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Intravital microscopy (IVM) is a powerful technique that enables imaging of internal tissues at (sub)cellular resolutions in living animals. Here, we present a silicone-based imaging window consisting of a fully flexible, sutureless design that is ideally suited for long-term, longitudinal IVM of growing tissues and tumors. Crucially, we show that this window, without any customization, is suitable for numerous anatomical locations in mice using a rapid and standardized implantation procedure. This low-cost device represents a substantial technological and performance advance that facilitates intravital imaging in diverse contexts in higher organisms, opening previously unattainable avenues for in vivo imaging of soft and fragile tissues.Newborns and hatchlings can perform incredibly sophisticated behaviors, but many animals abstain from sexual activity at the beginning of life. Hormonal changes have long been known to drive both physical and behavioral changes during adolescence, leading to the largely untested assumption that sexuality emerges from organizational changes to neuronal circuitry. We show that the transition to sexuality in male Drosophila is controlled by hormonal changes, but this regulation is functional rather than structural. In very young males, a broadly acting hormone directly inhibits the activity of three courtship-motivating circuit elements, ensuring the complete suppression of sexual motivation and behavior. Blocking or overriding these inhibitory mechanisms evokes immediate and robust sexual behavior from very young and otherwise asexual males. Similarities to mammalian adolescence suggest a general principle in which hormonal changes gate the transition to sexuality not by constructing new circuitry but by permitting activity in otherwise latent motivational circuit elements.β-Amyloid (Aβ) plaque formation is the major pathological hallmark of Alzheimer's disease (AD) and constitutes a potentially critical, early inducer driving AD pathogenesis as it precedes other pathological events and cognitive symptoms by decades. It is therefore critical to understand how Aβ pathology is initiated and where and when distinct Aβ species aggregate. Here, we used metabolic isotope labeling in APPNL-G-F knock-in mice together with mass spectrometry imaging to monitor the earliest seeds of Aβ deposition through ongoing plaque development. This allowed visualizing Aβ aggregation dynamics within single plaques across different brain regions. We show that formation of structurally distinct plaques is associated with differential Aβ peptide deposition. Specifically, Aβ1-42 is forming an initial core structure followed by radial outgrowth and late secretion and deposition of Aβ1-38. These data describe a detailed picture of the earliest events of precipitating amyloid pathology at scales not previously possible.In cortical microcircuits, it is generally assumed that fast-spiking parvalbumin interneurons mediate dense and nonselective inhibition. Some reports indicate sparse and structured inhibitory connectivity, but the computational relevance and the underlying spatial organization remain unresolved. In the rat superficial presubiculum, we find that inhibition by fast-spiking interneurons is organized in the form of a dominant super-reciprocal microcircuit motif where multiple pyramidal cells recurrently inhibit each other via a single interneuron. Multineuron recordings and subsequent 3D reconstructions and analysis further show that this nonrandom connectivity arises from an asymmetric, polarized morphology of fast-spiking interneuron axons, which individually cover different directions in the same volume. Network simulations assuming topographically organized input demonstrate that such polarized inhibition can improve head direction tuning of pyramidal cells in comparison to a "blanket of inhibition." We propose that structured inhibition based on asymmetrical axons is an overarching spatial connectivity principle for tailored computation across brain regions.The next generation of silicon-based photonic processors and neural and quantum networks need to be adaptable, reconfigurable, and programmable. Phase change technology offers proven nonvolatile electronic programmability; however, the materials used to date have shown prohibitively high optical losses, which are incompatible with integrated photonic platforms. Here, we demonstrate the capability of the previously unexplored material Sb2Se3 for ultralow-loss programmable silicon photonics. The favorable combination of large refractive index contrast and ultralow losses seen in Sb2Se3 facilitates an unprecedented optical phase control exceeding 10π radians in a Mach-Zehnder interferometer. To demonstrate full control over the flow of light, we introduce nanophotonic digital patterning as a previously unexplored conceptual approach with a footprint orders of magnitude smaller than state-of-the-art interferometer meshes. Our approach enables a wealth of possibilities in high-density reconfiguration of optical functionalities on silicon chip.Magnetic skyrmions are self-organized topological spin textures that behave like particles. Because of their fast creation and typically long lifetime, experimental verification of skyrmion's creation/annihilation processes has been challenging. https://www.selleckchem.com/products/bozitinib.html Here, we successfully track skyrmion dynamics in defect-introduced Co9Zn9Mn2 by using pump-probe Lorentz transmission electron microscope. Following the nanosecond photothermal excitation, we resolve 160-nm skyrmion's proliferation at less then 1 ns, contraction at 5 ns, drift from 10 ns to 4 μs, and coalescence at ~5 μs. These motions relay the multiscale arrangement and relaxation of skyrmion clusters in a repeatable cycle of 20 kHz. Such repeatable dynamics of skyrmions, arising from the weakened but still persistent topological protection around defects, enables us to visualize the whole life of the skyrmions and demonstrates the possible high-frequency manipulations of topological charges brought by skyrmions.Plants have a high ability to cope with changing environments and grow continuously throughout life. However, the mechanisms by which plants strike a balance between stress response and organ growth remain elusive. Here, we found that DNA double-strand breaks enhance the accumulation of cytokinin hormones through the DNA damage signaling pathway in the Arabidopsis root tip. Our data showed that activation of cytokinin signaling suppresses the expression of some of the PIN-FORMED genes that encode efflux carriers of another hormone, auxin, thereby decreasing the auxin signals in the root tip and causing cell cycle arrest at G2 phase and stem cell death. Elevated cytokinin signaling also promotes an early transition from cell division to endoreplication in the basal part of the root apex. We propose that plant hormones spatially coordinate differential DNA damage responses, thereby maintaining genome integrity and minimizing cell death to ensure continuous root growth.
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