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Biomedical subjects

S Takata

Publications and source records attributed to S Takata.

At least 73 records · Page 4Linked to original sources
PubMed1997

Primary antiphospholipid syndrome and pulmonary hypertension with prolonged survival. A case report.

The outcome of patients with pulmonary hypertension (PHT) and antiphospholipid syndrome (APS) is usually fatal. The authors report the rare case of a patient with primary APS and nonthrombotic PHT who has survived for twenty years after the onset of PHT. In this case, the patient's PHT resembled the primary idiopathic variety with clear lung fields and normal perfusion on the lung scan, and the combination therapy with nitrate, digoxin, and diuretics had been performed. During her clinical course over twenty years, she had not experienced any critical pulmonary thrombosis that influenced the progression of nonthrombotic PHT or any other severe systemic involvement of APS.

Adult↗
PubMed1997

L-NAME-sensitive and -insensitive nonadrenergic noncholinergic relaxation of cat airway in vivo and in vitro.

The neurotransmitters responsible for neurogenic airway relaxation are still unknown. We investigated the effects of N omega-nitro-L-arginine methylester (L-NAME) on nonadrenergic and noncholinergic (NANC) relaxation evoked by electrical stimulation of vagus nerves in vivo and in vitro in cat. To that end, we measured pulmonary resistance during vagal nerve stimulation (VS) in vivo, and isometric tension of small bronchi (1-3 mm outer diameter) during electrical field stimulation (EFS) in vitro. During infusion of 5-hydroxytryptamine (5-HT), VS transiently decreased total pulmonary resistance in the presence of atropine and propranolol, with peak relaxation at several seconds after the VS and a gradual return to baseline within 2-3 min. L-NAME abolished the initial peak relaxation and reduced the peak amplitude, but did not affect the duration of the NANC relaxation. In small bronchi obtained from control cats, EFS evoked a biphasic NANC relaxation, comprising an initial fast component followed by a second slow component, and L-NAME (10(-5) M) selectively abolished the first component without affecting the second. Whilst in the small bronchi obtained from L-NAME pretreated cats, EFS elicited only the slow component of NANC relaxation, which was insensitive to L-NAME but sensitive to tetrodotoxin. These results indicate that nonadrenergic noncholinergic relaxation induced by vagal nerve stimulation during infusion of 5-hydroxytryptamine can be classified into two components, and that at least two neurotransmitters, including nitric oxide, are involved in the relaxation.

Airway Resistance↗
PubMed1997

[Effects of head-up tilting on vagal nerve activity in man].

OBJECTIVES: To evaluate the contribution of the vagal nerve activity in the cardiovascular postural adaptation, effects of decremental head-up tilting (90 degrees, 64 degrees, 53 degrees, 44 degrees, 37 degrees, 30 degrees, 24 degrees, 17 degrees, 12 degrees, 6 degrees and 0 degree) on time- and frequency-domain heart rate variability variables were analyzed in healthy young female. BACKGROUND: During head-up tilting, a hydrostatic venous pooling in the extremities occurs owing to gravity. To pump up the blood toward the upper body, the sympathetic nerve activity has been shown to play an important role. So, to date, few studies evaluated the effects of vagal nerve activity to stabilize the cerebral blood flow during head-up tilting. METHODS: Eight young female volunteers (age, 23.3 +/- 0.8 years; mean +/- SD) were evaluated. The electrocardiogram (ECG) by bipolar chest leads was recorded continuously during procedures, and the bed was tilted at 0.1 interval of sine function of tilting angle from upright position (90 degrees) to supine position (0 degree). The time domain measurements of cycle length variability (co-efficient of variance in percent for R-R intervals [CVRR], number of differences between adjacent R-R intervals that are > 50ms [RR50]) and the frequency domain measurements of low (0.08 to 0.15Hz, LF), high (0.15 to 0.40Hz, HF) and total (0.08 to 0.40, TF) power were performed to assess the cardiac sympathetic and vagal nerve activity. RESULTS: The CVRR showed no significant change during decremental head-up tilting, whereas the RR50 and the square root of HF power, more specific indices of cardiac parasympathetic tone, showed significant negative linear correlations to the sine of the tilting angle. In markers of cardiac sympathetic tone, there were significant positive correlations between the sine of the tilting angle and the normalized LF power or the LF-to-HF power ratio (LF/HF). CONCLUSION: These findings suggest that, in healthy young female, not only cardiac sympathetic nervous system but also cardiac vagal nervous system respond linearly to the change in body axis component of gravity, and they may contribute reciprocally and coordinately to cardiovascular postural adaptation.

