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  • Articles  (12)
  • Bone resorption  (12)
  • Springer  (12)
  • American Institute of Physics
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  • 1995-1999
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  • Physics  (12)
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  • Articles  (12)
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  • Springer  (12)
  • American Institute of Physics
  • Elsevier
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  • 1995-1999
  • 1990-1994  (12)
  • 1965-1969
  • 1955-1959
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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 51 (1992), S. 18-19 
    ISSN: 1432-0827
    Keywords: Hypercalcemia ; Calcitonin ; Cancer ; Bone resorption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary We treated four hypercalcemic cancer patients by nasal hCT, 3×2 mg daily, which has been reported to be active in Paget's disease at lower doses. Only one patient became normocalcemic and mean (± SEM) calcium levels fell from 11.6±0.2 mg/dl before therapy to 10.7±0.6 mg/dl 2–3 days after starting hCT. The tolerance was excellent but, because of insufficient efficacy, we do not recommend this form of therapy for cancer hypercalcemia.
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 51 (1992), S. S27 
    ISSN: 1432-0827
    Keywords: Ipriflavone ; Calcitonin ; Estrone ; Bone resorption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Ipriflavone is known to stimulate calcitonin (CT) secretion from the thyroid glands of female animals, but the exact mechanism of this action remains unknown. In the present study, an increase of CT production in thyroid C cells of female rats, but not of male rats, was proven immunohistochemically. Furthermore, the parallel increase of CT mRNA in those thyroid glands was confirmed by Northern blot analysis. These results proved that ipriflavone stimulates not only CT secretion but also CT synthesis in thyroid C cells and that the changes were gender dependent (greater in females). In order to investigate the effect of estrogen on the ipriflavone-induced increase of CT in female rat thyroid gland, CT and CT mRNA in the thyroid glands of untreated, ovariectomized, and estrone-treated (postovariectomy) rats were examined by both immunohistochemistry and Northern blot technique. Serum levels of CT and calcium were also examined. Against expectation, estrone failed to produce any significant effect on the ability of ipriflavone to induce CT synthesis and secretion.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 50 (1992), S. 189-192 
    ISSN: 1432-0827
    Keywords: Bone resorption ; Glucocorticoid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Chronic glucocorticoid excess is associated with the development of osteoporosis and, in human subjects, there is histomorphometric evidence of increased bone resorption. Paradoxically, most in vitro studies have suggested that glucocorticoids inhibit bone resorption but recently two groups have demonstrated increased osteolysis in glucocorticoid-treated bone organ cultures. The present study reexamines the effect of cortisol on basal bone resorption in neonatal mouse calvaria with particular emphasis on the effect of serum supplementation of the media. In the absence of serum, 45Ca release was significantly stimulated by 10-7 M cortisol (treatment/control 1.37+-0.06, P〈0.005) and by 10-6 M cortisol (treatment/control 1.27+-0.08, P〈0.005). The stimulation of resorption by 10-7 M hydrocortisone was progressive from 24 to 96 hours of incubation. In contrast, when calvaria were incubated in the presence of 5% serum, bone resorption was not increased by cortisol (10-8 M-10-6 M). In the presence of 5% charcoal-stripped, heat-inactivated serum, there was a small stimulation of 45Ca release at 10-6 M hydrocortisone only (treatment/control 1.19 +-0.06, P〈0.01). Incubation of bones with indomethacin did not modify the effect of cortisol in either the presence or absence of serum. In serum-free conditions, cortisol 10-8 M significantly inhibited the rate of thymidine incorporation, though at higher concentrations this effect was not seen. Cortisol produced a dose-related inhibition of serumstimulated thymidine incorporation. It is concluded that the presence of serum substantially modifies the effect of cortisol on basal bone resorption. The cortisol-induced stimulation of bone resorption which is seen in serum-free conditions is sustained over time and is not mediated by alterations in prostaglandin synthesis.
