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  • 1995-1999  (2)
  • Alkylstannylhydrid  (1)
  • Key words Atherosclerosis – extracellular matrix – HMG-CoA reductase inhibitors – smooth muscle – thrombospondin  (1)
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Years
  • 1995-1999  (2)
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Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Hydrierung von Silicium-Halogen-Verbindungen mittels Trialkylstannylchlorid/Natriumhydrid (1995)
    Springer
    Monatshefte für Chemie 126 (1995), S. 549-555 
    Details
    ISSN: 1434-4475
    Keywords: Alkylstannylhydrid ; Hydrierung ; Organochlorsilane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Description / Table of Contents: Summary Organotinchlorides of the general formula R3SnCl and R2SnCl2 (R=Me,n-Bu, Ph) can easily be converted into the corresponding hydrides R3SiH and R2SiH2 employing NaH in diethylene glycol dialkyl ethers. Using trialkyltinhydrides like Bu3SnH in combination with a catalyst (tertiary amines, N-heterocycles, phosphonium or ammonium salts), Si-Cl bonds in mono- and disilanes are hydrogenated. In the case of disilanes, Si-Si bond cleavage and concurrent hydrogenation can be afforded with strongly nucleophilic catalysts. Partial hydrogenation is also possible. The whole process can be run cyclically.
    Notes: Zusammenfassung Organostannylchloride vom Typ R3SnCl und R2SnCl2 (R=Me,n-Bu, Ph) können in einfacher Weise mit NaH zu den entsprechenden Hydriden R3SnH und R2SnH2 umgesetzt werden, wenn als Lösungsmittel Diethylenglykoldialkylether verwendet werden. Trialkylzinnhydrid wie Bu3SnH können zur Hydrierung von Si-Cl-Bindungen in Mono- und Disilanen eingesetzt werden, wobei in Abhängigkeit vom notwendigen Katalysator (tertiäre Amine, N-Heterocyclen, λ3-Phosphorverbindungen, Ammonium- und Phosphoniumsalze) nur hydriert oder (mit stark nucleophilen Katalysatoren) auch die Si-Si-Bindung gespalten werden kann. Durch Verwendung eines Unterschusses an Bu3SnH können auch gezielt teilhydrierte Produkte erhalten werden. Das Verfahren kann als Kreislaufprozeß geführt werden.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00807428
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Effect of HMG-CoA reductase inhibitors on extracellular matrix expression in human vascular smooth muscle cells (1999)
    Springer
    Basic research in cardiology 94 (1999), S. 322-332 
    Details
    ISSN: 1435-1803
    Keywords: Key words Atherosclerosis – extracellular matrix – HMG-CoA reductase inhibitors – smooth muscle – thrombospondin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Clinical studies have shown that treatment with 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors can stabilize atherosclerotic plaques and slow their progression. One determinant of plaque stability and size is the composition of the vascular extracellular matrix. The aim of this study was to evaluate the effects of different HMG-CoA reductase inhibitors on the expression of major components of the vascular extracellular matrix in smooth muscle cells. Cultured human vascular smooth muscle cells were incubated for 24–72 h with the HMG-CoA reductase inhibitors lovastatin (1–50 μmol/L), simvastatin (0.05–20 μmol/L), and pravastatin ( 1–100 μmol/L). RNA expression of the extracellular matrix proteins thrombospondin-1, fibronectin, collagen type I, and biglycan as well as expression of the cytokine TGF-β1 was determined by Northern blotting. Extracellular matrix protein secretion was visualized by immunofluorescence. In addition, cell proliferation and viability were measured using BrDU-ELISAs, MTT-tests, and direct cell counting. Expression of thrombospondin-1 was significantly decreased after 24 h incubations with lovastatin in concentrations as low as 1 μmol/L. Coincubation with the cholesterol precursor mevalonate completely reversed this effect. The downregulation of thrombospondin-1 expression occured in the same concentration range that also inhibited cell proliferation. In contrast, lovatatin did not affect expression of fibronectin, whereas collagen type I and biglycan expression decreased only after long incubations with high, toxic lovastatin concentrations. Simvastatin, but not the very hydrophilic compound pravastatin, had a similar effect on extracellular matrix expression as lovastatin. In summary, lovastatin and simvastatin predominantly decrease the expression of the glycoprotein thrombospondin-1, which is functionally associated with smooth muscle cell migration and proliferation. In contrast, expression of plaque-stabilizing extracellular proteins such as collagen type I and biglycan are much less affected.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003950050158
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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