In this study, we report a rapid sonochemical synthesis of monodisperse nonaggregated Fe(3)O(4)@SiO(2) magnetic nanoparticles (NPs). We found that coprecipitation of Fe(II) and Fe(III) in aqueous solutions under the effect of power ultrasound yields smaller Fe(3)O(4) NPs with a narrow size distribution (4-8 nm) compared to the silent reaction. Moreover, the coating of Fe(3)O(4) NPs with silica using an alkaline hydrolysis of tetraethyl orthosilicate in ethanol-water mixture is accelerated many-fold in the presence of a 20 kHz ultrasonic field. The thickness of the silica shell can be easily controlled in the range of several nanometers during sonication. Mossbauer spectra revealed that nonsuperparamagnetic behavior of obtained core-shell NPs is mostly related to the dipole-dipole interactions of magnetic cores and not to the particle size effect. Core-shell Fe(3)O(4)@SiO(2) NPs prepared with sonochemistry exhibit a higher magnetization value than that for NPs obtained under silent conditions owing to better control of the deposited silica quantities as well as to the high speed of sonochemical coating, which prevents the magnetite from oxidizing.

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Angiogenesis is a process of development and of growth of new capillary blood vessels from pre-existing vessels. When pathological, it contributes to the development of numerous types of tumors, and the formation of metastases. In order to grow, carcinoma need new blood vessels to form so that they can feed themselves. Therefore, nowadays the concept according to which the development of cancer is angiogenesis dependent is generally recognized. This concept makes the control of tumoral angiogenesis one of the promising therapeutic ways in cancerology. The transition from the latent phase to the invasive and metastatic phase of a cancer is linked to what is called the angiogenic switch. It implies complex cellular and molecular interactions between cancerous cells, endothelial cells and the components of the extra-cellular matrix and namely the existence of specific proteins secreted by the tumoral cells able to stimulate the proliferation of capillary endothelial cells. Among them, VEGF, Vascular Endothelial Growth Factor was found in several types of tumors. It has shown a tumoral angiogenic activity in vitro and in vivo, and thus is a privileged target for the control of angiogenesis in an anti-tumoral goal. The role of VEGF in tumoral angiogenesis has been extensively studied. It has been proved to undergo as well autocrine as paracrine stimulation of tumoral angiogenesis. During the last few years, several members of the VEGF family have been described namely the VEGF-A, B, C, D, E and placenta growth factor (PlGF) among which VEGF-A (121 aminoacids) plays a role of prime importance in angiogenesis. VEGF is a 45 kDA glycoprotein, homodimeric, basic, and able to bind heparin. The three-dimensional structure of VEGF has been recently determined, by X-rays diffraction, and NMR spectroscopy. The different forms of the VEGF bind to receptors that exhibit a tyrosine-kinase activity (RTK). The specific action of the VEGF on the endothelial cells is mainly regulated by two types of RTK of the VEGF family, VEGFR1, or Flt-1, and VEGFR2, or KDR/Flk-1. Mutagenesis studies have shown that only a small number of VEGF residues are important and essential for the binding with RTK. Data described to date from the studies of VEGF/RTK interactions agree to the hypothesis that KDR receptor is the main human receptor responsible for the VEGF activity in both physiological and pathological vascular development, and VEGF-KDR signalling pathway has been validated as a priority target for the development of anti- and pro- angiogenic agents. Therefore angiogenesis mediated by VEGF constitutes a new target for anti-cancer therapy which has explored through different ways of intervention aiming at the blocking of the tumoral angiogenesis. The main ones are: -Struggle against the stroma degradation and invasion by the neo-vessels -Inhibition of activated endothelial cells. -Inhibition of angiogenic factors production and of their receptors. -Inhibition of the VEGF signal pathway, by peptides blocking the bond between VEGF and its recepto...

Blocking angiogenesis is an attractive strategy to inhibit tumor growth, invasion, and metastasis. We describe here the structure and the biological action of a new cyclic peptide derived from vascular endothelial growth factor (VEGF). This 17-amino acid molecule designated cyclopeptidic vascular endothelial growth inhibitor (cyclo-VEGI, CBO-P11) encompasses residues 79 -93 of VEGF which are involved in the interaction with VEGF receptor-2. In aqueous solution, cyclo-VEGI presents a propensity to adopt a helix conformation that was largely unexpected because only ␤-sheet structures or random coil conformations have been observed for macrocyclic peptides. Cyclo-VEGI inhibits binding of iodinated VEGF 165 to endothelial cells, endothelial cells proliferation, migration, and signaling induced by VEGF 165 . This peptide also exhibits anti-angiogenic activity in vivo on the differentiated chicken chorioallantoic membrane. Furthermore, cyclo-VEGI significantly blocks the growth of established intracranial glioma in nude and syngeneic mice and improves survival without side effects. Taken together, these results suggest that cyclo-VEGI is an attractive candidate for the development of novel angiogenesis inhibitor molecules useful for the treatment of cancer and other angiogenesis-related diseases.Angiogenesis takes place during embryonic development and in the adult during wound healing and the female ovulatory cycle. In pathological states, angiogenesis is observed during solid tumor growth and metastasis, diabetic retinopathy, and chronic inflammatory disorders. A number of angiogenic regulators such as vascular endothelial growth factors (VEGFs),

Top-level performances in endurance sports require several years of hard training loads. A major objective of this endurance training is to reach the most elevated metabolic adaptations the athlete will be able to support. As a consequence, overtraining is a recurrent problem that highly-trained athletes may experience during their career. Many studies have revealed that overtraining could be highlighted by various biochemical markers but a principal discrepancy in the diagnosis of overtraining stems from the fact that none of these markers may be considered as universal. In endurance sports, the metabolic aspects of training fatigue appear to be the most relevant parameters that may characterise overtraining when recovery is not sufficient, or when dietary habits do not allow an optimal replenishment of substrate stores. From the skeletal muscle functions to the overall energetic substrate availability during exercise, six metabolic schemes have been studied in relation to overtraining, each one related to a central parameter, i.e. carbohydrates, branched-chain amino acids, glutamine, polyunsaturated fatty acids, leptin, and proteins. We summarise the current knowledge on these metabolic hypotheses regarding the occurrence of overtraining in endurance sports.