Adult↗
PubMed1997

Assessment of improvement of myocardial fatty acid uptake and function after revascularization using iodine-123-BMIPP.

UNLABELLED: We used beta-methyl iodophenyl pentadecanoic acid (BMIPP) to evaluate changes in myocardial fatty acid utilization before and after revascularization and the ability of BMIPP to predict functional recovery in patients with chronic coronary artery disease. METHODS: Thirty-four patients with chronic coronary artery disease (60 +/- 10 yr) underwent BMIPP and 201Tl SPECT (stress-reinjection 201Tl in 29 patients and resting 201Tl in 5 patients) before and 2-5 wk after percutaneous transluminal angioplasty (n = 23) or coronary artery bypass surgery (n = 11). Cardiac function was evaluated by gated blood-pool scintigraphy (n = 26) or two-dimensional echocardiography (n = 8) before and after revascularization. RESULTS: In 32 patients with reduced BMIPP uptake before revascularization, scintigraphic findings with 201Tl improved in 28 patients after revascularization. In these 28 patients, BMIPP uptake improved in 20 patients (71%). Wall motion abnormality was observed in 16 of these 20 patients before revascularization, with 15 showing wall motion improvement after revascularization. In eight patients without improvement of BMIPP uptake, despite 201Tl uptake improvement, wall motion abnormality was observed in four patients before revascularization; after revascularization, one showed wall motion recovery, and three did not. Ejection fraction (EF) improvement after revascularization correlated best with the area of improved BMIPP uptake (r = 0.84, p < 0.0005). EF improvement also correlated with the area of improved reinjection 201Tl uptake (r = 0.54, p < 0.05) and improved 201Tl uptake at stress after revascularization (r = 0.48, p < 0.05). The area of discordant uptake of BMIPP less than reinjection 201Tl uptake before revascularization was a good predictor of EF improvement after revascularization (r = 0.58, p < 0.01); however, the area of reversible 201Tl defect was not (r = 0.34, p = 0.15). CONCLUSION: In patients with chronic coronary artery disease, functional improvement after revascularization is closely related to the recovery of BMIPP uptake. Discordant BMIPP uptake less than reinjection 201Tl uptake is a potential predictor of functional recovery.

Angioplasty, Balloon, Coronary↗
PubMed1996

Anti-DNA antibody kinetics following selective removal by adsorption using dextran sulphate cellulose columns in patients with systemic lupus erythematosus.

The aim of this study is to determine by mathematical analysis which of two models, the one- or the two-compartment model, more closely approximates the kinetics of anti-dsDNA following immunoadsorption procedures in patients with systemic lupus erythematosus. Titers of anti-dsDNA were measured at specified intervals after apheresis to each model by nonlinear least-squares methods, and Akaike's Information Criterion (AIC) was calculated to determine which model most approximately described the kinetics. The AIC of the two-compartment model was larger than that of the one-compartment model in all 14 SLE patients (P < .001). Therefore, the one-compartment model is thought to be suitable. The generation rate and catabolic rate of anti-dsDNA were obtainable using this model. The anti-dsDNA replenishment curve after an immunoadsorption session was defined by only two parameters: the generation and catabolic rates of anti-dsDNA.

Adolescent↗
PubMed1996

Thromboxane A2 mimetic (U-46619) induces hyperresponsiveness of smooth muscle in the canine bronchiole, but not in the trachea.

