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Biomedical subjects

K Konno

Publications and source records attributed to K Konno.

At least 181 records · Page 10Linked to original sources
PubMed1994

Nicotine prevents a reduction in neutrophil filterability induced by cigarette smoke exposure.

Decreased deformability of neutrophils exposed to cigarette smoke is considered a determinant of neutrophil sequestration within the pulmonary microvasculature, which may be a risk for the development of pulmonary emphysema. In this study we examined the effect of nicotine, a major cigarette component, on the reduction in neutrophil deformability, measured as cell filterability, after exposed to cigarette smoke. Neutrophils were exposed to smoke by incubating them in an aqueous solution of smoke extracts. Filterability of neutrophils was studied by a vertical filtration technique by measuring their ability to pass through a micropore membrane and expressed as membrane resistance. There was a negative relationship between membrane resistance after exposure to whole smoke and the nicotine content of the cigarettes tested. Whole smoke increased the membrane resistance less than gas-phase smoke, from which almost all nicotine had been excluded. Addition of nicotine, glutathione, alpha-tocopherol, thymol, and erythrocytes prevented the increase in membrane resistance following gas-phase smoke exposure. Nicotine also protected against an increase in membrane resistance against the effect of chloramine-T and hydrogen peroxide, but it provided no protection from superoxide radical generated from a xanthine-xanthine oxidase mixture of N-formylmethionylleucylphenylalanine. These results suggest that nicotine prevents the reduction in neutrophil filterability, probably by scavenging oxidants present in the cigarette smoke.

Analysis of Variance↗
PubMed1994

Effect of platelet-activating factor on intracellular free calcium in cow tracheal epithelium.

The effect of platelet activating factor (PAF) on the intracellular cytosolic levels of free calcium ([Ca2+]i) was studied in cultured epithelium from cow trachea. In fura-2-loaded cells, PAF (10(-9) to 10(-5) M), but not lyso-PAF, increased [Ca2+]i in a concentration-dependent manner, from 106 +/- 15 to 270 +/- 40 nM (P < 0.05). This [Ca2+]i response consisted of a transient increase that peaked within 15 s after addition and a subsequent sustained elevation that reached a plateau after 1 min. The potency for the sustained response was greater by approximately 1 log U than that for the transient response. Preincubation of the cells with the PAF receptor antagonist CV6209 (10(-6) M) inhibited the increase in [Ca2+]i. Ca(2+)-free medium (2 mM EGTA) totally abolished the sustained response to PAF, but it only partially inhibited the transient response. Verapamil (10(-5) M) also largely inhibited the sustained response. Moreover, PAF transiently increased inositol triphosphate (IP3) levels, peaking 10 s after addition. These data suggest that (1) a PAF-induced increase in [Ca2+]i is mediated via PAF receptors, (2) PAF causes both transient [Ca2+]i release from intracellular stores through IP3 production and sustained [Ca2+]i influx from extracellular solution, and (3) Ca2+ influx may be a major pathway of PAF-induced increase in [Ca2+]i in cow tracheal epithelium.

Animals↗
PubMed1994

Immunoblotting analysis of somatic components of Dirofilaria immitis.

SDS-PAGE analysis of Dirofilaria immitis extracts demonstrated the complexicity of protein components of microfilariae, similar to that of adult male and female worms. Immunoblotting analysis using sera from microfilaremic and amicrofilaremic dogs with D. immitis infection suggest that antigenic components in the low molecular weight region may be related to the anti-microfilarial mechanism of the host.

Animals↗
PubMed1994

Metastatic leiomyosarcoma of the skull--case report.

A 65-year-old female presented with a rare intestinal leiomyosarcoma metastasis to the skull manifesting as a mass beneath the scalp. She was free of neurological and physical symptoms on admission. The tumor was totally removed with normal surrounding bone and dura. The histological diagnosis was leiomyosarcoma. Ultrastructural and immunohistochemical studies demonstrated the smooth muscle origin of the tumor. Such patients in good physical condition should be immediately treated surgically to achieve the best chance of survival.

Aged↗
PubMed1994

[Effect of Sei-hai-to on ion transport in airway epithelial cells].

