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  • 1
    ISSN: 1436-2813
    Keywords: Key Worlds: short bowel syndrome ; T-cell-mediated immunity ; TCR ζ molecule
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1436-2813
    Keywords: short bowel syndrome ; T-cell-mediated immunity ; TCR σ molecule
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We describe herein the case of a 48-year-old man who underwent emergency massive resection of the small intestine due to strangulated ileus, which led to short bowel syndrome (SBS) as he was left with 7 cm of jejunum and 8 cm of ileum. We evaluated the immune function in this patient, focusing particular attention on T-cell-mediated immunity. Biochemical and nutritional parameters, including minerals and trace elements, indicated that the patient was in relatively good health; however, the proliferative response to mitogen and tumor necrosis factor-α production in response to the anti-CD3 monoclonal antibody in peripheral blood lymphocytes (PBL) were impaired compared with age-matched postgastrectomy patients and healthy donors. Moreover, the expression of T-cell receptor (TCR) ζ, which is involved in signal transduction and the subsequent activation of T cells, was downregulated in this patient compared with that in the age-matched postgastrectomy patients and healthy donors. These observations suggest that T-cell function was disturbed in our patient, and that this dysfunction was associated with the decreased expression of TCR ζ molecules.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2013
    Keywords: Ca2+-activated K+ channels ; Maxi-K+ channel ; Tetraethylammonium ; Salivary gland ; Fluid secretion ; K+ efflux ; Epithelial transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The involvement of large-conductance, voltage- and Ca2+-activated K+ channels (maxi-K+ channels) in basolateral Ca2+-dependent K+-efflux pathways and fluid secretion by the rat submandibular gland was investigated. Basolateral K+ efflux was monitored by measuring the change in K+ concentration in the perfusate collected from the vein of the isolated, perfused rat submandibular gland every 30 s. Under conditions in which the Na+/K+-ATPase and Na+-K+-2Cl− cotransporter were inhibited by ouabain (1 mmol/l) and bumeta-nide (50 μmol/l) respectively, continuous stimulation with acetylcholine (ACh) (1 μmol/l) caused a transient large net K+ efflux, followed by a smaller K+ efflux, which gradually returned to the basal level within 10 min. These two components of the K+ efflux appear to be dependent on an increase in cytosolic Ca2+ concentration. The initial transient K+ efflux was not affected by charybdotoxin (100 nmol/l) or tetraethylammonium (TEA) (5 mmol/l) but the smaller second component was strongly and reversibly inhibited by charybdotoxin (100 nmol/l) and TEA (0.1 and 5 mmol/l). The initial K+ efflux transient induced by ACh was inhibited by quinine (0.1–3 mmol/l), quinidine (1–3 mmol/l) and Ba2+ (5 mmol/l), but not by verapamil (0.1 mmol/l), lidocaine (1 mmol/l), 4-aminopyridine (1 mmol/l) or apamin (1 μmol/l). Ca2+-dependent transient large K+ effluxes induced by substance P (0.01 μmol/l) and A23187 (3 μmol/l) were not inhibited by TEA (5 mmol/l or 10 mmol/l). A23187 (3 μmol/l) evoked a biphasic fluid-secretory response, which was not inhibited by TEA (5 mmol/l). Patch-clamp studies confirmed that the whole-cell outward K+ current attributable to maxi-K+ channels obtained from rat submandibular endpiece cells was strongly inhibited by the addition of TEA (1–10 mmol/l) to the bath. It is concluded that maxi-K+ channels are not responsible for the major part of the Ca2+-dependent basolateral K+ efflux and fluid secretion by the rat submandibular gland.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 429 (1995), S. 748-750 
    ISSN: 1432-2013
    Keywords: Whole-cell current ; Ca2+-dependent K+ channels ; Tetraethylammonium ; Salivary secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Using whole-cell patch-clamp techniques, we demonstrate, for the first time, that rat submandibular acinar cells contain a tetraethylammonium (TEA)-insensitive, Ca2+-activated K+ conductance which is not attributable to large conductance, voltage-sensitive, Ca2+-dependent K+ channels (maxi-K+ channels). Taken together with our recent K+ efflux and fluid secretion studies in intact rat submandibular gland, we postulate that the K+ conductance reported here may be involved in the basolateral K+ efflux pathway activated by cytosolic Ca2+ concentration during secretion by this gland.
    Type of Medium: Electronic Resource
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