Effect of oral calcium carbonate on aortic calcification in apolipoprotein E-deficient (apoE−/−) mice with chronic renal failure

Background. In chronic kidney disease (CKD) patients, the intake of calcium-based phosphate binders is associated with a marked progression of coronary artery and aortic calcification, in contrast to patients receiving calcium-free phosphate binders. The aim of this study was to reexamine the role of calcium carbonate in vascular calcification and to analyse its effect on aortic calcification-related gene expression in chronic renal failure (CRF). Methods. Mice deficient in apolipoprotein E underwent either sham operation or subtotal nephrectomy to create CRF. They were then randomly assigned to one of the three following groups: a control non-CRF group and a CRF group fed on standard diet, and a CRF group fed on calcium carbonate enriched diet, for a period of 8 weeks. Aortic atherosclerotic plaque and calcification were evaluated using quantitative morphologic image processing. Aortic gene and protein expression was examined using immunohistochemistry and Q-PCR methods. Results. Calcium carbonate supplementation was effective in decreasing serum phosphorus but was associated with a higher serum calcium concentration. Compared with standard diet, calcium carbonate enriched diet unexpectedly induced a significant decrease of both plaque (p < 0.05) and non-plaque-associated calcification surface (p < 0.05) in CRF mice. It also increased osteopontin (OPN) protein expression in atherosclerotic lesion areas of aortic root. There was also a numerical increase in OPN and osteoprotegerin gene expression in total thoracic aorta but the difference did not reach the level of significance. Finally, calcium carbonate did not change the severity of atherosclerotic lesions. Conclusion. In this experimental model of CRF, calcium carbonate supplementation did not accelerate but instead decreased vascular calcification. If our observation can be extrapolated to humans, it appears to question the contention that calcium carbonate supplementation, at least when given in moderate amounts, necessarily enhances vascular calcification. It is also compatible with the hypothesis of a preponderant role of phosphorus over that of calcium in promoting vascular calcification in CR

The Bois de Boulogne and the Bois de Vincennes, the nature reserves of Paris

Quoique constitués pour seulement 1/3 de massifs boisés, les bois de Boulogne (846 ha) et de Vincennes (995 ha) remplissent des fonctions de réserve naturelle et de promenade pour les Parisiens comme le traduit leur fréquentation de 6 000 à 7 000 visiteurs par hectare et par an. L'examen détaillé des facteurs de perturbation de l'équilibre biologique conduit à des règles de sylviculture et d'aménagement; la méthode de régénération par enclos de reboisement et le choix d'essences s'appliquent en gros à une surface de 6 ha à reboiser par an, effort nécessaire au rétablissement de l'équilibre biologique et à la garantie de l'avenir des massifs boisés.Although only a Third of their area is woodland, the Bois de Boulogne (846 ha) and the Bois de Vincennes (995 ha) fulfil the functions of a nature reserve and a place for walks for the people of Paris. This can be seen from the frequency of Visitation - 6 000 to 7 000 visitors per ha per year. A detailed examination of the factors which disturb the biological equilibrium leads to silvicultural and management rules. The method of regeneration by reforestation enclosures, and the choice of species, are applied over all to an area of 6 ha to be reforested each year. This is the effort needed to restore the biological equilibrium and to ensure the future of the woodlands

Synthesis of N-, S-, and C-glycoside castanospermine analogues with selective neutral α-glucosidase inhibitory activity as antitumour agents

3 páginas, 2 figuras, 1 tabla, 1 esquemasp2-Iminosugar-type castanospermine analogues bearing an α-configured N-, S-, or C-linked pseudoanomeric group have been designed as selective inhibitors of the neutral α-glucosidases involved in N-glycoprotein processing; evaluation in breast cancer cell growth indicated a significant antiproliferative potential that was dependent on the nature of the pseudoanomeric group.This work was supported by the Spanish Ministerio de Educación y Ciencia (contract numbers CTQ2006-15515-C02-01/BQU, CTQ2009-14551-C02-01/BQU and TQ2007-61180/PPQ) and the Junta de Andalucía.Peer reviewe

Effect of oral calcium carbonate on aortic calcification in apolipoprotein E-deficient (apoE-/-) mice with chronic renal failure.

BACKGROUND: In chronic kidney disease (CKD) patients, the intake of calcium-based phosphate binders is associated with a marked progression of coronary artery and aortic calcification, in contrast to patients receiving calcium-free phosphate binders. The aim of this study was to reexamine the role of calcium carbonate in vascular calcification and to analyse its effect on aortic calcification-related gene expression in chronic renal failure (CRF). METHODS: Mice deficient in apolipoprotein E underwent either sham operation or subtotal nephrectomy to create CRF. They were then randomly assigned to one of the three following groups: a control non-CRF group and a CRF group fed on standard diet, and a CRF group fed on calcium carbonate enriched diet, for a period of 8 weeks. Aortic atherosclerotic plaque and calcification were evaluated using quantitative morphologic image processing. Aortic gene and protein expression was examined using immunohistochemistry and Q-PCR methods. RESULTS: Calcium carbonate supplementation was effective in decreasing serum phosphorus but was associated with a higher serum calcium concentration. Compared with standard diet, calcium carbonate enriched diet unexpectedly induced a significant decrease of both plaque (p&lt;0.05) and non-plaque-associated calcification surface (p&lt;0.05) in CRF mice. It also increased osteopontin (OPN) protein expression in atherosclerotic lesion areas of aortic root. There was also a numerical increase in OPN and osteoprotegerin gene expression in total thoracic aorta but the difference did not reach the level of significance. Finally, calcium carbonate did not change the severity of atherosclerotic lesions. CONCLUSION: In this experimental model of CRF, calcium carbonate supplementation did not accelerate but instead decreased vascular calcification. If our observation can be extrapolated to humans, it appears to question the contention that calcium carbonate supplementation, at least when given in moderate amounts, necessarily enhances vascular calcification. It is also compatible with the hypothesis of a preponderant role of phosphorus over that of calcium in promoting vascular calcification in CRF