Biomedical subjects

S Takata

Publications and source records attributed to S Takata.

At least 91 records · Page 5Linked to original sources

PubMed1995

Lipoxygenase product formation and cell adhesion during neutrophil-glomerular endothelial cell interaction.

Leukotriene (LT) and lipoxin (LX) levels were monitored in ionophore-stimulated coincubations of polymorphonuclear neutrophils (PMN) and microvascular kidney glomerular endothelial cells (GEN) to determine the profile of lipoxygenase (LO) products generated during cell-cell interactions and the relative contributions of transcellular pathways to LO product biosynthesis in this setting. LTB4 and LTC4 were the major products formed, as determined by reverse-phase high-performance liquid chromatography and radioimmunoassay. LTB4 and LTC4 levels were increased by 23 and 185%, respectively, in coincubations of PMN and GEN, compared with incubations of PMN alone. In contrast, LXA4 and LXB4 levels were not changed in the presence of GEN. These data suggested that GEN utilize PMN-derived LTA4 to generate LT. In keeping with this hypothesis, LT biosynthesis was enhanced if PMN were primed with human granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine that augments LTA4 biosynthesis by activated PMN. The influence of LT on PMN adhesion to GEN was also assessed, since adhesion appears to be a pivotal event in recruitment of PMN in acute glomerulonephritis. Under basal conditions, LTB4 provoked low levels of adhesion via a PMN-directed CD11/CD18-dependent mechanism. The level of adhesion was markedly enhanced by prior priming of PMN with GM-CSF or activation of GEN with tumor necrosis factor-alpha (TNF). LTB4 was as potent in this regard as the complement component C5a, platelet-activating factor (PAF), and interleukin-8 (IL-8), other mediators that contribute to the entrapment of PMN in inflamed glomeruli. LTC4 also provoked PMN-GEN adhesion via a CD11/CD18-dependent mechanism, but, in contrast to LTB4, via actions with GEN. This action of LTC4 appeared to be mediated, at least in part, by induction of PAF synthesis by GEN. Interestingly, LT-induced PMN-GEN adhesion was markedly attenuated following remodeling of PMN phospholipids with 15(S)-hydroxyeicosatetraenoic acid, a product of 15-LO, which has been implicated as an anti-inflammatory eicosanoid in some experimental and human inflammatory diseases. Taken together, these results provide further evidence that 1) transcellular biosynthetic pathways may amplify the profiles of inflammatory mediators and thereby contribute to leukocyte recruitment in acute glomerulonephritis and 2) that products of the 5-LO and 15-LO pathways may exert opposing actions on PMN trafficking during glomerular inflammation in vivo.

Amino Acid Sequence↗

PubMed1995

An important role of tachykinins in ozone-induced airway hyperresponsiveness.

We investigated the role of tachykinins in ozone-induced airway hyperresponsiveness (AHR) in guinea pigs. Airway responsiveness was assessed by determining the provocative concentration (PC200) of a histamine aerosol. Ozone exposure (3.0 ppm for 2 h) caused significant AHR. For vehicle-pretreated animals, the geometric mean pre- and post-ozone PC200 values were 0.87 mg/ml (GSEM 1.33) and 0.11 mg/ml (GSEM 1.17), respectively. Tachykinin depletion by capsaicin (50 mg/kg) prevented this AHR, whereas it did not alter pre-ozone airway responsiveness. The PC200 was 0.36 mg/kg (GSEM 1.64) before ozone and 0.24 mg/kg (GSEM 1.72) after ozone for this group. Ozone also caused a significant increase in neutrophils in bronchoalveolar lavage fluid (BALF) compared with BALF from a normal control group (1.71 +/- 0.69 versus 0.07 +/- 0.02 x 10(5)/ml, respectively). Capsaicin pretreatment attenuated this neutrophil influx (0.23 +/- 0.16 x 10(5)/ml). Morphometric assessment revealed edema of the bronchiolar wall after ozone exposure, which was not observed in the capsaicin group. BAL and morphometry revealed that the degree of ozone-induced epithelial desquamation was similar in both groups. These results suggest that tachykinins may be responsible for ozone-induced AHR, possibly via neurogenic inflammation.

Animals↗

PubMed1995

Assay of magnesium in serum and urine with use of only one enzyme, isocitrate dehydrogenase (NADP+).

