2.

Chromosome Mapping↗

PubMed1996

BAY u3405, a thromboxane A2 antagonist, reduces bronchial hyperresponsiveness in asthmatics.

OBJECTIVE: Thromboxane A2 (TXA2) is reported to induce bronchial hyperresponsiveness along with the well-documented bronchoconstrictor action on smooth muscles. We examined the effect of the TXA2 antagonist, BAY u3405, on bronchial hyperresponsiveness to methacholine (MCh) in asthmatics. PATIENTS: Twelve adult asthmatics were studied in a randomized, double-blind, placebo-controlled, crossover fashion. DESIGN: Following a 2-week run-in period, the subjects were administered 75 mg of BAY u3405 or placebo orally, twice a day for 2 weeks each in a crossover design, interposing a 2-week washout period. Bronchial hyperresponsiveness was measured by the astograph method. Briefly, the respiratory resistance (Rrs) was measured by the forced oscillation method during continuous inhalation of MCh in stepwise incremental concentrations, until Rrs reached twice the baseline value. Bronchial hyperresponsiveness was evaluated as the minimum cumulative dose (Dmin) of MCh that induced an increase in Rrs. Dmin was calculated so that 1 U of Dmin equals to 1 min of inhalation of aerosol solution at 1.0 mg/mL during quiet breathing. RESULTS: Three subjects were withdrawn from the evaluation because they had asthmatic attacks or wheezing during the study. The Dmin value of 0.533 U (GSEM 1.675) after the BAY u3405 treatment was significantly greater than that of 0.135 U (GSEM 1.969) after the placebo treatment (p = 0.0139). There were no safety concerns in either treatment group. CONCLUSION: We conclude that BAY u3405 may be a useful drug for attenuating bronchial hyperresponsiveness in bronchial asthma.

Adult↗

PubMed1996

[Clinical usefulness of helical computed tomography in evaluating chronic obstructive pulmonary diseases].

To assess the usefulness of healical computed tomography (CT) in evaluating pathophysiological abnormalities in chronic obstructive pulmonary disease, we compared the results of helical CT with those of pulmonary-function tests in 46 subjects with pulmonary emphysema. We obtained 3-D images of emphysematous lung tissue by choosing voxels with values less than -930 HU because the mean CT score in 10 normal subjects was -869 +/- 29 HU. For each patient the total lung volume (TLV) was computed from the 3-D image of the entire lung with CT score less than -600 HU, and the volume of emphysematous lung tissue (ELV) was computed from the lung with CT score less than -930 HU. TLV measured on inspiration correlated significantly with TLC (r = 0.601, p < 0.001), and TLV measured on expiration correlated significantly with RV (r = 0.836, p < 0.0001). The difference between inspiratory TLV and expiratory TLV correlated significantly with VC (r = 0.781, p < 0.001). ELV both on inspiration and on expiration correlated significantly with FEV1/FVC (p < 0.001) and with RV (p < 0.01, p < 0.001, respectively). These results suggest that the volume data obtained by helical CT reflect functional abnormalities of the lung. In addition to volume data, the distribution of abnormal lung tissue is easily assessed by helical CT. We conclude that helical CT is useful in evaluating pathophysiological abnormalities in chronic obstructive pulmonary disease.

Humans↗

PubMed1995

Effect of BAY u3405, a thromboxane A2 receptor antagonist, on neuro-effector transmission in canine tracheal tissue.

