Propulsion of bubble-based acoustic microswimmers

Acoustic microswimmers present a great potential for microfluidic applications and targeted drug delivery. Here, we introduce armored microbubbles (size range, 10–20 μm) made by three-dimensional microfabrication, which allows the bubbles to last for hours even under forced oscillations. The acoustic resonance of the armored microbubbles is found to be dictated by capillary forces and not by gas volume, and its measurements agree with a theoretical calculation. We further measure experimentally and predict theoretically the net propulsive flow generated by the bubble vibration. This flow, due to steady streaming in the fluid, can reach 100 mm/s, and is affected by the presence of nearby walls. Finally, microswimmers in motion are shown, either as spinning devices or free swimmers.P. M. acknowledges financial support from the European Community’s Seventh Framework Programme (FP7/2007-2013) ERC Grant Agreement Bubbleboost No. 614655. This work has been performed with the help of the “Plateforme Technologique Amont” de Grenoble, with the financial support of the “Nanosciences aux limites de la Nanoélectronique” Foundation. Support from the EPSRC (T. A. S.) and from a Marie Curie Grant (E. L.) is also gratefully acknowledged.This is the author accepted manuscript. The final version is available from American Physical Society via http://dx.doi.org/10.1103/PhysRevApplied.4.06401

La liaison éthylénique: Étude de quelques hexènes linéaires ou ramifiés

La pagination indiquée dans la zone "Pages" est celle du tiré à part, numérisé par les Bibliothèques de l'ULB. La pagination telle qu'elle apparaît dans la revue est pp. 938-.info:eu-repo/semantics/publishe

SPRED2 loss-of-function causes a recessive Noonan syndrome-like phenotype

Upregulated signal flow through RAS and the mitogen-associated protein kinase (MAPK) cascade is the unifying mechanistic theme of the RASopathies, a family of disorders affecting development and growth. Pathogenic variants in more than 20 genes have been causally linked to RASopathies, the majority having a dominant role in promoting enhanced signaling. Here, we report that SPRED2 loss of function is causally linked to a recessive phenotype evocative of Noonan syndrome. Homozygosity for three different variants-c.187C>T (p.Arg63∗), c.299T>C (p.Leu100Pro), and c.1142_1143delTT (p.Leu381Hisfs∗95)-were identified in four subjects from three families. All variants severely affected protein stability, causing accelerated degradation, and variably perturbed SPRED2 functional behavior. When overexpressed in cells, all variants were unable to negatively modulate EGF-promoted RAF1, MEK, and ERK phosphorylation, and time-course experiments in primary fibroblasts (p.Leu100Pro and p.Leu381Hisfs∗95) documented an increased and prolonged activation of the MAPK cascade in response to EGF stimulation. Morpholino-mediated knockdown of spred2a and spred2b in zebrafish induced defects in convergence and extension cell movements indicating upregulated RAS-MAPK signaling, which were rescued by expressing wild-type SPRED2 but not the SPRED2Leu381Hisfs∗95 protein. The clinical phenotype of the four affected individuals included developmental delay, intellectual disability, cardiac defects, short stature, skeletal anomalies, and a typical facial gestalt as major features, without the occurrence of the distinctive skin signs characterizing Legius syndrome. These features, in part, characterize the phenotype of Spred2-/- mice. Our findings identify the second recessive form of Noonan syndrome and document pleiotropic consequences of SPRED2 loss of function in development.s