We report a method for assaying magnesium in serum and urine involving only one enzyme, isocitrate dehydrogenase (NADP+)(EC 1.1.1.42), which requires magnesium ion for activity. The enzymatic reduction of NADP+ by isocitrate increases in rate linearly up to at least 20 mmol/L magnesium in the presence of appropriate concentrations of the two metal-chelating reagents, EDTA and glycol ether diamine-N,N,N',N'-tetraacetate. Within-run (n = 20) CVs and day-to-day (n = 10) CVs for sera are < or = 1.5% and < or = 2.6%, respectively. Analytical recovery of magnesium in sera averages 96-100%. This method is not affected by bilirubin, hemoglobin, or lipemia. The method (y) gives the following results correlating with atomic absorption spectrophotometry (x): y = 1.03x + 0.06 mmol/L (n = 62, r = 0.995, Sylx = 0.03) for sera, and y = 1.03x - 0.10 mmol/L (n = 62, r = 0.989, Sylx = 0.19) for urines; with the calmagite method (x): y = 0.99x + 0.04 mmol/L (n = 62, r = 0.991, Sylx = 0.03) for sera, and y = 0.98x + 0.03 mmol/L (n = 62, r = 0.999, Sylx = 0.02) for urines.

Autoanalysis↗

PubMed1995

[QRST isointegral maps on exercise in patients with congenital long QT syndrome].

UNLABELLED: To clarify the influence of exercise on ventricular repolarization abnormality, QRST isointegral maps (I-map) were analyzed in long QT syndrome (LQTS). The subjects were six LQTS patients. Body surface mapping data were sampled immediately and six min after exercise and at rest. At rest, three patients had a multipolar pattern (MP) in I-map and one patient had a larger negative area (LNA) extending beyond the mid-sternal line. After the handgrip exercise, two patients had a MP and two patients had a LNA. After the ergometer exercise, all five patients had a MP and three of five patients had a LNA. CONCLUSION: On exercise, abnormal findings were more frequent than those at rest. It showed greater dispersion of ventricular repolarization on exercise in patients with LQTS.

Adult↗

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

Vasomotor response to ergonovine of epicardial and resistance coronary arteries in the nonspastic vascular bed in patients with vasospastic angina.

The hypothesis that a coronary vasomotion disorder may exist in the entire coronary artery tree in patients with vasospastic angina was investigated by examining the coronary responses to atrial pacing (130 beats/min) before and after the administration of ergonovine (16 micrograms) into nonspastic coronary arteries. Seven patients with angiographically normal coronary arteries and focal spasm in the right coronary artery and 7 control patients with atypical chest pain and angiographically normal coronary arteries without spasm were studied. Great cardiac vein flow (GCVF) and left anterior descending coronary artery diameters (CDs) were measured by the thermodilution method and quantitative arteriography, respectively. Although the CDs before ergonovine were similar in the 2 groups, the pacing-induced increased in GCVF before ergonovine administration was smaller in patients with vasospastic angina than in control patients (22 +/- 4% vs 49 +/- 11%, respectively; p < 0.05). After ergonovine administration, pacing both increased GCVF and decreased anterior regional coronary resistance (ACR) to a lesser extent in patients with vasospastic angina than in control patients (GCVF, 16 +/- 4% vs 47 +/- 8%, respectively [p < 0.01]; ACR, -12 +/- 3% vs -29 +/- 3%, respectively [p < 0.01]). The decreases in CDs in patients with vasospastic angina observed after ergonovine administration were greater than those in control patients (-18 +/- 2% vs -9 +/- 2%, respectively; p < 0.05). Thus, not only epicardial, but also resistance coronary arteries are affected by the coronary vasomotion disorder in the nonspastic vascular bed in patients with vasospastic angina.

Adult↗

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↗

PubMed1994

Effects of lead on osteoclast-like cell formation in mouse bone marrow cell cultures.

To examine an effect of lead (Pb) on the process of osteoclast-like cell formation from its progenitors, we used a mouse bone marrow culture system in which osteoclast-like multinucleated cells (MNCs) were formed in response to bone-resorbing agents. In a 9-day culture period, Pb dose-dependently stimulated MNC formation over the concentration range 2-10 microM, whereas at 40 microM Pb, MNC formation declined. In an 11-day culture period, MNC formation reached a maximum at 5 microM Pb and decreased with increasing concentration of Pb at 10-40 microM. Pb-stimulated MNC formation was inhibited by both indomethacin and SC19220, an antagonist of prostaglandin E2 (PGE2) receptor. Pb stimulated the production of PGE2 in marrow cell cultures, suggesting that Pb-stimulated MNC formation is dependent on the production of PGE2. 3-Isobutyl-1-methylxanthine potentiated Pb-stimulated MNC formation and 2',5'-dideoxyadenosine, an inhibitor of adenylate cyclase, inhibited it. A calcium ionophore A23187 increased Pb-induced MNC formation and verapamil, a calcium channel blocker, depressed it. It is possible that a PGE2-induced increase in the levels of cyclic adenosine 3',5'-monophosphate (cAMP) and calcium ions in marrow cells is involved in Pb-induced MNC formation. Pb and parathyroid hormone showed a synergistic stimulation on MNC formation. From these results, Pb is thought to induce osteoclast-like cell formation by a mechanism involving PGE2 which increases the intracellular levels of cAMP and calcium ions.

