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Active plasmonic and nanophotonic systems require switchable materials with extreme material contrast, short switching times, and negligible degradation. On the quest for these supreme properties, an in-depth understanding of the nanoscopic processes is essential. Here, we unravel the nanoscopic details of the phase transition dynamics of metallic magnesium (Mg) to dielectric magnesium hydride (MgH2) using free-standing films for in situ nanoimaging. A characteristic MgH2 phonon resonance is used to achieve unprecedented chemical specificity between the material states. Our results reveal that the hydride phase nucleates at grain boundaries, from where the hydrogenation progresses into the adjoining nanocrystallites. We measure a much faster nanoscopic hydride phase propagation in comparison to the macroscopic propagation dynamics. Our innovative method offers an engineering strategy to overcome the hitherto limited diffusion coefficients and has substantial impact on the further design, development, and analysis of switchable phase transition as well as hydrogen storage and generation materials.The plant cuticle is often considered a passive barrier from the environment. We show that the cuticle regulates active transport of the defense hormone salicylic acid (SA). SA, an important regulator of systemic acquired resistance (SAR), is preferentially transported from pathogen-infected to uninfected parts via the apoplast. Apoplastic accumulation of SA, which precedes its accumulation in the cytosol, is driven by the pH gradient and deprotonation of SA. In cuticle-defective mutants, increased transpiration and reduced water potential preferentially routes SA to cuticle wax rather than to the apoplast. This results in defective long-distance transport of SA, which in turn impairs distal accumulation of the SAR-inducer pipecolic acid. High humidity reduces transpiration to restore systemic SA transport and, thereby, SAR in cuticle-defective mutants. Together, our results demonstrate that long-distance mobility of SA is essential for SAR and that partitioning of SA between the symplast and cuticle is regulated by transpiration.Plant viruses are natural, self-assembling nanostructures with versatile and genetically programmable shells, making them useful in diverse applications ranging from the development of new materials to diagnostics and therapeutics. SID791 Here, we describe the design and synthesis of plant virus nanoparticles displaying peptides associated with two different autoimmune diseases. Using animal models, we show that the recombinant nanoparticles can prevent autoimmune diabetes and ameliorate rheumatoid arthritis. In both cases, this effect is based on a strictly peptide-related mechanism in which the virus nanoparticle acts both as a peptide scaffold and as an adjuvant, showing an overlapping mechanism of action. This successful preclinical testing could pave the way for the development of plant viruses for the clinical treatment of human autoimmune diseases.Bacterial CRISPR-Cas9 nucleases have been repurposed as powerful genome editing tools. Whereas engineering guide RNAs or Cas nucleases have proven to improve the efficiency of CRISPR editing, modulation of protospacer-adjacent motif (PAM), indispensable for CRISPR, has been less explored. Here, we develop a DNA origami-based platform to program a PAM antenna microenvironment and address its performance at the single-molecule level with submolecular resolution. To mimic spatially controlled in vivo PAM distribution as may occur in chromatin, we investigate the effect of PAM antennae surrounding target DNA. We find that PAM antennae effectively sensitize the DNA cleavage by recruiting Cas9 molecules. Super-resolution tracking of single single-guide RNA/Cas9s reveals localized translocation of Cas9 among spatially proximal PAMs. We find that the introduction of the PAM antennae effectively modulates the microenvironment for enhanced target cleavage (up to ~50%). These results provide insight into factors that promote more efficient genome editing.The cardiac and hematopoietic progenitors (CPs and HPs, respectively) in the mesoderm ultimately form a well-organized circulation system, but mechanisms that reconcile their development remain elusive. We found that activating transcription factor 3 (atf3) was highly expressed in the CPs, HPs, and mesoderm, in zebrafish. The atf3 -/- mutants exhibited atrial dilated cardiomyopathy and a high ratio of immature myeloid cells. These manifestations were primarily caused by the blockade of differentiation of both CPs and HPs within the anterior lateral plate mesoderm. Mechanistically, Atf3 targets cebpγ to repress slc2a1a-mediated glucose utilization. The high rate of glucose metabolism in atf3 -/- mutants inhibited the differentiation of progenitors by