Exploring the impact of the inverse Faraday effect on all-optical helicity-dependent magnetization switching

All-optical helicity-dependent magnetization switching (AO-HDS) is the quickest deterministic technique for data storage by solely using ultrashort laser pulses. Granular high data density magnetic storage media developed for heat-assisted magnetic recording (HAMR) provide an ideal playground to investigate the interplay of effects leading to magnetization switching. In the latest perception, we identify two effects, the magnetic circular dichroism (MCD) and the inverse Faraday effect (IFE), as the forces driving the switching process. During photon absorption, which leads to a rapid temperature rise and thus to magnetization quenching, the MCD ensures two distinct electron temperatures due to helicity-dependent absorption. This effect already holds a nonvanishing probability for magnetization switching. At the same time, the IFE induces a magnetic moment within the material, enhancing the switching probability. We present AO-HDS experiments using ultrashort laser pulses ($\lesssim 200\,\mathrm{fs}$) in the near-infrared range from $800\,\mathrm{nm}$ to $1500\,\mathrm{nm}$. The experiments demonstrate a strong dependence of the switching efficiency on the absorbed energy density, elevating the electron temperature in the vicinity of the Curie point, allowing for the IFE to take full effect, inducing a magnetic moment for deterministic switching in the quenched magnetization state. While we do not observe an enhanced switching due to an increased MCD, a higher induced magnetization usually improves the switching rate if the electron temperature reaches the transition temperature vicinity. Therefore, we conclude that the magnetic moment generated by the IFE is crucial for the switching efficiency and the distinct deterministic character of the switching process. Laser pulses with a higher absorption induce a higher magnetic moment and switch magnetization at lower fluences

Modeling Edar expression reveals the hidden dynamics of tooth signaling center patterning.

When patterns are set during embryogenesis, it is expected that they are straightly established rather than subsequently modified. The patterning of the three mouse molars is, however, far from straight, likely as a result of mouse evolutionary history. The first-formed tooth signaling centers, called MS and R2, disappear before driving tooth formation and are thought to be vestiges of the premolars found in mouse ancestors. Moreover, the mature signaling center of the first molar (M1) is formed from the fusion of two signaling centers (R2 and early M1). Here, we report that broad activation of Edar expression precedes its spatial restriction to tooth signaling centers. This reveals a hidden two-step patterning process for tooth signaling centers, which was modeled with a single activator-inhibitor pair subject to reaction-diffusion (RD). The study of Edar expression also unveiled successive phases of signaling center formation, erasing, recovering, and fusion. Our model, in which R2 signaling center is not intrinsically defective but erased by the broad activation preceding M1 signaling center formation, predicted the surprising rescue of R2 in Edar mutant mice, where activation is reduced. The importance of this R2-M1 interaction was confirmed by ex vivo cultures showing that R2 is capable of forming a tooth. Finally, by introducing chemotaxis as a secondary process to RD, we recapitulated in silico different conditions in which R2 and M1 centers fuse or not. In conclusion, pattern formation in the mouse molar field relies on basic mechanisms whose dynamics produce embryonic patterns that are plastic objects rather than fixed end points

Three-dimensional analysis of molar development in the mouse from the cap to bell stage

During four days of prenatal development in the mouse, the morphology of the first lower molar moves from the early cap to the bell stage. Five phenomena characterize this period: growth of the tooth germ; development of the cervical loop; histogenesis of the enamel organ; folding of the epithelial-mesenchymal junction associated with cusp formation; and change in cellular heterogeneity in the mesenchyme. All these processes are controlled by epithelial-mesenchymal interactions. These complex histo-morphogenetic events have been documented using histological sections and 3D reconstructions. When combined with functional tests in vitro, this approach allowed searching for possible relationships between simultaneous changes occurring in both the epithelial and ecto-mesenchymal compartments. Parallel changes that occur in the two tissues could result from different mechanisms, as illustrated by the increasing number of pre-odontoblasts and pre-ameloblasts during crown growth. Cell division was involved mainly in the ecto-mesenchyme, while proliferation and cell re-organization occurred in the inner dental epithelium. 3D reconstructions also raised still unsolved questions, such as the possible relationship between cusp size and spatial specification of cell kinetic parameters, changes in cell position within the inner dental epithelium, and tracing cell migration in the mesenchyme during development

Development of the Vestibular Lamina in Human Embryos: Morphogenesis and Vestibule Formation

The vestibular lamina (VL) is a transient developmental structure that forms the lip furrow, creating a gap between the lips/cheeks and teeth (oral vestibule). Surprisingly, little is known about the development of the VL and its relationship to the adjacent dental lamina (DL), which forms the teeth. In some congenital disorders, such as Ellis-van Creveld (EVC) syndrome, development of the VL is disrupted and multiple supernumerary frenula form, physically linking the lips and teeth. Here, we assess the normal development of the VL in human embryos from 6.5 (CS19) to 13 weeks of development, showing the close relationship between the VL and DL, from initiation to differentiation. In the anterior lower region, the two structures arise from the same epithelial thickening. The VL then undergoes complex morphogenetic changes during development, forming a branched structure that separates to create the vestibule. Changing expression of keratins highlight the differentiation patterns in the VL, with fissure formation linked to the onset of filaggrin. Apoptosis is involved in removal of the central portion of the VL to create a broad furrow between the future cheek and gum. This research forms an essential base to further explore developmental defects in this part of the oral cavity

Prenatal development of Crocodylus niloticus niloticus Laurenti,1768.

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