Thromboxane A2 (TXA2) is reported to potentiate vagal nerve neuro-effector transmission in airway smooth muscle tissue. We investigated the effects of BAY u3405 (3(R)-[[4-fluorophenyl)sulfonyl]amino]-1,2,3,4,-tetrahydro-9H-carbazole - 9-propanoic acid), a potent and selective TXA2 receptor antagonist, on the increase in vagal nerve neuro-effector transmission induced by a TXA2 mimetic, U-46619, in the canine trachea. We measured the contractions of canine tracheal smooth muscle evoked by electrical field stimulation (EFS) and by acetylcholine (ACh) in the presence and absence of a subthreshold dose of U-46619 (the highest dose that did not induce any smooth muscle contraction). We then examined whether BAY u3405 inhibited the effect of U-46619 on tracheal smooth muscle. The following results were obtained: (i) subthreshold doses of U-46619 (10(-10) M and 10(-9) M) significantly increased the amplitude of the contractions evoked by EFS; (ii) by contrast, U-46619 had no effect on the contractile response of smooth muscle to exogenously applied ACh; (iii) the contraction evoked by EFS was completely abolished by the application of atropine (10(-6) M) or tetrodotoxin (10(-7) M), indicating that EFS caused the smooth muscle contraction through the release of ACh from vagal nerve terminals; and (iv) pretreatment with BAY u3405 (10(-6) M) abolished the excitatory action of U-46619 on the amplitude of twitch contraction evoked by EFS in the trachea. These results indicate that U-46619, at low concentrations, has a prejunctional action stimulating neuro-effector transmission, presumably increasing ACh release from vagal nerve terminals through TXA2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

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

PubMed1995

[Clinical efficacy of neoadjuvant M-VAC chemotherapy for invasive bladder cancer].

We clinically evaluated the efficacy of neoadjuvant M-VAC (methotrexate, vinblastine, doxorubicin and cisplatin) therapy followed by radical cystectomy. A total of 21 patients with locally invasive bladder cancer received neoadjuvant M-VAC therapy with an average of 2.4 courses (range 2-4). Of the 21 patients, 4 had stage T2N0M0, 11 had stage T3aN0M0, 5 had stage T3bN0M0 and 1 had stage T4N0M0 at diagnosis. Of the 21 patients, 3 had clinically complete responses (cCR) and 12 had partial responses (cPR), for an overall response rate of 71.4%. The patients who responded to the chemotherapy (cCR + cPR) had a 2-year disease free rate of 80.0% in contrast to 50.0% for the remaining patients who did not respond. A pathological response (pT0, pT1) was achieved in 6 (28.6%) of the 21 patients. The 5 patients in this group remain free of disease for 15 to 79 months (mean 58.8 months). These preliminary results suggest that the patients who achieve either a complete or partial response, in particular those had pathological stage of pT0 or pT1, may have a favorable clinical course.

Adult↗

PubMed1995

A rare case of disseminated intravascular coagulation caused by the nonionic contrast medium iohexol.

Nonionic contrast media are reported to cause serious adverse reactions less often than ionic contrast media. However, we treated an otherwise healthy woman with a left ureteral stone in whom disseminated intravascular coagulation developed due to intravenous administration of the nonionic contrast medium iohexol. We discuss the clinical course and possible causes of disseminated intravascular coagulation. Our case emphasizes that nonionic contrast media are not free from serious adverse reactions although the incidence seems extremely low.

Disseminated Intravascular Coagulation↗

PubMed1995

[Inhibitory non-adrenergic, non-cholinergic nerves and nitric oxide].

We studied the role of nitric oxide and inhibitory non-adrenergic, non-cholinergic (i-NANC) nerves in the regulation of airway responsiveness in anesthetized and mechanically ventilated cats. Vagal stimulation caused marked bronchodilation in the cats with sustained bronchoconstriction in the presence of atropine and propranolol. The bronchodilation evoked by vagal stimulation was completely abolished by hexamethonium (2 mg/kg). L-NG-nitroarginine methyl ester (L-NAME; 8 mg/kg + 2 mg/kg/min) significantly suppressed the relaxation evoked by vagal stimulation; the effect was particularly noticeable soon after the stimulation. Hexamethonium significantly increased airway responsiveness to serotonin: the PC200 decreased from 0.346 mg/ml (GSEM 1.23) without hexamethonium to 0.44 mg/ml (GSEM 1.63) with hexamethonium (p < 0.05). L-NAME shifted the dose-response curve to serotonin significantly to the left: the PC200 decreased from 0.261 mg/ml (GSEM 1.,40) without L-NAME to 0.056mg/dl (GSEM 1.38) with L-NAME (p < 0.05). Inhalation of citric acid (20%) caused marked bronchodilation during serotonin-induced bronchoconstriction. This bronchodilation occurred in the presence of atropine and propranolol and was inhibited by hexamethonium, therefore it was probably caused by a reflex mediated by i-NANC nerves. Furthermore, the bronchodilation induced by i-NANC nerves was significantly suppressed by L-NAME. These results suggest that nitric oxide is an important i-NANC transmitter that can modulate airway responsiveness.