1-Methyl-3-isobutylxanthine↗

PubMed1994

Case of cough syncope with seizure.

A rare case of cough syncope accompanied by seizure is presented. Interseizure electroencephalogram revealed in this 55-year-old man spikes and sharp waves over the bilateral temporal regions. Bronchodilators and antiepileptic medication effectively controlled cough syncope and seizure in this patient.

Bronchial Provocation Tests↗

PubMed1994

Remodeling of neutrophil phospholipids with 15(S)-hydroxyeicosatetraenoic acid inhibits leukotriene B4-induced neutrophil migration across endothelium.

5-Lipoxygenase products, such as leukotrienes, are important stimuli for leukocyte-mediated tissue injury in acute inflammation. 15-Hydroxyeicosatetraenoic acid (15-HETE) is an eicosanoid generated by a variety of cell types via the actions of 15-lipoxygenases and, in addition, cyclooxygenases and epoxygenases. 15-HETE levels are frequently elevated at sites of inflammation, and extracellular 15(S)-HETE is esterified rapidly into neutrophil (PMN) phospholipids in vitro to levels that are comparable with arachidonic acid. We present evidence that remodeling of PMN phospholipids with 15(S)-HETE stereoselectively inhibits PMN migration across endothelium in response to leukotriene B4 (LTB4) and other chemoattractants. Esterified 15(S)-HETE causes a striking reduction in the affinity of LTB4 cell-surface receptors for their ligand and inhibition of LTB4-triggered stimulus-response coupling. As a result of these actions, esterified 15(S)-HETE attenuates the cytoskeletal rearrangements and CD11/CD18-mediated adhesive events that subserve directed locomotion of PMN across endothelium. These observations indicate that products of the 5-lipoxygenase and 15-lipoxygenase pathways can exert counterbalancing influences on PMN trafficking across endothelium. They suggest that 15(S)-HETE may be a potent endogenous inhibitor of PMN-endothelial interactions in vivo and serve to limit or reverse acute inflammation.

Antigens, CD↗

PubMed1994

Angina pectoris associated with ST segment elevation in the absence of epicardial coronary arterial obstruction. Case reports.

Two cases are presented in which angina pectoris associated with ST segment elevation occurred during either an ergonovine provocation test or coronary angioplasty, despite the absence of epicardial coronary artery obstruction. In both cases, no epicardial coronary spasm, thromboembolic occlusion, coronary air embolus, vessel dissection, or side-branch occlusion was observed. These findings suggest that transmural myocardial ischemia without epicardial coronary artery obstruction can occur owing to abnormalities of the coronary microcirculation. Microvascular vasoconstriction leading to transmural myocardial ischemia may be induced by ergonovine or by the release of potent vasoconstrictors from disrupted coronary lesions during angioplasty.

Angina Pectoris↗

PubMed1994

Effect of stimulation frequency on metabolism of skeletal muscles.

We studied the effects of stimulation frequency on the energy metabolism of rat skeletal muscles during electrical low-frequency stimulation, using in vivo phosphorus-31 magnetic resonance spectroscopy. The sciatic nerve of Wistar-Kyoto rats (n = 16) was stimulated electrically using low frequency stimulation (LFS) at 30 Hz and high frequency stimulation (HFS) at 100 Hz as tetanizing frequencies. The initial tension during LFS was significantly different from that during HFS, 200.49 +/- 19.47 vs. 516.67 +/- 5.38 dynes (mean +/- S.E.; n = 8) (p < 0.01). In the first 2 min of stimulation, the ratio of phosphocreatine (PCr) to inorganic phosphate (Pi) + sugar phosphate (SP) during LFS and HFS were 0.28 +/- 0.04 and 0.53 +/- 0.06 (mean +/- S.E.; n = 8), respectively. Subsequently, the ratio during LFS remained lower than that during HFS. The intracellular pH during LFS and HFS in the first 2 min of stimulation was 6.27 +/- 0.02 and 6.75 +/- 0.03 (mean +/- S.E.; n = 8), respectively. From 2 min to 12 min of stimulation, the intracellular pH during LFS remained lower than that during HFS. The results showed that lower levels of both energy and intracellular pH of skeletal muscles were maintained during LFS than during HFS, facilitating aerobic glycolysis to produce ATP during stimulation.

Animals↗

PubMed1994

15-Hydroxyeicosatetraenoic acid inhibits neutrophil migration across cytokine-activated endothelium.

