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International audience; Nous étudions la fonte de grosses billes de glace dans un écoulement turbulent de von Kármán à très hauts nombres de Reynolds à l'aide d'un montage optique couplant suivi de particules et ombroscopie. La mesure de la variation de taille d'une particule au cours du temps permet de mesurer le ux ther-mique à sa surface en fonction du nombre de Reynolds à l'échelle de la particule Re D. Trois situations d'écoulement sont considérées : billes librement advectées dans tout l'écoulement, billes maintenues xes dans une zone d'écoulement moyen nul, et billes maintenues xes en présence d'un écoulement moyen fort. Dans les deux cas où les billes sont xes, nous observons que le transfert thermique dans ce régime turbulent est toujours beaucoup plus fort que pour un régime laminaire, le nombre de Nusselt s'exprimant comme une loi de puissance en fonction du nombre de Reynolds : N u ∝ Re 0,8 D. Dans le cas des particules librement advectées, le transfert turbulent est encore augmenté et le nombre de Nusselt devient proportionnel au nombre de Reynolds. Le ux thermique par unité de surface est alors indé-pendant de la taille de la particule, ce qui correspond à un régime ultime de transfert de chaleur atteint lorsque la couche limite thermique est pleinement turbulente. Abstract : We study the melting dynamics of large ice balls in a turbulent von Kármán ow at very high Reynolds numbers with an optical setup based on both particles tracking and shadowgraphy. By recording the particle size variation along time, we obtain the heat ux at the ice ball surface as a function of the particle scale Reynolds number Re D. Three cases of ow are studied : ice balls freely advected in the whole ow, ice balls xed in a zero mean ow region and ice balls xed in a strong mean ow. For the two xed cases, we observe heat transfers much stronger than in laminar ows, the Nusselt number behaving as a power law as a function of the Reynolds number: N u ∝ Re 0.8 D. For freely advected ice balls, the turbulent transfert is further enhanced and the Nusselt number is proportionnal to the Reynolds number. The surface heat ux is then independant of the particles size, leading to an ultimate regime of heat transfert reached when the thermal boundary layer is fully turbulent.

International audience; We study the melting dynamics of large ice balls in a turbulent von Kármán flow at very high Reynolds number. Using an optical shadowgraphy setup, we record the time evolution of particle sizes. We study the heat transfer as a function of the particle scale Reynolds number Re D for three cases: fixed ice balls melting in a region of strong turbulence with zero mean flow, fixed ice balls melting under the action of a strong mean flow with lower fluctuations, and ice balls freely advected in the whole apparatus. For the fixed particles cases, heat transfer is observed to be much stronger than in laminar flows, the Nusselt number behaving as a power law of the Reynolds number: Nu ∝ Re 0.8 D. For freely advected ice balls, the turbulent transfer is further enhanced and the Nusselt number is proportional to the Reynolds number Nu ∝ Re D. Furthermore, the surface heat flux is found to be independent of the particles size, leading to an ultimate regime of heat transfer reached when the thermal boundary layer is fully turbulent. C 2013 AIP Publishing LLC. [http://dx.

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The Wnt/beta-catenin signaling pathway plays a key role in several cellular functions during embryonic development and adult homeostasis. The deregulation of this pathway may lead to the development of cancer, including melanoma. Deregulation of the Wnt/beta-catenin pathway occurs through either the induction/repression of, or specific mutations in, various members of this signaling pathway; this results in the stabilization of beta-catenin and its translocation from the cytoplasm to the nucleus, where it regulates transcription. Although nuclear beta-catenin is clearly involved in malignant transformation, the mechanism by which it exerts its effects remains elusive. This review focuses on the molecular and cellular mechanisms that are driven by beta-catenin and lead to melanocyte transformation. In particular, we describe how beta-catenin induces melanocyte immortalization, a novel activity of this multifunction protein. Finally, we discuss how beta-catenin-induced immortalization can cooperate with MAPKinase pathways to produce melanoma. (C) 2008 Elsevier Masson SAS. All rights reserved.

The Wnt/beta-catenin signaling pathway plays a key role in several cellular functions during embryonic development and adult homeostasis. The deregulation of this pathway may lead to the development of cancer, including melanoma. Deregulation of the Wnt/beta-catenin pathway occurs through either the induction/repression of, or specific mutations in, various members of this signaling pathway; this results in the stabilization of beta-catenin and its translocation from the cytoplasm to the nucleus, where it regulates transcription. Although nuclear beta-catenin is clearly involved in malignant transformation, the mechanism by which it exerts its effects remains elusive. This review focuses on the molecular and cellular mechanisms that are driven by beta-catenin and lead to melanocyte transformation. In particular, we describe how beta-catenin induces melanocyte immortalization, a novel activity of this multifunction protein. Finally, we discuss how beta-catenin-induced immortalization can cooperate with MAPKinase pathways to produce melanoma. (C) 2008 Elsevier Masson SAS. All rights reserved.

The Wnt/β-catenin signaling pathway plays a key role in several cellular functions during embryonic development and adult homeostasis. The deregulation of this pathway may lead to the development of cancer, including melanoma. Deregulation of the Wnt/β-catenin pathway occurs through either the induction/repression of, or specific mutations in, various members of this signaling pathway; this results in the stabilization of β-catenin and its translocation from the cytoplasm to the nucleus, where it regulates transcription. Although nuclear β-catenin is clearly involved in malignant transformation, the mechanism by which it exerts its effects remains elusive. This review focuses on the molecular and cellular mechanisms that are driven by β-catenin and lead to melanocyte transformation. In particular, we describe how β-catenin induces melanocyte immortalization, a novel activity of this multifunction protein. Finally, we discuss how β-catenin-induced immortalization can cooperate with MAPKinase pathways to produce melanoma. © 2008 Elsevier Masson SAS. All rights reserved.

A recurrent point mutation in the fibroblast growth factor receptor 3 (FGFR3) gene that converts proline 250 into arginine is commonly associated with coronal craniosynostosis and has allowed definition of a new syndrome on a molecular basis. Sixty-two patients with sporadic or familial forms of coronal craniosynostosis were investigated for the P250R FGFR3 mutation. It was identified in 20 probands originating from 27 unrelated families (74%), while only 6/35 sporadic cases (17%) harboured the mutation. In both familial and sporadic cases, females were significantly more severely affected than males. Hence, while 68% of females carrying the P250R mutation showed brachycephaly, only 35% of males had the same phenotype. In the most severe forms of the disease, the association of bicoronal craniosynostosis with hypertelorism and marked bulging of the temporal fossae were common hallmarks that might be helpful for clinical diagnosis. Taken together, these results indicate that the P250R FGFR3 mutation is mostly familial and is associated with a more severe phenotype in females than in males. The sex related severity of the condition points to the possible implication of modifier genes in this syndrome. Keywords: coronal craniosynostosis; P250R FGFR3 mutation; sex related expressivity