The effect of Sei-hai-to on ion transport in airway epithelial cells and its mechanism of action were investigated. Measurement of short-circuit current (Isc) using cultured epithelial cells from canine tracheal mucosa under short-circuit conditions showed that Isc was dose-dependently increased by the submucosal administration of Sei-hai-to. The response of Isc to this drug was not affected by pretreatment the cells with amiloride, but abolished by furosemide, or Cl-free condition. These results suggest that Sei-hai-to stimulates Cl ion transport selectively and may affect the subsequent movement of water across the airway mucosa to the lumen.

Animals↗
PubMed1994

[Cell-to-cell interaction in airway mucosa--effect of eosinophils on airway epithelial ion transport].

We examined the interaction between eosinophil-derived mediators and ion transport in airway epithelial cells. Eosinophils were obtained by peritoneal lavage from polymyxin B-treated guinea-pigs and were purified over discontinuous Percoll density gradients. The activated eosinophil supernatant was prepared with a two-stage method in the presence of A23187. The effects of eosinophil supernatant on the electric properties of cultured epithelial cells from cow trachea were examined in an Ussing chamber under short-circuit conditions. The eosinophil supernatant added to the serosal and mucosal sides increased the short-circuit current (Isc) in an eosinophil number-dependent manner (3 x 10(6), 10(7) eosinophils: delta Isc 9 +/- 1 microA/cm2, 18 +/- 3 microA/cm2). The response was inhibited by treatment of epithelial cells with diphenylamine-2-carboxylate but not by amiloride. The increase in Isc induced by the supermatant from eosinophils treated with indomethacin or the lipoxygenase inhibitor AA861 was significantly less than that induced by untreated eosinophils. These results indicate that activated eosinophils stimulate C1 secretion in airway epithelium via release of metabolites of arachidonic acid.

Animals↗
PubMed1994

[Continuous monitoring of nitric oxide release from airway mucosa].

There is increasing evidence that nitric oxide (NO) plays a role in the regulation of airway and vascular smooth muscle tone, pulmonary microvascular permeability, and host defense. However, it remains uncertain whether NO is actually released from airway mucosa. We therefore directly measured NO concentrations in the perfusate of rabbit tracheal mucosal surface, with an NO-selective electrode. The electrode was made of Pt/Ir alloy coated with a three-layered membrane that consisted of KCl, No-selective silicone resin, and a normal silicone membrane. Termination of tracheal perfusion with Krebs-Henseleit solution increased the electrical current derived from oxidation of NO at the electrode, and reperfusion rapidly decreased the current to the baseline value. Addition of L-NG-arginine methylester (L-NAME, 10(-3) M) to the perfusate decreased NO release, but D-NAME had no effect. Subsequent addition of L-arginine (10(-3) M) reversed the inhibition by L-NAME and greatly increased NO release above the baseline value. Histochemical staining to reveal NADPH diaphorase activity in the tracheal tissue showed a strong blue reaction mainly in the epithelial cells. These results suggest that NO is continuously released in the airway mucosal surface, probably from the epithelial cells rich in NO synthase.

Animals↗
PubMed1994

Niacin attenuates acute lung injury induced by lipopolysaccharide in the hamster.

Lipopolysaccharide plays a major role in the development of lung injury induced by Gram-negative bacteria, but a protective agent to attenuate the LPS-induced lung injury has not been found. The aim of this study was to examine the effects of niacin on LPS-induced acute lung injury. We administered LPS (Escherichia coli) 0.01 mg.100 g-1 body weight, transtracheally into the lungs of hamsters. Niacin (250 or 500 mg.kg-1 body weight) was injected intraperitoneally 24 h before, and 1 h after the LPS administration. LPS treatment increased wet/dry lung weight, albumin content and neutrophil counts in bronchoalveolar lavage fluid. In hamsters treated with niacin, wet/dry lung weight, albumin content and intra-alveolar cell counts were normal. Nicotinamide adenine dinucleotide (NAD) was significantly decreased in lung tissue of hamsters treated with LPS alone, but was increased in hamsters treated with LPS and niacin. Histopathological examination revealed that niacin-treated LPS-administered hamsters had lungs with no or occasional inflammatory cell infiltration in alveolar spaces, in contrast to the lungs of LPS-treated hamsters, which were infiltrated with numerous inflammatory cells. We conclude that niacin attenuates LPS-induced acute lung injury, probably, in part, by preventing the depletion of NAD.

Animals↗
PubMed1994

Erythromycin inhibits cholinergic neuro-effector transmission in canine airway smooth muscle.

