| 1. |
- Bouyoucef, S E, et al.
(författare)
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Poster Session 2 : Monday 4 May 2015, 08
- 2015
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Ingår i: European Heart Journal Cardiovascular Imaging. - : Oxford University Press (OUP). - 2047-2404 .- 2047-2412. ; 16 Suppl 1
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Tidskriftsartikel (refereegranskat)
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| 2. |
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| 3. |
- Malinkin, Sergey O., et al.
(författare)
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Zinc(II) Complexes with Asymmetric 3,5-Substituted 1H-Pyrazoles
- 2012
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Ingår i: European Journal of Inorganic Chemistry. - : Wiley. - 1099-0682 .- 1434-1948. ; :10, s. 1639-1649
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Tidskriftsartikel (refereegranskat)abstract
- Two new pyrazolate-based ligands, N'-[1-(3-acetyl-4-methyl-1H-pyrazol-5-yl)ethylidene]-2-(hydroxyimino)propanehydrazide (L1) and 5-[(E)-1-(2-{(E)-2-(hydroxyimino}propanoyl}hydrazono)ethyl]-4-methyl-1H-pyrazole-3-carboxylic acid (L2), were synthesized and studied for zinc(II) complexation. A set of pH-dependent UV/Vis measurements has been performed to determine the complex formation properties of L2. According to the calculations, in solution, L2 forms variously protonated mononuclear (ZnII/L2 = 1:1) and dinuclear (ZnII/L2 = 2:1) complexes. The reaction of the deprotonated ligands with hydrated ZnII salts and slow diffusion of ammonia into the reaction mixtures gave mononuclear [Zn(L1-2H)(NH3)2]center dot DMF (1) and trinuclear mu-pyrazolato-bridged [Zn3(L2-3H)2(NH3)5]center dot 4H2O (3). In both complexes, the zinc ions are in the same distorted trigonal-bipyramidal environment, coordinated to two nitrogen atoms of the ammonia and one oxygen and two nitrogen atoms of the pyrazolate and hydrazide groups. The molecular structures of all of the ligands and complexes have been elucidated by X-ray crystallography.
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| 4. |
- Mandinov, L., et al.
(författare)
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Inhibition of in-stent restenosis by oral copper chelation in porcine coronary arteries
- 2006
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Ingår i: American Journal of Physiology. Heart and Circulatory Physiology. - : American Physiological Society. - 0363-6135 .- 1522-1539. ; 291:6, s. H2692-H2697
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Tidskriftsartikel (refereegranskat)abstract
- Stress-induced release of IL-1 alpha and fibroblast growth factor-1 is dependent on intracellular copper and is a major driver of neointimal hyperplasia. Therefore, we assessed the effect of tetrathiomolybdate (TTM), a clinically proven copper chelator, on in-stent restenosis. Nine pigs were treated with TTM (5 mg/kg po) twice daily for 2 wk before stent implantation and for 4 wk thereafter, and nine pigs served as controls. In-stent restenosis was assessed by quantitative coronary angiography (QCA), intravascular ultrasound (IVUS), and histomorphometry. Serum ceruloplasmin activity was used as a surrogate marker of copper bioavailability. In TTM-treated animals, ceruloplasmin dropped 70 +/- 10% below baseline levels. Baseline characteristics were comparable in TTM-treated and control animals. At 4-wk follow-up, all parameters relevant to in-stent restenosis were significantly reduced in TTM-treated animals: minimal lumen diameter by QCA was 2.03 +/- 0.57 and 1.47 +/- 0.45 mm in TTM-treated and control animals, respectively (P less than 0.05), percent stenosis diameter was 39% less in TTM-treated animals (27.1 +/- 16.6% vs. 44.5 +/- 16.1%, P less than 0.05), minimal lumen area by IVUS was 60% larger in TTM-treated animals (4.27 +/- 1.56 vs. 2.67 +/- 1.19 mm(2), P less than 0.05), and neointimal volume by histomorphometry was 37% less in TTM-treated animals (34.9 +/- 11.5 vs. 55.2 +/- 19.6 mm(3), P less than 0.05). We conclude that systemic copper chelation with a clinically approved chelator significantly inhibits in-stent restenosis.
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