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Biomedical subjects

S Takata

Publications and source records attributed to S Takata.

At least 55 records · Page 3Linked to original sources
PubMed1999

Circular vection in patients with age-related macular degeneration.

We have used optokinetic stimulation in patients with unilateral age-related macular degeneration (AMD) and central scotoma to investigate the possible contribution of the central visual field to circular vection (CV). Six patients aged 42-73 years with unilateral AMD and an aged-matched control group of nine elderly adults aged 47-75 years were examined. Monocular visual field defects were verified with the Goldmann perimeter by kinetic perimetry. The device used to induce CV was a random dot pattern projected onto a hemispherical dome with a radius of 75 cm. The pattern was rotated horizontally at a constant acceleration of 1 deg/s2. Monocular stimuli were randomly repeated two to three times in both temporal-nasal (T-N) and nasal-temporal (N-T) directions. The latency of onset of CV was measured for each stimulus presentation. In the age-matched control group the CV latencies varied from 4.2 to 72.0 s. In each case, however, the CV latencies were stable. No significant differences in CV latencies were found between right and left eyes in both stimulus directions (p > 0.05). In patients with AMD, no statistically significant difference in CV latency was found between the affected and unaffected eyes (p > 0.05). Marked central visual field loss in AMD does not significantly impair peripherally induced CV. Our results are compatible with the hypothesis that the peripheral retina dominates CV.

Aged↗
PubMed1998

Role of adrenergic nervous system in cigarette smoke-induced bronchoconstriction in guinea pigs.

The goal of this study was to clarify the role of the adrenergic nervous system in bronchoconstriction induced by exposure to cigarette smoke in guinea pigs. Artificially ventilated animals were exposed to 160 puffs of smoke for 8 min. Bronchoconstriction was assessed as a percentage of the baseline total pulmonary resistance (RL). The effects of pretreatment with phentolamine (0.1 mg/kg, i.v.), propranolol (1 mg/kg, i.v.), and/or atropine (1 mg/kg, i.v.) were evaluated. Exposure to cigarette smoke caused significant bronchoconstriction. Phentolamine, an alpha-adrenoceptor antagonist, significantly inhibited cigarette smoke-induced bronchoconstriction, while propranolol, a beta-adrenoceptor antagonist, significantly enhanced it. Combined use of these compounds further enhanced the bronchoconstriction. All of modulations of the bronchoconstriction by adrenoceptor antagonists were completely abolished by pretreatment with atropine. Phentolamine and/or propranolol had no effect on the bronchoconstriction induced by inhaled acetylcholine. Pretreatment with yohimbine (0.5 mg/kg, i.v.), a selective alpha2-adrenoceptor antagonist, showed modulatory effects similar to those of phentolamine on cigarette smoke-induced bronchoconstriction. These results suggest that cigarette smoke-induced bronchoconstriction is regulated by the prejunctional modulation of the cholinergic system via alpha- and beta-adrenoceptors. This mechanism may be modulated by the autoregulation of adrenergic nerves via the alpha2-autoreceptor.

Acetylcholine↗
PubMed1998

Myocardial fatty acid imaging with 123I-labelled 9-methyl-branched pentadecanoic acid (9MPA) using SPET.

123I-labelled 15-(p-iodophenyl)-9-(R,S)-methylpentadecanoic acid (9MPA) is a modified long-chain fatty acid that shows some beta-oxidation. Some basic aspects of this fatty acid, including myocardial uptake, distribution, clearance and differences from 201Tl myocardial perfusion, have yet to be evaluated. An average of 150 MBq of 123I-9MPA was injected intravenously into 16 patients with coronary artery disease. Planar images were obtained 45, 120 and 240 min post-injection, and single photon emission tomography (SPET) was performed at the initial (5 min), middle (45 min) and late (120 min) phases after injection. Myocardial uptake and clearance were evaluated by planar imaging, and a segmental comparison between 123I-9MPA and reinjection or resting 201Tl was performed on the SPET images. 123I-9MPA showed good uptake between 5 and 60 min, but a severe decrease was seen after 120 min in three (19%) patients. The heart-to-mediastinum ratio was 1.68 +/- 0.19, 1.55 +/- 0.19 and 1.40 +/- 1.40 at 45, 120 and 240 min, respectively. The washout rate after background subtraction was 28% for 45 min to 2 h and 47% for 45 min to 4 h. The segmental comparison (n = 182) between 123I-9MPA and 201Tl showed complete agreement of 72, 75 and 65% at 10, 45 and 120 min, respectively. The grading of the uptake of 123I-9MPA was less than that of 201Tl in 20-30% of the segments indicating myocardial fatty acid metabolic impairment relative to perfusion. The regional clearance from 5 to 120 min in the reduced-count region was lower than that in the normal region (28 +/- 7% vs 36 +/- 8%, P < 0.01). All 123I-9MPA SPET images showed good contrast if the data were acquired within 60 min. Based on the clearance of 123I-9MPA from the myocardium, imaging within 120 min is desirable. A mismatch of fatty acids and perfusion was seen in one-quarter of patients, and differential regional clearance may be clinically significant and should be investigated.

