Drop deformation by laser-pulse impact

A free-falling absorbing liquid drop hit by a nanosecond laser-pulse experiences a strong recoil-pressure kick. As a consequence, the drop propels forward and deforms into a thin sheet which eventually fragments. We study how the drop deformation depends on the pulse shape and drop properties. We first derive the velocity field inside the drop on the timescale of the pressure pulse, when the drop is still spherical. This yields the kinetic-energy partition inside the drop, which precisely measures the deformation rate with respect to the propulsion rate, before surface tension comes into play. On the timescale where surface tension is important the drop has evolved into a thin sheet. Its expansion dynamics is described with a slender-slope model, which uses the impulsive energy-partition as an initial condition. Completed with boundary integral simulations, this two-stage model explains the entire drop dynamics and its dependance on the pulse shape: for a given propulsion, a tightly focused pulse results in a thin curved sheet which maximizes the lateral expansion, while a uniform illumination yields a smaller expansion but a flat symmetric sheet, in good agreement with experimental observations.Comment: submitted to J. Fluid Mec

Drop Shaping by Laser-Pulse Impact

We show how the deposition of laser energy induces propulsion and strong deformation of an absorbing liquid body. Combining high speed with stroboscopic imaging, we observe that a millimeter-sized dyed water drop hit by a millijoule nanosecond laser pulse propels forward at several meters per second and deforms until it eventually fragments. The drop motion results from the recoil momentum imparted at the drop surface by water vaporization. We measure the propulsion speed and the time-deformation law of the drop, complemented by boundary-integral simulations. The drop propulsion and shaping are explained in terms of the laser-pulse energy, the drop size, and the liquid properties. These findings are, for instance, crucial for the generation of extreme ultraviolet light in nanolithography machines.Comment: Submitted as research article to Physical Review Applied, 6 pages with 6 figure

Drop Fragmentation at Impact onto a Bath of an Immiscible Liquid

The impact of a drop onto a deep bath of an immiscible liquid is studied with emphasis on the drop fragmentation into a collection of noncoalescing daughter drops. At impact the drop flattens and spreads at the surface of the crater it transiently opens in the bath and reaches a maximum deformation, which gets larger with increasing impact velocity, before surface tension drives its recession. This recession can promote the fragmentation by two different mechanisms: At moderate impact velocity, the drop recession converges to the axis of symmetry to form a jet which then fragments by a Plateau-Rayleigh mechanism. At higher velocity the edge of the receding drop destabilizes and shapes into radial ligaments which subsequently fragment. For this latter mechanism the number N / We 3 and the size distribution of the daughter drops pðdÞ / d À4 as a function of the impact Weber number We are explained on the basis of the observed spreading of the drop. The universality of this model for the fragmentation of receding liquid sheets might be relevant for other configurations. DOI: 10.1103/PhysRevLett.110.264503 PACS numbers: 47.20.Ma, 47.20.Ky, 47.55.DÀ, 47.55.nb A drop impacting onto a deep liquid bath is well known to transiently open a crater in the bath and possibly eject a liquid sheet and a jet. Since Worthington's drawings and photographs more than a century ago [1,2], much attention has been paid to the impact with identical or miscible drop and bath liquids. Although the long term state itself, the coalescence of the drop, was not an issue, the description of the transient structures Our experiment consists of a water drop (with density and surface tensio

A Model for the Development of the Rhizobial and Arbuscular Mycorrhizal Symbioses in Legumes and Its Use to Understand the Roles of Ethylene in the Establishment of these two Symbioses

We propose a model depicting the development of nodulation and arbuscular mycorrhizae. Both processes are dissected into many steps, using Pisum sativum L. nodulation mutants as a guideline. For nodulation, we distinguish two main developmental programs, one epidermal and one cortical. Whereas Nod factors alone affect the cortical program, bacteria are required to trigger the epidermal events. We propose that the two programs of the rhizobial symbiosis evolved separately and that, over time, they came to function together. The distinction between these two programs does not exist for arbuscular mycorrhizae development despite events occurring in both root tissues. Mutations that affect both symbioses are restricted to the epidermal program. We propose here sites of action and potential roles for ethylene during the formation of the two symbioses with a specific hypothesis for nodule organogenesis. Assuming the epidermis does not make ethylene, the microsymbionts probably first encounter a regulatory level of ethylene at the epidermis–outermost cortical cell layer interface. Depending on the hormone concentrations there, infection will either progress or be blocked. In the former case, ethylene affects the cortex cytoskeleton, allowing reorganization that facilitates infection; in the latter case, ethylene acts on several enzymes that interfere with infection thread growth, causing it to abort. Throughout this review, the difficulty of generalizing the roles of ethylene is emphasized and numerous examples are given to demonstrate the diversity that exists in plants

3-Deazaneplanocin A (DZNep), an Inhibitor of the Histone Methyltransferase EZH2, Induces Apoptosis and Reduces Cell Migration in Chondrosarcoma Cells

ObjectiveGrowing evidences indicate that the histone methyltransferase EZH2 (enhancer of zeste homolog 2) may be an appropriate therapeutic target in some tumors. Indeed, a high expression of EZH2 is correlated with poor prognosis and metastasis in many cancers. In addition, 3-Deazaneplanocin A (DZNep), an S-adenosyl-L homocysteine hydrolase inhibitor which induces EZH2 protein depletion, leads to cell death in several cancers and tumors. The aim of this study was to determine whether an epigenetic therapy targeting EZH2 with DZNep may be also efficient to treat chondrosarcomas.MethodsEZH2 expression was determined by immunohistochemistry and western-blot. Chondrosarcoma cell line CH2879 was cultured in the presence of DZNep, and its growth and survival were evaluated by counting adherent cells periodically. Apoptosis was assayed by cell cycle analysis, Apo2.7 expression using flow cytometry, and by PARP cleavage using western-blot. Cell migration was assessed by wound healing assay.ResultsChondrosarcomas (at least with high grade) highly express EZH2, at contrary to enchondromas or chondrocytes. In vitro, DZNep inhibits EZH2 protein expression, and subsequently reduces the trimethylation of lysine 27 on histone H3 (H3K27me3). Interestingly, DZNep induces cell death of chondrosarcoma cell lines by apoptosis, while it slightly reduces growth of normal chondrocytes. In addition, DZNep reduces cell migration.ConclusionThese results indicate that an epigenetic therapy that pharmacologically targets EZH2 via DZNep may constitute a novel approach to treat chondrosarcomas