Animals↗

PubMed1994

Ipratropium bromide protects against bronchoconstriction during bronchoscopy.

Pulmonary function is reportedly impaired by fiberoptic bronchoscopy. We investigated the effect of two anticholinergic agents, intramuscular atropine and inhaled ipratropium bromide, on bronchoconstriction in 29 patients who were undergoing diagnostic bronchoscopy. The patients were divided into three groups; the first received 0.5 mg of atropine intramuscularly; the second took four puffs of 0.02 mg ipratropium bromide aerosolized by a metered-dose inhaler, and the third inhaled four puffs of a placebo. Fifteen minutes later a standardized topical anesthetic, lidocaine, was administered, and a bronchoscopic examination was performed. Pulmonary function was measured before and 15 minutes after each step. Pulmonary function was not affected by the treatment with anticholinergics or the placebo. In the placebo and the atropine groups, the topical anesthesia produced significant reductions in forced expiratory volume in 1 second (FEV1) and peak expiratory flow rate (PEFR); further reductions in these values were observed after bronchoscopy. In the group treated with ipratropium bromide there were no significant changes in FEV1 and PEFR after topical anesthesia. Bronchoscopy induced significant reductions in FEV1 and PEFR, but the changes were significantly smaller than those seen in the placebo and atropine groups. The results suggest that the deleterious effect of bronchoscopy on pulmonary function is due to topical lidocaine anesthesia and to the bronchoscopic examination itself. Inhaled ipratropium bromide protects against these deleterious effects, whereas intramuscular atropine does not.

Administration, Inhalation↗

PubMed1994

Airway epithelial cells modulate cholinergic neurotransmission in dog trachea.

We investigated the effects of epithelial cells on excitatory cholinergic neurotransmission in dog trachea, to shed more light on the role of airway epithelial cells in regulating airway responsiveness. Airway epithelial cells were prepared by an enzymatic dissociation of the tracheal mucosa using protease-free collagenase. Tracheal smooth muscle contractions evoked by electrical field stimulation (EFS) or acetylcholine (ACh) were measured before and after the application of epithelial cells. Isolated and dispersed epithelial cells (3 x 10(5) cells/ml) suppressed the amplitude of the twitch-like contractions evoked by EFS in the combined presence of guanethidine sulfate (10(-6) M) and indomethacin (10(-5) M). In contrast, epithelial cells did not affect the contraction evoked by exogenously applied ACh. Atropine (10(-6) M) or tetrodotoxin (10(-7) M) abolished the contraction evoked by electrical field stimulation. These findings indicate that airway epithelial cells inhibit the excitatory neurotransmission of the vagus nerve, presumably by suppressing the release of ACh. Airway epithelial cells may therefore play an important role in regulating the response of smooth muscle.

Acetylcholine↗

PubMed1994

VIP antagonists enhance excitatory cholinergic neurotransmission in the human airway.

It has been reported that a low concentration of exogenously applied vasoactive intestinal peptide (VIP) suppresses the release of acetylcholine (ACh) from vagus nerve terminals in the ferret and feline trachea. There has been, however, no documentation of the prejunctional action of VIP in the human airway. We observed the effects of VIP and VIP antagonists on cholinergic excitatory neuro-effector transmission in the human bronchus to study the possible role of endogenous VIP on excitatory neurotransmission. In the human bronchus, VIP (10(-10) to 10(-7) M) showed no effect on either the contractions evoked by electrical field stimulation (EPS) or those evoked by ACh. To investigate the possible role of endogenous VIP on the human bronchus, we observed the effects of the VIP antagonists [4-Cl-D-Phe6,Leu17]-VIP and [Ac-Tyr1,D-Phe2]-GRF(1-29)-NH2 on excitatory neuro-effector transmission. Both VIP antagonists (10(-8) M) significantly enhances the contractions evoked by EFS without affecting the ACh sensitivity of smooth muscle cells. These results indicate that VIP antagonists have a prejunctional action that enhances excitatory neurotransmission. This study suggests that endogenous VIP may suppresses ACh release from the vagus nerve terminals in the human airway. It is also suggested that exogenously applied VIP may be inactivated by some mechanism in the human airway.

