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  • 1
    Electronic Resource
    Electronic Resource
    Effects of the immunosuppressant cyclosporin A on neurotransmitter release from peripheral non-adrenergic, non-cholinergic nerves (1997)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 356 (1997), S. 398-403 
    Details
    ISSN: 1432-1912
    Keywords: Key words Cyclosporin A ; Substance P ; Nicardipine ; Voltage-dependent Ca2+ channels ; Neurotransmitter ; release ; Smooth muscle contraction ; Tachykininergic ; nerves ; Rabbit iris sphincter muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study was undertaken to determine the effect of the immunosuppressant cyclosporin A on neurotransmitter release from non-adrenergic, non-cholinergic nerves (tachykininergic nerves) in the rabbit iris sphincter muscle. Cumulative application of cyclosporin A (0.1 to 10 μM) caused a slow onset of contraction in a concentration-dependent manner. Both FK888 (1 μM) and capsaicin (10 μM), a substance P receptor antagonist and a substance P-depleting agent, respectively, inhibited the contractile effect of cyclosporin A, whereas atropine (1 μM) had no effect. Both cyclosporin A and capsaicin (10 μM) stimulated the release of substance P-like immunoreactivity in the iris. Neither the sodium channel blocker tetrodotoxin (1 μM), the N-type voltage-dependent Ca2+ channel blocker ω-conotoxin GVIA (1 μM) nor the P-type channel blocker ω-agatoxin IVA (0.2 μM) affected cyclosporin A (1 μM)-induced contraction. In contrast, the L-type Ca2+ channel blocker nicardipine (10 μM) inhibited this contractile effect. These results suggest that cyclosporin A stimulates substance P-like tachykinin release by activating L-type voltage-dependent Ca2+ channels, resulting in contraction of the rabbit iris sphincter muscle.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005068
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  • 2
    Electronic Resource
    Electronic Resource
    Involvement of both L- and N-type voltage-dependent Ca2+ channels in KCl- and veratridine-evoked transmitter release from non-adrenergic, non-cholinergic nerves in the rabbit iris sphincter muscle (1997)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 355 (1997), S. 638-644 
    Details
    ISSN: 1432-1912
    Keywords: Key words Voltage-dependent Ca2+ channels ; x-Agatoxin IVA ; ω-Conotoxin GVIA ; Nicardipine ; Neurotransmitter release ; Tachykininergic nerves ; Smooth muscle contractions ; Rabbit iris sphincter muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To determine which types of voltage-dependent Ca2+ channels mediate tachykinin release in the isolated rabbit iris sphincter muscle, we examined the effects of several Ca2+ channel modulators on contractions induced by either an elevation of the extracellular KCl concentration or application of the Na+ channel activator veratridine. Contractions caused by either 45.9mMKCl or veratridine (10μM) were inhibited by spantide (10μM), a tachykinin receptor antagonist, and capsaicin (10μM), a tachykinin-depleting agent, but were not changed by atropine. Nicardipine, an L-type Ca2+ channel blocker, inhibited contractions induced by KCl and veratridine in a concentration-dependent manner. ω-Conotoxin GVIA (1μM), an N-type Ca2+ channel blocker, inhibited only contractions induced by lower concentrations of KCl, both when applied alone and when combined with nicardipine. Bay K8644, an L-type Ca2+ channel activator, caused a spantide- and nicardipine-sensitive contraction in muscles partially depolarized with 15.9mMKCl, and enhanced contractions induced by 15.9mMKCl and veratridine (2μM). ω-Agatoxin IVA (0.3μM), a P-type voltage-dependent Ca2+ channel blocker, did not affect contractions induced by either KCl or veratridine. Contractions induced by exogenous substance P were not modified by any of the Ca2+ channel blockers or by Bay K8644. These results suggest that, in the rabbit iris sphincter muscle, L- and N-type voltage-dependent Ca2+ channels are involved in neurotransmitter release from tachykininergic nerves elicited by high KCl and by veratridine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00004995
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  • 3
    Electronic Resource
    Electronic Resource
    Cytokine-Induced Neutrophil Chemoattractants in Healing of Gastric Ulcers in Rats (Expression of 〉40-kDa Chemoattractant in Delayed Ulcer Healing by Indomethacin) (1999)
    Springer
    Digestive diseases and sciences 44 (1999), S. 889-895 
    Details
    ISSN: 1573-2568
    Keywords: GASTRIC ULCERS ; NEUTROPHIL INFILTRATION ; CHEMOTACTIC ACTIVITY
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined the roles of cytokine-inducedneutrophil chemoattractants (CINCs) in neutrophilinfiltration of ulcerated gastric tissue in rats.Neutrophil chemotactic and myeloperoxidase (MPO)activities were negligible in the normal mucosa but weremarkedly elevated by ulceration. The activitiesdecreased with spontaneous ulcer healing, but remainedquite high when the healing was prevented byindomethacin. Neither CINC-1 nor CINC-2α was detected,and CINC-3 was negligible in the normal mucosa. Theexpression of these CINCs was also promoted byulceration, but the expression patterns during ulcerhealing were apparently different among them. Thechange in net content of CINCs was well associated withthose in chemotactic and MPO activities duringspontaneous healing. The chemotactic activity due to the net CINCs was equivalent to most parts of theactivity extracted from the tissue. On the other hand,indomethacin did not affect CINC expression, comparedwith that in spontaneous healing, but induced the expression of high-molecular-weight(〉40-kDa) chemoattractant when ulcer healing wasimpaired. The chemotactic activity due to 〉40-kDachemoattractant was equivalent to the activity extractedfrom the tissue. We conclude that CINCs play crucialroles in neutrophil infiltration of ulcerated gastrictissue in the spontaneous healing in rats and that theexpression of CINCs might be differentially regulated. Furthermore, the 〉40-kDa chemoattractantmight be the predominant contributor to the increasedneutrophil infiltration in the delayed healing byindomethacin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026683824850