Adult↗
PubMed1998

New adsorption column (Lixelle) to eliminate beta2-microglobulin for direct hemoperfusion.

The Lixelle column is an adsorbent column used to eliminate beta2-microglobulin (beta2M) selectively from circulating blood of dialysis related amyloidosis (DRA) patients, which is used in combination with a dialyzer in series. The column has such a high capacity for adsorbing beta2M that the most intensive removal of beta2M has been possible. In clinical trials of the column, the obvious improvement of subjective symptoms such as decreases in the frequency of nocturnal awakening, the joint pain severity index, and the joint mobility index were observed. Hypotension has been the most frequent adverse event observed during treatment since the column was put on the market. It is very important to clarify the causes of both the efficacy and the side effects. A controlled prospective study is now in progress to clarify the efficacy more scientifically. The results will be published soon elsewhere.

Amyloidosis↗
PubMed1998

Therapeutic selective adsorption of anti-DNA antibody using dextran sulfate cellulose column (Selesorb) for the treatment of systemic lupus erythematosus.

The Selesorb therapeutic dextran sulfate cellulose column (Kaneka Corporation, Osaka, Japan) selectively adsorbs anti-DNA antibody, anti-cardiolipin antibody, and immune complex from the plasma of patients with systemic lupus erythematosus (SLE). The Selesorb system is composed of twin columns attached to an automated regeneration apheresis unit. Anti-DNA antibody in plasma is continuously removed through 1 of the 2 columns alternately. Clinical application of the Selesorb system to SLE patients with high titers of anti-DNA antibody showed improvement of proteinurea, arthralgia, rash, lymphocytopenia, etc., with the concurrent use of steroid and/or immnosuppressant. Angiotensin converting enzyme inhibitor should not be administered to patients treated with the Selesorb system to avoid anaphylactoid reactions based on rapid increases of bradykinin concentrations in the blood.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Spectral analysis of heart rate, arterial pressure, and muscle sympathetic nerve activity in normal humans.

We investigated the frequency components of fluctuations in heart rate, arterial pressure, respiration, and muscle sympathetic nerve activity (MSNA) in 11 healthy women using an autoregressive model and examined the relation among variables using Akaike's relative power contribution analysis with multivariate autoregressive model fitting. Power spectral analysis of MSNA revealed two peaks, with low-frequency (LF) and high-frequency (HF) components. The LF component of MSNA was a major determinant of the LF component of arterial pressure and R-R interval variability (0.70 +/- 0.07 and 0.18 +/- 0.05, respectively). The effect of the LF component of MSNA on arterial pressure showed no change in response to propranolol but was diminished (0.35 +/- 0.08) by phentolamine (P < 0.02). The effect of the LF component of MSNA on R-R interval was not altered by pharmacological sympathetic nerve blockade. The HF component of MSNA did not influence other variables but was influenced by R-R interval, arterial pressure, and respiration. These findings indicate that the LF component of MSNA reflects autonomic oscillations, whereas the HF component is passive and influenced by other cardiovascular variables.

Adolescent↗
PubMed1998

Enhanced insulin response to oral glucose load in patients with angina pectoris associated with ST segment elevation in the absence of epicardial coronary arterial obstruction.