15-hydroxyeicosatetraenoic acid (15-HETE) is an eicosanoid, formed by the actions of 15-lipoxygenase, epoxygenases, and cyclooxygenases on arachidonic acid, whose tissue levels are often elevated during inflammation. The present study demonstrates that 15(S)-HETE is a potent inhibitor of polymorphonuclear neutrophil (PMN) migration across cytokine-activated endothelium in vitro. 15(S)-HETE is rapidly esterified into PMN phospholipids, and we report that 15-(S)-HETE-remodeled PMN displayed blunted adhesion to, and migration across, human endothelial cells that had been activated with either interleukin-1 beta or tumor necrosis factor-alpha Several lines of evidence suggested that 15(S)-HETE inhibited PMN transmigration by attenuating PMN responsiveness to endothelial cell-derived platelet-activating factor (PAF). The inhibitory action of 15(S)-HETE on transmigration was not restricted by the profile of adhesion molecules expressed by cytokine-activated endothelium. Interleukin-1 beta and tumor necrosis factor-alpha induce PAF production by endothelium, and PMN migration across cytokine-activated endothelium was inhibited by a PAF receptor antagonist. PMN migration across endothelium in response to exogenous PAF was dramatically inhibited following exposure of PMN to 15(S)-HETE. Furthermore, 15(S)-HETE-remodeled PMN displayed impaired cytoskeletal and adhesion responses when stimulated by exogenous PAF, two pivotal events in PMN migration across activated endothelium. 15(S)-HETE seemed to attenuate PMN responsiveness to PAF by inhibiting membrane-associated signal transduction events. In keeping with this interpretation, remodeling of PMN phospholipids with 15(S)-HETE was associated with a sixfold reduction in the affinity of specific high-affinity PAF receptors for their ligand and impaired PAF-triggered IP3 generation. In contrast, PMN adhesion responses stimulated by calcium ionophore or activators of protein kinase C remained intact. These results provide further evidence that 15(S)-HETE may be an important endogenous inhibitor of PMN-endothelial cell interaction that serves to limit or reverse neutrophil-mediated inflammation in vivo.

Cell Adhesion↗

PubMed1993

Effects of bed rest on bone metabolism in patients with femoral neck fracture.

The effect of continuous 1 week bed rest during traction on bone metabolism were studied in patients with femoral neck fracture. Bone demineralization was assessed by measuring serum calcium (Ca), phosphorus (P), and alkaline phosphatase (AlkP) before, during, and after 1 week-bed rest with skeletal traction. In addition, 24-hour urinary excretion of calcium and phosphorus were measured. Serum Ca did not change significantly before, during, and after bed rest, whereas serum P increased after 1 week bed rest and postoperatively remained significantly elevated. Serum AlkP did not increase with bed rest, but became elevated postoperatively. Urinary Ca excretion increased from 105.8 +/- 15.2 to 138.0 +/- 15.4 mg/24h after 1 week of bed rest, and remained elevated postoperatively. In contrast, urinary P excretion initially increased 495.1 +/- 65.0 to 610.8 +/- 87.7 mg/24h, and subsequently decreased to a level significantly less than the admission level. These results suggest that 1 week bed rest for the patients with femoral neck fracture resulted in bone atrophy and demineralization.

Aged↗

PubMed1993

A new treatment for dialysis-related amyloidosis with beta 2-microglobulin adsorbent column.

Dialysis-related amyloidosis (DRA) is characterized by the presence of beta 2-microglobulin (beta 2-m) in the plasma. In order to eliminate beta 2-m from the circulating blood, the beta 2-m selective adsorbent for direct hemoperfusion (DHP) was developed. A DHP column (BM-01), containing 350 ml of the adsorbent, was subjected to clinical trials. The column was connected with a PAN (AN69) membrane dialyzer in series and used 3 times a week for 1 week (11 patients), 4 weeks (5 patients), 6 months (1 patient) and 12 months (2 patients). The percent reduction (%) of beta 2-m was for 16 patients (for 1 or 4 weeks), more than 65, and for 3 patients (for more than 6 months), 76.5 +/- 4.9, 73.5 +/- 5.7, 72.2 +/- 6.2. At the end of each session, beta 2-m plasma levels were found to be below 10 mg/L, with 3.4 mg/L being the lowest. The total amounts of beta 2-m removed were 172.5 +/- 22.3, 257.0 +/- 75.6, 157.6 +/- 32.2 and 429.8 mg/session at max. Two out of these three patients had a favorable effect on joint symptoms and ocular fundus. It can be concluded that this selective adsorption therapy may delay the progression of DRA, and is worth considering for wide application.

Adsorption↗

PubMed1993

Acute interstitial pneumonitis induced by carbamazepine.

A 62 year old man treated with carbamazepine for 3 months developed eczema and acute interstitial pneumonitis. A lymphocyte-stimulation test was reactive to carbamazepine. Withdrawal of the drug resulted in prompt improvement. Only 10 cases of this type of drug-induced lung disease have previously been reported.

Acute Disease↗