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  • 1
    Electronic Resource
    Electronic Resource
    A novel synthetic vitamin D analogue, 2β-(3-hydroxypropoxy)1α, 25-dihydroxyvitamin D3 (ED-71), increases bone mass by stimulating the bone formation in normal and ovariectomized rats (1994)
    Springer
    Calcified tissue international 54 (1994), S. 142-149 
    Details
    ISSN: 1432-0827
    Keywords: Normal and ovariectomized rats ; Lumbar vertebra ; Bone formation ; Histomorphometry ; 2β-(3-hydroxypropoxy)-1α,25(OH)2D3
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Abstract We performed dosing experiments to evaluate the bone mass increasing action of a novel, synthetic vitamin D derivative, 2β-(3-hydroxypropoxy)-1α, 25(OH)2D3 (ED-71), in normal and estrogen-deficient rats. The first experiment consisted of 31 Sprague-Dawley rats, 28 weeks of age. The second experiment consisted of 44 animals who were ovariectomized (OVX) or sham operated at the age of 12 weeks. ED-71 was given twice a week for the duration of 12 weeks. At the end of the experiments, serum chemistries were examined and lumbar vertebrae were assessed histomorphometrically. Serum alkaline-phosphatase levels tended to decrease by ED-71 administration in the first experiment and their elevated values after ovariectomy were also depressed by ED-71 in the second experiment. Serum osteocalcin levels, however, increased by the agent. In the first experiment, cancellous bone volume (BV/TV) increased dose dependently. Bone formation rates (BFR/BS) also increased. In the second experiment, BV/TV significantly decreased by ovariectomy and it increased in ED-71-treated groups, but not in 1α-(OH)D3-treated group. BFR/BS increased by ED-71. Activation frequency did not decreased by ED-71 in either experiment. These data clearly demonstrated that ED-71 administration was capable of increasing the bone mass by stimulating bone formation in normal and estrogen-deficient rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296065
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  • 2
    Electronic Resource
    Electronic Resource
    Ionic basis of methacholine-induced shrinkage of dissociated eccrine clear cells (1991)
    Springer
    The journal of membrane biology 123 (1991), S. 33-41 
    Details
    ISSN: 1432-1424
    Keywords: eccrine ; sweat gland ; cell volume ; cholinergic ; Ca ; potassium ; chloride ; channels ; quinidine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The goal of the present study was to elucidate the ionic mechanisms by which cholinergic stimulation induces cell shrinkage in eccrine clear cells. Dissociated Rhesus monkey eccrine sweat clear cells were prepared by collagenase digestion of freshly isolated secretory coils and immobilized on a glass slide in a perfusion chamber at 30°C. The cell was visualized by light microscopy with differential interference contract (DIC) and was recorded with a video system (15,000× total magnification). The cell volume was calculated from the maximal cross section of the cell. Methacholine (MCh)-induced cell shrinkage, which was as much as 30% of resting cell volume, was dose dependent and pharmacologically specific. MCh-induced cell shrinkage was persistent in some cells but tended to partially wane with time in others. MCh-induced cell shrinkage was dependent on the chemical potential gradient for KCl, i.e., increasing [K] in the bath ([K] o ) from 5 to 120mm caused MCh to induce cell swelling, whereas removing [Cl] o at 120mm K partially restored the MCh-induced cell shrinkage. The interpolated null [K] o (medium [K] where the cell volume did not change by MCh) of 71mm agreed with the predicted [K] o,null. MCh-induced cell shrinkage was inhibited completely by 1mm quinidine (K-channel blocker) and partially by 1mm diphenylamine-2-carboxylic acid (DPC, a Cl-channel blocker), but not by 0.1mm ouabain or 0.1mm bumetanide, suggesting that MCh-induced cell shrinkage may be due to activation of both K and Cl channels with the resultant net KCl efflux down the chemical potential gradient. That Ca/calmodulin may be involved in cholinergic regulation of Cl and K channels is suggested because 10 μm ionomycin also induced cell shrinkage, MCh failed to induce cell shrinkage in a Ca-free medium after the endogenous Ca store was depleted, and (6-aminohexyl)-5-chlorol-naphthalenesulfonamide (W-7, a putative inhibitor of calmodulin) also inhibited MCh-induced cell shrinkage in a reversible manner.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01993960
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    Paper (German National Licenses)
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