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  • 4
    ISSN: 1432-0827
    Keywords: Ipriflavone ; Osteoclasts ; Pit formation ; Bone resorption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Effects of ipriflavone (7-isopropoxyisoflavone) on osteoclast-induced bone resorption were evaluated using an unfractionated bone cell culture system containing mature osteoclasts from the femur and tibia of newborn mice. When cells were cultured for 4 days on dentin slices in the presence of 5% fetal bovine serum and 10−8 M 1α,25(OH)2D3, ipriflavone (3 x 10−7-3 x 10−5 M) inhibited pit formation and caused a decrease in the number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells (MNCs). The lowest significant effect was observed at a concentration of 10−6 M. Unlike ipriflavone, calcitonin inhibited pit formation 4 days after the culture was started without affecting the number of TRAP-positive MNCs. Ipriflavone still inhibited pit formation when the culture period was 13 days, when new osteoclasts were expected to be formed. These findings suggest that ipriflavone inhibits new osteoclast formation and bone resorption at the cellular level.
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 51 (1992), S. 387-392 
    ISSN: 1432-0827
    Keywords: Tumor necrosis factor ; Cytokine ; Bone resorption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary In many tissues the actions of tumor necrosis factor-α (TNF) are indirectly mediated through the production of autacoids or other cytokines. To determine the role that these factors might have in the action of TNF on bone resorption, we examined the effects of several selective inhibitors on TNF-stimulated resorption. The cyclooxygenase inhibitor indomethacin did not prevent TNF-stimulated resorption in fetal rat limb bones. Stimulation of resorption by TNF was also unaffected by the platelet activating factor antagonist WEB 2086. A 17.5 kD interleukin receptor antagonist protein, at concentrations that completely blocked the bone-resorbing actions of maximally effective concentrations of interleukin (IL)-1β, failed to affect the stimulatory actions of TNF. TNF-stimulated resorption was inhibited by both interferon-γ and dexamethasone. Dexamethasone inhibited TNF-stimulated resorption more effectively than it inhibited parathyroid hormone (PTH)-stimulated resorption. When bones were treated simultaneously with low concentrations of TNF and PTH, potentiation of the bone-resorbing effects was elicited. These results suggest that TNF stimulates resorption through a pathway different from that by which PTH produces its effects. Transforming growth factor-β (TGF-β) enhanced responses to TNF; TGF-β failed to inhibit the effects of TNF, even in long-term culture or when bones were pretreated with TGF-β. Synergistic interactions between TNF and several other bone-resorbing factors have now been demonstrated. In contrast to the actions of TNF on certain other functions, the bone-resorbing effects of TNF, as determined in the fetal rat limb bone system, do not seem to be mediated by PAF, IL-1, or prostaglandins.
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  • 6
    ISSN: 1432-0827
    Keywords: Prostaglandin E2 ; Long-term treatment ; Cancellous bone ; Bone formation ; Bone resorption ; Bone turnover ; Remodeling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The effects of long-term prostaglandin E2 (PGE2) on cancellous bone in proximal tibial metaphysis were studied in 7-month-old male Sprague-Dawley rats given daily subcutaneous injections of 0, 1, 3, and 6 mg PGE2/kg/day and sacrificed after 60, 120, and 180 days. Histomorphometric analyses were performed on double fluorescent-labeled undecalcified bone specimens. After 60 days of treatment, PGE2 produced diffusely labeled trabecular bone area, increased trabecular bone area, eroded and labeled trabecular perimeter, mineral apposition rate, and bone formation rate at all dose levels when compared with age-matched controls. In rats given PGE2 for longer time periods (120 and 180 days), trabecular bone area, diffusely labeled trabecular bone area, labeled perimeter, mineral apposition, and bone formation rates were sustained at the elevated levels achieved earlier at 60-day treatment. The eroded perimeter continued to increase until 120 days, then plateau. The observation that continuous systemic PGE2 administration to adult male rats elevated metaphyseal cancellous bone mass to 3.5-fold of the control level within 60 days and maintained it for another 120 days indicates that the powerful skeletal anabolic effects of PGE2 can be sustained with continuous administration.