The authors treated 10 patients with microvascular angina (MVA) manifesting angina pectoris, ST segment elevation suggestive of transmural myocardial ischemia, and no epicardial arterial obstruction. Since such patients frequently showed abnormal responses to oral glucose loading, the authors investigated the glucose and insulin responses to glucose loading in 10 MVA patients, 25 patients with vasospastic angina (VAP), 25 patients with effort angina (EAP), and 25 control subjects. Insulinogenic index, peripheral insulin activity [= 10(4)/(peak glucose x insulin at glucose peak)], glucose area, and insulin area were calculated. The MVA group included two patients with impaired glucose tolerance and two newly diagnosed diabetic patients. These proportions were similar to those in the VAP and EAP groups. Glucose levels at 30 to 180 min and insulin levels at 90 to 120 min in the MVA group were higher than in the control group. Peak glucose, glucose area, peak insulin, and insulin area were higher in the MVA group than in the control group (p<0.01). Those in the VAP and EAP groups were also higher. Insulin/glucose ratio at 120 min was higher, peripheral insulin activity, lower, in the disease groups than in the control group (p<0.05). The MVA patients showed a hyperglycemic and hyperinsulinemic response to oral glucose loading, as did the patients with EAP and VAP. Enhanced insulin response to oral glucose loading may also contribute to the pathogenesis of MVA.

Adult↗
PubMed1998

Pituitary adenylate cyclase activating peptide regulates neurally mediated airway responses.

To clarify the protective effects of pituitary adenylate cyclase activating peptide (PACAP) on airway narrowing, we examined the effects of PACAP on smooth muscle contraction and plasma extravasation in guinea-pig airways. Smooth muscle contraction evoked by electrical field stimulation (EFS) or exogenously applied acetylcholine (ACh) or substance P (SP) was measured before and after PACAP in vitro. The effect of PACAP on airway plasma extravasation was also measured in vivo. In trachea, PACAP (10(-9) - 10(-7) M) significantly suppressed smooth muscle contraction evoked by EFS without affecting ACh sensitivity, suggesting that PACAP inhibits cholinergic neuroeffector transmission. In the main bronchi, PACAP (10(-9) - 10(-8) M) significantly suppressed the contraction evoked by EFS without affecting SP sensitivity in the presence of atropine, suggesting that PACAP inhibits SP release from excitatory nonadrenergic noncholinergic (eNANC) nerves. In animals treated with atropine and propranolol, PACAP attenuated the increase in plasma extravasation induced by electrical vagus stimulation or by SP. These results suggest that pituitary adenylate cyclase activating peptide may play a role in modulation of airway responses through inhibition of cholinergic and noncholinergic mechanisms.

Acetylcholine↗
PubMed1998

Eosinophilic airway inflammation induced by repeated exposure to cigarette smoke.

Acute exposure to cigarette smoke causes airway hyperresponsiveness (AHR) in guinea-pigs, which resolves within a few hours. Repeated exposure may have a different effect on the airways. To address this question, guinea-pigs were repeatedly exposed to cigarette smoke (six cigarettes for 1 h x day(-1)) for 14 consecutive days. Airway responsiveness to inhaled histamine and differential cell counts in bronchoalveolar lavage fluid (BALF) were evaluated 1 day after the last exposure. Significant neutrophilia in BALF was observed after 3 days of smoke exposure. Significant eosinophilia in BALF and AHR were observed after 14 days of smoke exposure, but not after 3 or 7 days of smoke exposure. These changes persisted until 3 days after the last exposure and resolved 7 days afterwards. Histologically, the recruited eosinophils were observed predominantly in the airways, but not in the alveoli. Treatment with E-6123, a specific platelet-activating factor receptor antagonist (1 mg x kg(-1) x day(-1) p.o. during smoke exposure) significantly inhibited the eosinophil influx and AHR. Repeated exposure to cigarette smoke may induce prolonged airway inflammation and airway hyperresponsiveness in guinea-pigs. Platelet-activating factor or platelet-activating factor-like lipids may play a key role in airway hyperresponsiveness, presumably by the induction of eosinophilic airway inflammation.

Animals↗
PubMed1998

Bilateral coronary artery fistulas with multiple sites of drainage.

A 49-year-old woman presented with bilateral coronary fistulas with multiple sites of drainage. She had been referred to hospital for evaluation of a cardiac murmur, and a coronary arteriogram revealed multiple coronary fistulas. One fistula originated from the proximal part of the left anterior descending coronary artery and connected to the main pulmonary artery. Three coronary artery fistulas arised from a conal branch of the right coronary artery and drained into the main pulmonary artery, the right atrium and the great cardiac vein. This is the first reported case of bilateral coronary fistulas with multiple sites of drainage.

Coronary Angiography↗
PubMed1997

Four novel KVLQT1 and four novel HERG mutations in familial long-QT syndrome.