Acetylcholine↗

PubMed1990

[Malignant lymphoma with acute renal failure and nephrotic syndrome].

A case of non-Hodgkin's lymphoma with nephrotic syndrome and acute renal failure is described. A 60-year-old Japanese male was admitted to our hospital in November, 1988, because of lymphadenopathy, fever, night sweat, weight loss. On physical examination, lymphadenopathy was present in both cervical, submandibular, supraclavicular, axillary and inguinal regions. The leukocyte count was 9,700/microliters with 85% neutrophils and 2% atypical lymphocytes. Renal function was normal. Lymph node biopsy showed non-Hodgkin's lymphoma of diffuse, large cell type. Immunohistologic examination showed T cell type. A few days later, he fell into acute renal failure. After systemic chemotherapy, he showed prompt improvement in renal function. Echo and computerized tomography (CT) of abdomen revealed no compression of the ureters and bladder. Renal biopsy findings suggested mesangium proliferative glomerulonephritis without invasion of tumor cells. Our case seemed to be rare and was compared with previous reports.

Acute Kidney Injury↗

PubMedDate not supplied

PACAP reverses airway hyperresponsiveness induced by ozone exposure in guinea pigs.

BACKGROUND: We previously demonstrated that pituitary adenylate cyclase activating peptide (PACAP) inhibits airway smooth muscle contraction and plasma extravasation. OBJECTIVE: We thus hypothesized that PACAP may regulate airway responsiveness through these effects and examined the effects of exogenously applied PACAP on the airway hyperresponsiveness induced by ozone exposure. METHODS: Ozone exposure was carried out in awake, spontaneously breathing guinea pigs using 3 ppm for 2 h. Airway responsiveness to histamine was determined before and 30 and 90 min after the termination of ozone exposure for 2 h in anesthetized animals. Extravasation of Evans blue was measured before and 90 min after the termination of ozone exposure. Either PACAP (10(-6) mol/kg) or vehicle was administered intravenously 60 min after exposure. The airway responsiveness was expressed as the concentration of histamine required to produce a 200% increase in total pulmonary resistance (PC(200)). RESULTS: Ozone exposure caused a significant decrease in PC(200) (n = 5, p < 0.05) 30 min after ozone exposure which persisted 90 min thereafter, thus suggesting that ozone caused airway hyperresponsiveness. PACAP significantly suppressed the increase in airway hyperresponsiveness induced by ozone 90 min after exposure (n = 5, p < 0.05). In contrast, this peptide did not have any effect on plasma extravasation. CONCLUSION: We thus conclude that PACAP decreases ozone-induced airway responsiveness, and, therefore, intravenously administered PACAP may be useful in reversing airway hyperresponsiveness.

Animals↗

PubMedDate not supplied

Once-daily administration of fluticasone propionate does not worsen controlled airway hyperresponsiveness in patients with asthma.

BACKGROUND: Inhaled steroids are currently the most important drugs for asthma patients, but compliance tends to be low. Compliance could be improved by reducing the number of daily administrations. OBJECTIVES: In the present study, we compared once- and twice-daily administration of fluticasone propionate (FP) to determine the differences in efficacy. METHODS: Subjects were 40 patients diagnosed with bronchial asthma with stable symptoms and pulmonary functions who were on twice-daily FP administration of 100 microg. There were 14 men and 26 women ranging from 29 to 72 years of age. After a 4-week observation period, subjects were randomized into two administration groups by the envelope method and followed for 8 weeks: group A, once-daily administration (200 microg of FP at night), and group B, twice-daily administration (100 microg of FP in the morning and at night). Clinical symptoms, pulmonary functions and airway responsiveness were compared between these two groups. RESULTS: No significant deterioration in clinical symptoms, pulmonary functions and airway responsiveness were observed in group A compared with group B. CONCLUSIONS: These results demonstrate that once-daily FP administration is as effective as twice-daily administration, and that it may improve the compliance for inhaled steroids.

Administration, Inhalation↗