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  • 4
    Electronic Resource
    Electronic Resource
    Novel stabilization pattern of thermolysin due to the binding substrate induced by electrostatic change in enzyme active site caused by the temperature elevation (2000)
    Springer
    Biotechnology letters 22 (2000), S. 295-300 
    Details
    ISSN: 1573-6776
    Keywords: fluorescence spectra ; phenylalanine methyl ester ; substrate binding ; thermolysin ; thermostabilization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract During the synthesis of the dipeptide, N-benzyloxycarbonyl-l-phenylalanyl-l-phenylalanine methyl ester, from N-benzyloxycarbonyl-l-phenylalanine and l-phenylalanine methyl ester by thermolysin, the enzyme was stabilized by 20 °C up to 110 °C. The stabilization was caused by the interaction of the enzyme with Phe-OMe, a counterpart of the substrate, which was bound at the enzyme active site due to the drop in pH and dielectric constant following the temperature elevation of the medium. The binding of the enzyme to Phe-OMe suggested the induction of the transition state formation at around 80 °C based on the UV spectra, resulting in the increase in the stability in the higher temperature region. The fluorescence second-order derivative spectra suggested that the binding Phe-OMe interacted with Trp 115 at the active site of the enzyme. The phenomenon was considered to be a novel stabilization pattern of the enzyme resulting from the conduction due to the chemical modification by the binding substrate.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005626516201
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  • 5
    Electronic Resource
    Electronic Resource
    Pathological Changes in the Formation of Helicobacter pylori-Induced Gastric Lesions in Mongolian Gerbils (1998)
    Springer
    Digestive diseases and sciences 43 (1998), S. 754-765 
    Details
    ISSN: 1573-2568
    Keywords: H. PYLORI ; MONGOLIAN GERBIL ; GASTRIC MUCOSAL LESIONS ; INFLAMMATION ; MYELOPEROXIDASE ; NEUTROPHIL CHEMOTAXIS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined pathological changes in theformation of Helicobacter pylori-induced gastric lesionsin Mongorian gerbils. H. pylori (NCTC11637) was orallyadministered once to the animals and was detected in the gastric mucosa of all gerbils given thebacteria. The number of viable H. pylori increasedduring the initial two weeks and thereafter reached aplateau level. The initial pathological changes were found at one week, ie, edema/congestion and awhite viscous substance only in the antrum. At twoweeks, superficial damage appeared in the antrum,although inflammatory cell infiltration had notoccurred. Gastritis with lymphoid follicles was observedin the antrum and fundus from three weeks. At fourweeks, mucosal lesions were detected as a fewhemorrhagic spots in the fundus adjacent to the antrum.In the control animals, however, no pathologicalchanges were observed even at four weeks. In the gastricmucosa infected with H. pylori , myeloperoxidaseactivity was negligible at two weeks, but was extremely elevated at four weeks. Similarly, neutrophilchemotactic activity was only slightly increased at twoweeks, but was markedly elevated at four weeks. Theseresults indicate that H. pylori infection induces initial pathological changes only in theantrum, but mucosal lesions occur in the fundus adjacentto the antrum. Furthermore, it is demonstrated that theinitial superficial damage is generated by factors other than chemokines and neutrophil-associatedfactors, although mucosal inflammation may contribute tothe subsequent formation of lesions andulcers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018861930068
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  • 6
    Electronic Resource
    Electronic Resource
    Correlation between the virulence ofFrancisella tularensis in experimental mice and its acriflavine reaction (1992)
    Springer
    Current microbiology 25 (1992), S. 95-97 
    Details
    ISSN: 1432-0991
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Correlation between the virulence ofFrancisella tularensis in experimental mice and its acriflavine reaction was studied. The cultures derived from all four strains (Ebina, CMB2, Schu, and N9) that had long been subcultured on agar media yielded two types of colonies, i.e., acriflavine reaction-positive (acf+) and acriflavine reaction-negative (acf−) colonies. All acf+ colonies, regardless of their parent strains, were shown to be low virulent in mice. Acf− colonies were shown to be either high (Ebina, CMB2) or low (Schu, N9) virulent. The low-virulent acf− colonies gained virulence during several passages in mice, whereas the acf+ colonies remained low virulent even after the animal passages.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01570966
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