To elucidate whether macrolide antibiotics affect cholinergic neuro-effector transmission in the airway, we studied canine isolated bronchial segments under isometric conditions in vitro. Addition of erythromycin (3 x 10(-4) M) attenuated the contractile responses to electrical field stimulation (EFS), so that the stimulus frequency required to produce a half-maximal contraction (ES50) increased from 1.3 +/- 0.3 to 5.1 +/- 0.5 Hz (p < 0.001). This effect was concentration-dependent and not influenced by propranolol, indomethacin, ouabain or mechanical removal of the epithelium. In contrast, contractile responses to acetylcholine were not altered by erythromycin. These results suggest that erythromycin may inhibit neuro-effector transmission in the airway cholinergic motor pathway, probably involving the reduction of exocytotic release of acetylcholine from the nerve terminals.

Acetylcholine↗
PubMed1994

[A case of tuberculous pleural effusion diagnosed by polymerase chain reaction (PCR)--with reference to tuberculous pleurisy using polymerase chain reaction].

A 38-year-old man was admitted to hospital because of chest pain and for the evaluation of a right pleural effusion on his chest X-ray film. Pleural effusion was characterized as exudative lymphocyte-predominant fluid with elevation of adenosine deaminase (ADA). Bacteriologic examination of pleural fluid was negative in both smear and culture of the fluid. PPD was positive and ESR was elevated. Mycobacterial DNA was detected in the pleural effusion using polymerase chain reaction (PCR) with primers which amplified a fragment of Is6110. Following treatment (INH, RFP and EB), the right pleural effusion disappeared. We conclude that PCR technique may be very useful in the rapid diagnosis of tuberculous pleurisy.

Adult↗
PubMed1994

[Modulation of cholinergic neurotransmission by Ca(2+)-activated K channel and Na(+)-K(+)-ATPase in canine airway smooth muscle].

Stimulation of Ca(2+)-activated K+ channel and Na(+)-K(+)-ATPase may play an important role in the relaxant responses of airway smooth muscle to certain bronchodilators. To elucidate whether cholinergic neuroeffector transmission can be modulated by Ca(2+)-activated K+ channel and Na(+)-K(+)-ATPase, we studied canine airway smooth muscle under isometric conditions in vitro. Addition of charybdotoxin (ChTx, 10(-7) M) did not alter the contractile responses to acetylcholine (ACh) but augmented electrical field stimulation (FES)-induced contractions at 1-10 Hz (p < 0.01), whereas apamin and glibenclamide were without effect. This effect was dose-dependent, with the maximal increase being 36.8 +/- 5.3% (p < 0.001). Ouabain at a concentration insufficient to alter the resting tension (10(-7) M) increased contractions induced by both EFS and ACh. The magnitude of the increase in contractile responses to EFS was similar to those to ACh at ouabain concentration of up to 3 x 10(-7) M, but the former was significantly greater at 10(-6) M ouabain (p < 0.05). These results suggest that each Ca(2+)-activated K+ channel and Na(+)-K(+)-ATPase may a modulatory role in the cholinergic neurotransmission by inhibiting the exocytotic ACh release from the vagal nerve terminals.

Acetylcholine↗
PubMed1993

Molecular cloning and expression of cDNA encoding rat skeletal muscle cytosolic sialidase.

We have isolated a cDNA clone encoding the cytosolic sialidase of rat skeletal muscle. Degenerate oligonucleotides, based on amino acid sequence data for the purified enzyme, were used as primers to amplify fragments of the gene from rat skeletal muscle cDNA by the polymerase chain reaction. The amplified cDNA fragment was then applied as probe to screen a rat skeletal muscle cDNA library. The longest cDNA clone thus isolated was incomplete at the 5'-end, and therefore an amplified cDNA from the 5'-end portion of the gene was further generated by polymerase chain reaction. These two cDNAs were used to construct a cDNA encoding the entire sequence of rat sialidase. The composite sequence encodes an open reading frame of 379 amino acids that include all sequenced peptides. Although the deduced amino acid sequence is not largely similar to those of bacterial and parasite sialidases, it contains two Asp blocks, the conserved sequence of the sialidases from these microorganisms. When the cDNA was inserted into an expression vector followed by transformation in Escherichia coli, sialidase activity appeared in the cell extract. The sialidase could be completely immunoprecipitated by antiserum against the cytosolic sialidase of rat skeletal muscle.

Amino Acid Sequence↗