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  • 7
    ISSN: 1432-0827
    Keywords: Osteoblast conditioned medium ; Osteoclast precursors ; Bone resorption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Osteoblasts are thought to secrete factors that regulate the rate of osteoclastic bone resorption. We studied the effect of osteoblast conditioned medium on bone degradation by multinucleated osteoclast-like cells generated in vitro from mononuclear precursors and found that the medium stimulates bone degradation primarily through interactions with osteoclast precursors. The conditioned medium also stimulates expression of the osteoclast-specific antigen 121F. The increased bone degradation, but not increased 121F expression, is due to the conditioned medium maintaining activity of the osteoclast precursors. Although the osteoclast precursors exhibit the DNA fragmentation characteristic of apoptosis, the osteoblast conditioned medium does not prevent such fragmentation. Chicken macrophage growth factor neither mimics nor augments the ability of the conditioned medium to stimulate bone degradation. Studies of osteoclast generation or function should carefully consider whether the effects are dependent on the viability of the resorbing cells.
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 51 (1992), S. 424-428 
    ISSN: 1432-0827
    Keywords: Bone resorption ; Caffeine ; Cyclic AMP ; Osieoporosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary In view of the possible association between ingestion of caffeine (a constituent of coffee, tea, and several beverages) and osteoporosis, we have studied the effect of caffeine on bone resorption in vitro. Caffeine caused a dose-dependent increase of the spontaneous release of 45Ca from neonatal mouse calvarial bones. The effect of caffeine was less pronounced than that of parathyroid hormone (PTH), but of the same magnitude as that of theophylline, a structurally related methylxanthine. The enhancement of 45Ca release induced by caffeine and PTH was observed in 5 days culture. In 2 days culture, however, only PTH stimulated mineral mobilization. The delayed stimulatory effect of caffeine in long-term cultures was abolished by indomethacin and flurbiprofen. In indomethacin-treated bones, however, caffeine potentiated the stimulatory effect on 45Ca release induced by choleratoxin and forskolin. In contrast, caffeine did not potentiate 45Ca release stimulated by PTH. These data show that caffeine can stimulate calcium release from bone in vitro and that this effect is due to potentiation of a stimulatory action of a bone resorptive agonist acting via the adenylate cyclase-cyclic AMP system.
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  • 9
    ISSN: 1432-0827
    Keywords: Bone resorption ; Osteoclast formation ; Bone Ca mobilization ; 26,27-Dialkyl-1α,25-dihydroxyvitamin ; D3-Osteopenia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary A series of analogs of 1α,25-dihydroxyvitamin D3[1,25(OH)2D3] with alkyl substitutions in 26- and 27-positions were tested for calcium (Ca) regulating activity. The potencies of dialkyl analogs in stimulating bone resorption in neonatal mouse calvaria cultures were the highest in 1α,25-dihydroxy-26,27-dimethylvitamin D3[1,25(OH)2-(Me)2D3], followed by 1,25(OH)2D3, 1α,25-dihydroxy-26,27-diethylvitamin D3[1,25(OH)2(Et)2D3], and 1α,25-dihydroxy-26,27-dipropylvitamin D3[1,25(OH)2(Pr)2D3] in that order. A similar order of potential regarding formation of osteoclast-like cells in mouse bone marrow cell cultures and on bone Ca mobilization with long-term vitamin D-deficient rats was observed in the same series. The relative potencies of 1,25(OH)2D3, 1,25(OH)2(Me)2D3, 1,25(OH)2(Et)2D3, and 1,25(OH)2(Pr)2D3 in competing with 1,25(OH)2D3 for binding to chick intestinal cytosol receptors were 1:1:0.16:0.036. A similar order of potential in case of intestinal Ca transport in situ was observed in the same series. The potencies of dialkyl analogs in competing with 25-hydroxy-vitamin D3 for binding to rat serum vitamin D binding protein were much lower than that of 1,25(OH)2D3. Effect of 1,25(OH)2(Me)2D3 on osteopenia in rats induced by ovariectomy and right sciatic neurotomy was higher than that of 1,25(OH)2D3. From these results, the lengthening by one carbon at 26- and 27-positions was shown to maintain the Ca regulatory activity of 1,25(OH)2D3.