It has been reported that cholinergic agonists induce bronchoconstriction by directly stimulating M3 muscarinic receptors on the surfaces of smooth muscle cells. Although thromboxane A2 (TXA2) has been demonstrated to induce airway hyperresponsiveness to cholinergic agonists in vivo, it does not affect the contractile response of smooth muscle to cholinergic agonists in vitro. To investigate the causes for the discrepancy between the in vivo and in vitro data, we compared the effects exerted by a TXA2 mimetic, U-46619, on the smooth muscle of canine trachea and bronchiole. We measured the contractile response to exogenously applied acetylcholine (ACh) before and after the application of a subthreshold dose of U-46619. The subthreshold dose was determined as that dose which did not induce smooth muscle contraction, this being 10(-9) M in the present study. The contractile responses of tracheal strips to ACh were not affected by the subthreshold dose of U-46619. By contrast, the responses of bronchiolar rings were significantly enhanced by this subthreshold dose. The excitatory effect of U-46619 on the ACh-induced contraction was completely prevented by treatment with a TXA2 antagonist, BAY u3405. These results indicate that TXA2 directly increases the responsiveness of smooth muscle in the bronchiole, and suggest that increases in the responsiveness of small airways may play an important role in the development of the airway hyperresponsiveness induced by TXA2.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1996

Thromboxane causes airway hyperresponsiveness after cigarette smoke-induced neurogenic inflammation.

We investigated the role of neurogenic inflammation and the subsequent mechanisms in cigarette smoke-induced airway hyperresponsiveness in guinea pigs. Exposure to cigarette smoke was carried out at tidal volume for 3 min. Airway responsiveness to histamine was determined before and after smoke exposure followed by bronchoalveolar lavage (BAL). Plasma extravasation was evaluated by measuring the extravasation of Evans blue dye in the airway. Cigarette smoke produced significant airway hyperresponsiveness and plasma extravasation, with an influx of neutrophils in BAL fluid. FK-224 (10 mg/kg i.v.), a tachykinin antagonist at NK1 and NK2 receptors, significantly inhibited these changes. The thromboxane (Tx) B2 concentration was increased in BAL fluid after smoke exposure and was significantly inhibited by FK-224. OKY-046 (10 mg/kg i.v.), a Tx synthase inhibitor, significantly inhibited airway hyperresponsiveness but had no effect on neutrophil influx or plasma extravasation. The results suggest that neurogenic inflammation and the subsequent generation of Tx in the airway are important in the development of the airway hyperresponsiveness induced by cigarette smoke.

Animals↗
PubMed1996

Cultured epithelial cells release cyclooxygenase-dependent and cyclooxygenase-independent factors that inhibit cholinergic contraction of canine airway smooth muscles.

We observed the effects of supernatants from cultured epithelial cells on the contraction of tracheal smooth muscle evoked by acetylcholine (ACh) or by electrical field stimulation (EFS). Cultured canine tracheal epithelial cells were incubated in Krebs solution with or without indomethacin (10(-5)M) for 30 and 120 min. The amplitude of the tracheal smooth muscle contractions evoked by EFS or exogenously applied ACh were measured before and after the application of each supernatant in the combined presence of both indomethacin (10(-5)M) and propranolol (10(-6)M). The control supernatant incubated without indomethacin markedly suppressed the amplitude of the contraction evoked by EFS, but not by ACh. The supernatant incubated with indomethacin for 30 min did not show any effects on the contractile responses evoked by EFS or ACh. However, the supernatants from the cultured epithelial cells incubated for a longer period (120 min) in the presence of indomethacin significantly suppressed the contraction evoked by EFS, but not by ACh. The prostaglandin E2 (PGE2) concentration was markedly higher in the supernatants incubated without indomethacin (1.39 +/- 0.51 ng/ml, 30 min incubation) than in those with indomethacin (0.02 +/- 0.01 ng/ml, 30 min incubation, and 0.06 +/- 0.01 ng/ml, 120 min incubation). To determine whether PGE2 is responsible for the inhibitory effect of the supernatants, we evaluated the effects of PGE2 on the resting tone, and EFS- or ACh-evoked contraction. 10(-12) to 10(-6) M of PGE2 showed no significant effect on the resting tone. 10(-9) M of PGE2, corresponding to the concentration of the supernatants incubated without indomethacin, and 10(-11) M of PGE2, to that of the supernatants incubated with indomethacin, showed a similar extent of inhibitory effects to the corresponding supernatants on the EFS-evoked contraction, and no effect on the ACh-evoked contraction. These results suggest that cultured airway epithelial cells release at least two factors spontaneously even without stimulation. One of these factors may be prostanoid (PGE2), which acts prejunctionally to inhibit the contractile response. The other factor is distinct from prostanoid and inhibits smooth muscle contraction, presumably by suppressing ACh release from vagus nerve termini.