BACKGROUND: Familial long-QT syndrome (LQTS) is characterized by prolonged ventricular repolarization. Clinical symptoms include recurrent syncopal attacks, and sudden death may occur due to ventricular tachyarrhythmias. Three genes responsible for this syndrome (KVLQT1, HERG, and SCN5A) have been identified so far. We investigated mutations of these genes in LQTS families. METHODS AND RESULTS: Thirty-two Japanese families with LQTS were brought together for screening for mutations. Genomic DNA from each proband was examined by the polymerase chain reaction-single-strand conformation polymorphism technique followed by direct DNA sequencing. In four of the families, comprising 16 patients, mutations were identified in KVLQT1; five other families (9 patients) segregated mutant alleles of HERG. All 25 of these patients carried the specific mutations present in their respective families, and none of 80 normal individuals carried these alleles. Mutations were confirmed by endonuclease digestion or hybridization of mutant allele-specific oligonucleotides. No mutation in SCN5A was found in any family. CONCLUSIONS: We identified nine different mutations among 32 families with LQTS. Eight of these were novel and account for 25% of all types of mutations reported to date. Such a variety of mutations makes it difficult to screen high-risk groups using simple methods such as endonuclease digestion or mutant allele-specific amplification.

Alleles↗
PubMed1997

Effect of peripheral nerve injury on nuclear magnetic resonance relaxation times of rat skeletal muscle.

RATIONALE AND OBJECTIVES: The authors evaluate the changes in magnetic resonance (MR) relaxation times of rat skeletal muscles in vivo after nerve injury and during neural recovery, and determine the major determinants of relaxation times. MATERIALS: Magnetic resonance relaxation times, blood volume, and water and fat content were examined after nerve injury and during recovery with time course. RESULTS: Nerve injury led to longer T2 values compared with controls, but there were no significant changes in T1 values. After the initial prolongation of T2 after nerve injury, no changes were observed. Neural recovery resulted in a return of T2 values to normal. The time course of changes in blood volume was similar to that of changes in T2, and T2 values were correlated strongly with 19-fluorine-MR spectroscopy estimates of blood volume (r2 = 0.94). CONCLUSIONS: T2 values may be useful to monitor recovery after nerve injury and may be related to the blood volume in skeletal muscle.

Animals↗
PubMed1997

The effects of a specific tachykinin receptor antagonist FK-224 on ozone-induced airway hyperresponsiveness and inflammation.

We have demonstrated previously that tachykinin depletion by capsaicin prevented the ozone-induced airway hyperresponsiveness and the bronchial wall oedema in guinea pigs. To further clarify the role of neurogenic inflammation in ozone-induced airway hyperresponsiveness, we investigated the effects of a specific tachykinin receptor antagonist (FK-224) in guinea pigs. Animals were anaesthetized, tracheostomized and mechanically ventilated. Total pulmonary resistance (RL) was calculated from transpulmonary pressure and box flow in a plethysmograph. Airway responsiveness was assessed by determining the provocative concentration of histamine aerosol that increased RL to twice the baseline value (PC200). Animals were injected with either FK-224 (10 mg/kg, dissolved in 0.2 mL/kg DMSO) or vehicle (0.2 mL/kg DMSO) intravenously, then pre-ozone PC200 was determined. Following this measurement, animals were exposed to 3 ppm ozone for 60 min. Immediately after exposure, the histamine dose response curve was evaluated again. Bronchoalveolar lavage (BAL) was performed in animals treated with FK-224 or vehicle. In animals treated with vehicle, ozone exposure caused significant decrease in PC200 and moderate increase in neutrophils in BAL fluid. FK-224 pre-treatment significantly inhibited ozone-induced hyperresponsiveness. Neutrophils in BAL fluid did not significantly increase after ozone exposure in animals treated with FK-224. By contrast, the degree of epithelial desquamation did not differ significantly between the two groups. We conclude that neurogenic inflammation caused by tachykinin release may be responsible for ozone-induced bronchial hyperresponsiveness, and that tachykinins may play a role in the initiation of airway inflammation.

Airway Resistance↗
PubMed1997

Time course of recovery from nerve injury in skeletal muscle: energy state and local circulation.

This study examined the time course of recovery from nerve injury on energy state assessed by phosphorus-31 magnetic resonance spectroscopy and local circulation dynamics by fluorine-19 magnetic resonance spectroscopy in skeletal muscles of rats. The hindlimb muscles that had undergone unilateral sciatic nerve compression for 2 wk (CN) were compared with sham-operated (SO) muscles and with muscles that had the compression removed after 2 wk and were allowed to recover for 4 wk (R4) or for 6 wk (R6). The energy state and local circulation dynamics of CN muscles were less than those of SO muscles (P < 0.01). The energy state of R4 muscles remained at levels similar to CN muscles, whereas the local circulation dynamics improved but not back to SO values. In R6 muscles, both parameters returned to SO values. These results showed that the recovery processes of circulation precede those of energy state in skeletal muscles.