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 51 (1992), S. S21 
    ISSN: 1432-0827
    Keywords: Ipriflavone ; Bone resorption ; Osteogenesis ; Confocal scanning laser microscope
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Bone labeling, histochemical, and fine structural studies were performed in order to clarify the effects of ipriflavone (IP) on rat bone tissuein vivo andin vitro. Labeling experiments showed a slight increase in bone formation during 3 days' administration. It was also noted that many osteoclasts detached from the bone surface at 1, 2, and 6 hours after administrationin vivo. In addition, irregular localization of tartrate-resistant acid phosphatase (TRACPase) activity was observed in osteoclasts. Fine structurally, IP-treated osteoclasts exhibited irregularity in their ruffled borders, as reported in calcitonin administration, and many enlarged rough endoplasmic reticuli and vacuoles were observed. However, osteoclasts at 12 hours after administration, as well as the control, indicated recovery features from the effect of IP. Osteoblast proliferation and differentiation led to increasing alkaline phosphatase activity (ALPase) with time as well as the development of rough endoplasmic reticuli and Golgi apparatus with well-developed fine structure. These findings imply active synthesis of bone matrix. In ourin vitro experiment, osteoclasts and osteoblasts displayed histochemical and fine structural characteristics Similar to those observed in ourin vivo experiment. Moreover, fewer TRACP-positive mononuclear cells were observed after 24-hour culture with IP than with the control. These results suggest that IP inhibits directly and/or indirectly differentiation and activity of osteoclasts and also promotes differentiation of osteoblast-lineage cells and their bone-forming activity.
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  • 11
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 50 (1992), S. 123-128 
    ISSN: 1432-0827
    Keywords: Thyroid hormones ; Cyclosporins ; TGFβ1 ; Bone resorption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary To study the mechanism of action of thyroid hormones on bone, we examined the effects of immunosuppresive and nonimmunosuppressive cyclosporins, as well as of transforming growth factor β1 (TGFβ1), 17β-estradiol (E2), and dihydroxytestosterone (DHT) on thyroxine (T4)-and triiodothyronine (T3)-stimulated bone resorption in fetal rat limb bones. The immunosuppressive cyclosporins A (CsA) and G (CsG) inhibited thyroid hormone (T4+T3)-stimulated resorption and β-glucuronidase release into the culture medium, whereas the weak or nonimmunosuppressive cyclosporins D (CsD) and H (CsH) did not show this effect. Increasing the medium calcium concentration reduced the ability of T4 to stimulate 45Ca release, while not significantly affecting the response to CsA. TGFβ1 elicited a biphasic effect when administered together with T4. During the first 3 days of culture, TGFβ1 elicited a small, nonsignificant decrease in released 45Ca; during a subsequent 3 days of culture, it enhanced T4-stimulated bone resorption significantly. These effects differed from those of TGFβ1 on parathormone-stimulated resorption. E2 and DHT did not influence the action of T4 on bone tissue. These results suggest that the mechanism of action of thyroid hormones on bone may involve immune factors, as well.
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  • 12
    ISSN: 1432-1017
    Keywords: Cell shape ; Cell motility ; Osteoclasts ; Bone resorption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Physics
    Notes: Abstract We describe the in vitro morphometric changes shown by rat osteoclasts that accompany their functional responses to the application of a range of regulatory agents of known physiological importance. We introduce a cellular motility parameter, µ, which was defined through a quantification of retraction-protrusion behaviour. This was used in conjunction with a net cell retraction, ϱ, which is derived from the change in total cell area following the application of an agent. These terms were used together for the description of cellular motility changes in response to specific cellular regulatory agents. The definition of retraction-protrusion was normalised against control cell area, to give a dimension-less variable independent of the net cell retraction. Thus, mutual terms present in either descriptor cancelled when the complementary parameter was held constant. Furthermore, the descriptor, µ remained time-invariant for extended intervals (around 20 min) even when ϱ was varying following cell introduction into culture. Interventions also with substances known to modify osteoclast function, were capable of altering each descriptor, to different extents. Thus elevation of the extracellular Ca2+ concentration ([Ca2+]e) at the osteoclast calcium “receptor” altered ϱ without changes in µ. In contrast, the polypeptide amylin (250 nM), within 20 minutes of application, elicited a marked change in µ, but only a relatively small change in ϱ. Finally, human calcitonin treatment (300 pM) influenced both descriptors. When combined together, these morphometric findings accordingly offer complementary descriptions of visible cellular changes in response to added agents of physiological relevance. Such an approach may be useful in the analysis of structure-function relationships in osteoclasts or other cell systems particularly in correlations between quantitative structure and functional responsiveness.
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