Acetylcholine↗
PubMed1996

Compensatory enlargement of angiographically normal coronary segments in patients with coronary artery disease. In vivo documentation using intravascular ultrasound.

Intravascular ultrasound (IVUS) frequently reveals plaque formation at sites with a normal angiographic appearance. However, whether angiographically normal coronary arteries undergo adaptive expansion in vivo remains uncertain. The authors studied 12 patients (11 men, 1 woman; mean age fifty-three +/- ten years [mean +/- SD]) with focal coronary stenosis. Sixty IVUS images from angiographically normal coronary segments were analyzed (14 left main, 44 left anterior descending, and 2 left circumflex coronary arteries). The mean percent area stenosis was 36 +/- 5% and the circular shape factor of the lumen cross section averaged 0.97 +/- 0.02. Both total arterial area and internal elastic lamina area increased as the plaque area expanded (y = 2.13x + 8.07, r = 0.87, P = 0.0001; y = 2.06x + 4.57, r = 0.87, P = 0.0001, respectively), suggesting that for every 1 mm2 increase in plaque area, the total arterial area increased by approximately 2.13 mm2 and the internal elastic lamina area increased by approximately 2.06 mm2. The lumen area also increased as the plaque area expanded (y = 1.06x + 4.57, r = 0.68, P = 0.0001), suggesting that for every 1 mm2 increase in plaque area, the lumen area increased by approximately 1.06 mm2. The medial area did not correlate with the plaque area (r = 0.15, P = 0.26). Thus, compensatory enlargement precedes development of angiographically, detectable coronary atherosclerosis. Furthermore, in early stages of atherosclerosis, arterial enlargement may overcompensate for plaque area. The reduction of the total medial mass does not appear to contribute to the mechanism of compensatory enlargement.

Adaptation, Physiological↗
PubMed1996

Role of thromboxane-A2 and cholinergic mechanisms in bronchoconstriction induced by cigarette smoke in guinea-pigs.

Acute exposure to cigarette smoke provokes bronchoconstriction and increases the concentration of thromboxane (Tx) A2 in bronchoalveolar lavage (BAL) fluid. The purpose of this study was to investigate the role of TxA2 and cholinergic mechanisms in the airway response induced by exposure to cigarette smoke in guinea-pigs. Anaesthetized animals were exposed to 200 puffs of smoke for 10 min. The amount of Evans blue dye extravasated into the bronchial tissue was then measured BAL was performed to determine cell counts and the concentration of TxB2, a stable metabolite of TxA2. The effects of pretreatment with a Tx synthase inhibitor, OKY-046 (10 mg.kg-1), and/or atropine (1 mg.kg-1) were evaluated. Exposure to cigarette smoke caused significant bronchoconstriction (284 +/- 33% of baseline pulmonary resistance (RL)) and plasma extravasation (30.0 +/- 3.8 vs 16.8 +/- 2.6 ng.mg-1 of sham control; main bronchi). OKY-046 or atropine significantly inhibited the bronchoconstriction to a similar extent, without affecting the plasma extravasation. Combined use of these compounds had no additive effect. The cigarette smoke caused significant increase in TxB2 (48 +/- 10 vs 14 +/- 1 pg.mL-1 of sham control) in BAL fluid, which was abolished by OKY-046 but not by atropine. The cellularity in BAL fluid was not different among groups. These results suggest that the bronchoconstriction induced by cigarette smoke is partially mediated by thromboxane A2, which is dependent on a cholinergic pathway.

Animals↗
PubMed1996

IgA2 genotyping by polymerase chain reaction (PCR) using allele-specific amplification primers.

A method of genotyping IgA2 alleles in the human immunoglobulin alpha 2 heavy chain constant region (C alpha 2 gene) was developed by using the polymerase chain reaction (PCR). By this method, the genotype was determined by discriminating base substitution in the 3'-flanking region of alleles, A2m*1 and A2m*2, which manifest A2m serum types, by nested PCR using allele-specific primers. Three types, IgA2*1/IgA2*1, IgA2*2/IgA2*1, and IgA2*2/IgA2*2, were detected from DNA extracted from lymphocytes. Genotyping was possible from 100 pg of DNA by this method. The estimated allele frequency in 318 Japanese subjects was 0.561 for IgA2*1 and 0.439 for IgA2*2. Analysis of 29 cases of paternity tests suggested that the data follow Mendel's law of inheritance. This genotype could also be detected in whole blood, blood stains, saliva stains, and various organs and tissues. These results suggest the usefulness of the present method for paternity testing and individual identification in forensic medicine.

