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  • 1995-1999  (2)
  • 1970-1974  (1)
  • 1965-1969
  • Apoptosis  (1)
  • Calcium  (1)
  • MKN 28  (1)
Material
Years
  • 1995-1999  (2)
  • 1970-1974  (1)
  • 1965-1969
Year
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 12 (1973), S. 8-15 
    ISSN: 1432-0827
    Keywords: Insulin ; Bone ; Calcium ; Resorption ; Orthophosphate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Description / Table of Contents: Résumé L'administration d'insuline cristallisée à des rats thyroparathyroidectomisés provoque une augmentation de la calcémie et de la phosphorémie. Le calcium plasmatique s'élève de façon linéaire entre 31 et 250 m Unités d'insuline/100 g de poids corporel. La courbe obtenue n'est guère différente de celle obtenue par extrait parathyroidien. L'administration simultanée d'insuline et d'extrait parathyroidien à des rats thyro-parathyroidectomisés agit sur la calcémie et la phosphorémie par un effet additif. Lorsque des os frontaux d'embryons de poulet sont cultivésin vitro en présence d'insuline cristallisée, le taux de résorption augmente. L'insuline augmente le taux de consommation en glucose des explants et induit une accumulation de citrate dans le milieu de culture. L'insuline stimule donc la résorption osseuse.
    Abstract: Zusammenfassung Der Plasmagehalt an Calcium und Phosphor bei thyroparathyreoidektomierten Ratten wurde durch die Verabreichung von kristallinem Insulin erhöht. Das Plasmacalcium verhielt sich zwischen 31 und 250 m Einheiten Insulin pro 100 g Körpergewicht linear. Die Steigung der erhaltenen Kurve ist nicht signifikant verschieden von derjenigen, die nach Parathyreoidea-Extrakt erhalten wird. Die gleichzeitige Verabreichung von Insulin und Parathyreoidea-Extrakt von thyroparathyreoidektomierten Ratten hatte eine kumulative Wirkung auf den Gehalt von Calcium und Phosphor im Plasma. Wenn Stirnbeine von Kükenembryos mit kristallinem Insulinin vitro kultiviert wurden, erhöhte sich die Resorptionsrate. Das Insulin steigerte den Glucoseverbrauch der Explantate und verursachte eine Anreicherung von Citrat im Kulturmedium. Die Ergebnisse deuten auf eine Stimulation der Knochenresorption durch Insulin.
    Notes: Abstract the administration of crystalline insulin to thyroparathyroidectomized rats raised their calcium and phosphorus plasma levels. The plasma calcium gave a linear response between 31 and 250 mU of insulin/100 g body weight. The slope obtained is not significantly different from that obtained with parathyroid extract. The simultaneous administration of insulin and parathyroid extract to thyroparathyroidectomized rats affected the calcium and phosphorus plasma levels in an additive fashion. When chick embryo frontal bones were cultivatedin vitro with crystalline insulin the rate of resorption increased. Insulin increased the rate of glucose consumption by the explants and induced the accumulation of citrate in the culture medium. It is concluded that insulin stimulates bone resorption.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-675X
    Keywords: Apoptosis ; CD95 (Fas/APO-1) ; NF-κB/Rel ; T lymphocytes.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The activity of NF-κB/Rel transcription factors can inhibit the apoptosis induced by TNF, UV or cancer therapy drugs in a number of cell types, including human T lymphocytes. Furthermore, the NF-κB/Rel inducer, phorbol-12-myristate-13-acetate (PMA), has been reported to suppress the CD95-induced apoptosis of human T lymphocytes. To verify whether the survival-enhancing effect of PMA required NF-κB/Rel activity, we generated two Jurkat cell sublines (AL.7 and AL.8) transfected with a pCMV4-IκBα construct, and two (AL.3 and AL.5) with the void pCMV4 vector. Compared to wild type, AL.3 and AL.5 cells, the AL.7 and AL.8 sublines displayed markedly lower amounts of NF-κB/Rel nuclear complexes and a reduced expression of a κB-controlled CAT reporter gene after 1 and 4 h of incubation with PMA, respectively. All the five cell types displayed negligible levels of apoptosis when cultured with medium or PMA alone; when stimulated with the mAb CH-11, the AL.7 and AL.8 sublines displayed apoptotic responses only slightly (〈0.5 fold) higher than control cells. On the other hand, the salvage activity of PMA was partially impaired in the AL.7 and AL.8 sublines. PMA inhibited apoptosis by 〉85% in wild type, AL.3 and AL.5 cells and by 〈60% in the AL.7 and AL.8 sublines; the apoptosis percentages in the mAb CH-11 + PMA cultures of the IκBα-transfected cells were 〉4-fold higher than in control cells. We conclude that the inhibition of the CD95-induced apoptosis by PMA relies on both NF-κB/Rel-dependent and -independent mechanisms. The partial contribution of these nuclear factors to the suppression of apoptosis indicates that the NF-κB/Rel activity can influence the extent of the CD95-induced T cell death.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-2568
    Keywords: roxatidine ; ranitidine ; MKN 28 ; cell proliferation ; cell migration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Gastric mucosal cell migration and proliferation are crucial events in the repair of gastric mucosal erosions. This study was designed to test the hypothesis that the H2 blockers roxatidine and ranitidine might stimulate migration and proliferation of gastric mucous cells derived from a human well-differentiated gastric adenocarcinoma cell line (MKN 28 cells)in vitro, in conditions independent of systemic factors and of acid inhibition. Confluent monolayers of MKN 28 cells were wounded with a razor blade and were then incubated with roxatidine or ranitidine. The number of cells migrating to the damaged area was determined 24 hr later. Cell proliferation was assessed by means of [3H]thymidine uptake and cell counts after incubation with roxatidine or ranitidine. Neither H2 antagonist significantly stimulated cell migration. On the other hand, cell proliferation was dose-dependently and significantly enhanced by incubation with roxatidine and ranitidine. Exogenous administration of TGF-α significantly stimulated MKN 28 cell division. However, incubation with roxatidine or ranitidine did not increase the steady-state mRNA expression of TGF-α or EGFR as assessed by northern blot analysis. Based on thesein vitro findings, we postulate that the ulcer healing effect of these H2 antagonistsin vivo might be due in part to stimulation of gastric mucosal cell proliferation.
    Type of Medium: Electronic Resource
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