Animals↗
PubMed1997

Nitric oxide derived from sympathetic nerves regulates airway responsiveness to histamine in guinea pigs.

Nitric oxide (NO), which can be derived from the nervous system or the epithelium of the airway, may modulate airway responsiveness. We investigated how NO derived from the airway nervous system would affect the airway responsiveness to histamine and acetylcholine in mechanically ventilated guinea pigs. An NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (1 mmol/kg i.p.) significantly enhanced airway responsiveness to histamine but not to acetylcholine. Its enantiomer D-NAME (1 mmol/kg i.p.), in contrast, had no effect. The L-NAME-induced airway hyperresponsiveness was still observed in animals pretreated with propranolol (1 mg/kg i.v.) and atropine (1 mg/kg i.v.). Pretreatment with the ganglionic blocker hexamethonium (2 mg/kg i.v.) completely abolished enhancing effect of L-NAME on airway responsiveness. Bilateral cervical vagotomy did not alter the L-NAME-induced airway hyperresponsiveness, whereas sympathetic stellatectomy completely abolished it. Results suggest that NO that was presumably derived from the sympathetic nervous system regulates airway responsiveness to histamine in guinea pigs.

Airway Resistance↗
PubMed1997

Pre- and post-junctional effects of VIP-like peptides in guinea pig tracheal smooth muscle.

To determine the role of VIP-like peptides on neurotransmission of vagus nerve, we evaluated the effects of helodermin, helospectin, and vasoactive intestinal peptide (VIP) on the contraction of guinea pig tracheal smooth muscle evoked by electrical field stimulation (EFS) or the exogenous application of actylcholine (ACh). Isometric tension of tracheal strips was measured in the presence of indomethacin (10(-6) M) and of guanethidine (10(-6) M). VIP (10(-9) M to 10(-7) M) significantly suppressed the contraction evoked by EFS. VIP, at concentrations of 10(-9) M and 10(-8) M, did not affect the ACh-evoked contraction, but a concentration of 10(-7) M suppressed ACh-evoked contraction. Helospectin and helodermin (10(-8) M and 10(-7) M) significantly suppressed the EFS-evoked contraction, but 10(-9) M showed no effect. Helospectin and helodermin had no effect on the ACh sensitivity of smooth muscle up to 10(-8) M, but a concentration of 10(-7) M suppressed the ACh-evoked contraction. These results indicate that helodermin, helospectin, and VIP exert both pre- and post-junctional inhibitory effects on the airway smooth muscle of guinea pigs. These peptides, thus, inhibited tracheal smooth muscle contraction prejunctionally at low concentrations, and acted postjunctionally at higher concentrations.

Acetylcholine↗
PubMed1997

Effect of beta 2-agonists on histamine-induced airway microvascular leakage in ozone-exposed guinea pigs.

beta 2-adrenergic agonists exhibit antipermeability effects in the airways. However, it is not known whether beta 2-agonists have this beneficial effect in airway mucosa that is already inflamed. We evaluated the effects of two inhaled beta 2-agonists, salbutamol and formoterol, on the histamine-induced bronchoconstriction and plasma extravasation in the airways of guinea pigs with or without ozone exposure. Total pulmonary resistance (RL) was measured before and after histamine inhalation in anesthetized animals that were pretreated with inhaled salbutamol, formoterol, or saline. Plasma extravasation in the airways was measured using Evans blue dye. In the control animals not exposed to ozone, salbutamol and formoterol each significantly reduced both the histamine-induced bronchoconstriction and the plasma extravasation in the trachea and main bronchi. In the ozone-exposed animals, the increase in RL after histamine was greater than that in control animals. Salbutamol and formoterol each significantly reduced histamine-induced bronchoconstriction, even in the ozone-exposed animals. Salbutamol did not affect the histamine-induced plasma extravasation, whereas formoterol reduced the plasma extravasation in the main bronchi, but not in the trachea, of the animals exposed to ozone. These results suggest that the anti-inflammatory properties of formoterol in inflamed airways may contribute to the beneficial effects in the treatment of airway inflammation.

Adrenergic beta-Agonists↗