Adult↗
PubMed1996

[Studies on anti-DNA antibodies associated with renal involvement by enzyme-linked immunosorbent assay in patients with systemic lupus erythematosus].

It has been reported that a significantly higher incidence of lupus nephritis was found in patients with high avidity anti-DNA antibodies. Radioimmunoassay (Farr's assay) is a method which enables to detect high avidity anti-DNA antibodies, whereas enzyme-linked immunosorbent assay (ELISA) can detect anti-DNA antibodies from low to high avidity. There are, however some patients who had high levels of anti-DNA antibodies by Farr's assay without renal involvement. In this study, ELISA was developed to detect IgG anti-DNA antibodies highly associated with lupus nephritis by changing salt concentration of reaction buffer solution. Levels of a fraction, we call [0.1 M - 0.3 M] fraction, which was obtained from the antibody levels measured under 0.1 molar of sodium chloride (NaCl) subtracted by antibodies levels under 0.3 molar of NaCl solution were found to be significantly higher in patients with urinary protein (p = 0.0074) and low serum complement (C 3 less than 50 mg/dl; p = 0.0026, C 4 less than 10 mg/dl; p = 0.0280 and CH 50 less than 30 U/mL; p = 0.0662). Among the patients with hypocomplementemia, levels of [0.1 M - 0.3 M] fraction were significantly higher in patients with urinary protein than in patients without renal involvement. This fraction might be consistent with anti-DNA antibodies with intermediate avidity that are related to lupus nephritis. The ELISA procedure established in this study is showed to be a available method to detect anti-DNA antibodies associated with renal disease in patients with systemic lupus erythematosus.

Antibodies, Antinuclear↗
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

Ozone exposure suppresses epithelium-dependent relaxation in feline airway.

We examined the effect of exposure to ozone on the epithelium-dependent relaxation (EpDR) of bronchioles evoked by electrical field stimulation (EFS) in a feline model with hyperresponsive airways induced by exposure to ozone. Airway responsiveness was assessed by measuring the increases in total pulmonary resistance (RL) produced by aerosolized acetylcholine (ACh) in vivo. Airway responsiveness was also measured in vitro in dissected bronchiolar ring preparations. Exposure to ozone (3 ppm, 2h) significantly increased the airway responsiveness in vivo. The concentration of ACh required increasing RL to 200% of the baseline value, decreased from 1.97 mg/ml (GSEM 1.94) to 0.12 mg/ml (GSEM 1.77, p < 0.01) after exposure to ozone. EFS evoked atropine-, guanethidine-, and tetrodotoxin-resistant relaxations in the control bronchiolar rings precontracted by 5-hydroxytryptamine. Such relaxation was significantly suppressed by the mechanical denudation of epithelium, confirming that it was epithelium dependent. The amplitude of the EpDR was significantly suppressed in the animals exposed to ozone. These results suggest that EpDR is present in cats, and that its inhibition may contribute to the development of airway hyperresponsiveness.

Acetylcholine↗
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

Long-term clinical evaluation of an adsorbent column (BM-01) of direct hemoperfusion type for beta 2-microglobulin on the treatment of dialysis-related amyloidosis.

The clinical efficacy and safety of a beta 2-microglobulin (beta 2M) adsorbent column, BM-01, on the treatment of dialysis-related amyloidosis were investigated in 7 hemodialysis patients for more than 6 months. The percent reduction of serum beta 2M was more than 60-70%, and the level at the end of each session was less than 10 mg/L in almost all patients. The amount of beta 2M removed was calculated as more than 200-300 mg/session. The results demonstrated that BM-01 performed very well for removing beta 2M, was capable of maintaining less than 25 mg/L of time average concentration (TAC) for beta 2M, and improved the clinical symptoms. Clinically severe side effects were not observed. We recommend that BM-01 should undergo further evaluation for its usefulness in the long-term treatment of dialysis-related amyloidosis, though treatment with the column may not be successful in preventing the onset of the disease.

Acrylic Resins↗