changing the redox state. Therefore, atf3 could provide CPs and HPs with metabolic adaptive capacity to changes in glucose levels. Our study provides new insights into the role of atf3 in the coordination of differentiation of CPs and HPs by regulating glucose metabolism.Alzheimer's disease (AD) is a neurodegenerative disorder that causes cognitive decline, memory loss, and inability to perform everyday functions. Hallmark features of AD-including generation of amyloid plaques, neurofibrillary tangles, gliosis, and inflammation in the brain-are well defined; however, the cause of the disease remains elusive. Growing evidence implicates pathogens in AD development, with herpes simplex virus type I (HSV-1) gaining increasing attention as a potential causative agent. Here, we describe a multidisciplinary approach to produce physiologically relevant human tissues to study AD using human-induced neural stem cells (hiNSCs) and HSV-1 infection in a 3D bioengineered brain model. We report a herpes-induced tissue model of AD that mimics human disease with multicellular amyloid plaque-like formations, gliosis, neuroinflammation, and decreased functionality, completely in the absence of any exogenous mediators of AD. This model will allow for future studies to identify potential downstream drug targets for treating this devastating disease.Presently, the Indian Ocean (IO) resides in a climate state that prevents strong year-to-year climate variations. This may change under greenhouse warming, but the mechanisms remain uncertain, thus limiting our ability to predict future changes in climate extremes. Using climate model simulations, we uncover the emergence of a mode of climate variability capable of generating unprecedented sea surface temperature and rainfall fluctuations across the IO. This mode, which is inhibited under present-day conditions, becomes active in climate states with a shallow thermocline and vigorous upwelling, consistent with the predictions of continued greenhouse warming. These predictions are supported by modeling and proxy evidence of an active mode during glacial intervals that favored such a state. Because of its impact on hydrological variability, the emergence of such a mode would become a first-order source of climate-related risks for the densely populated IO rim.Hundreds of YouTube videos show people running on cornstarch suspensions demonstrating that dense shear thickening suspensions solidify under impact. Such processes are mimicked by impacting and pulling out a plate from the surface of a thickening cornstarch suspension. Here, using both experiments and simulations, we show that applying fast oscillatory shear transverse to the primary impact or extension directions tunes the degree of solidification. The forces acting on the impacting surface are modified by varying the dimensionless ratio of the orthogonal shear to the compression and extension flow rate. Simulations show varying this parameter changes the number of particle contacts governing solidification. To demonstrate this strategy in an untethered context, we show the sinking speed of a cylinder dropped onto the suspension varies markedly by changing this dimensionless ratio. These results suggest applying orthogonal shear while people are running on cornstarch would de-solidify the suspension and cause them to sink.The Tibetan Plateau exerts a major influence on Asian climate, but its long-term environmental history remains largely unknown. We present a detailed record of vegetation and climate changes over the past 1.74 million years in a lake sediment core from the Zoige Basin, eastern Tibetan Plateau. Results show three intervals with different orbital- and millennial-scale features superimposed on a stepwise long-term cooling trend. The interval of 1.74-1.54 million years ago is characterized by an insolation-dominated mode with strong ~20,000-year cyclicity and quasi-absent millennial-scale signal. The interval of 1.54-0.62 million years ago represents a transitional insolation-ice mode marked by ~20,000- and ~40,000-year cycles, with superimposed millennial-scale oscillations. The past 620,000 years are characterized by an ice-driven mode with 100,000-year cyclicity and less frequent millennial-scale variability. A pronounced transition occurred 620,000 years ago, as glacial cycles intensified. These new findings reveal how the interaction of low-latitude insolation and high-latitude ice-volume forcing shaped the evolution of the Tibetan Plateau climate.Sensory processing requires mechanisms of fast coincidence detection to discriminate synchronous from asynchronous inputs. Spike threshold adaptation enables such a discrimination but is ineffective in transmitting this information to the network. We show here that presynaptic axonal sodium channels read and transmit precise levels of input synchrony to the postsynaptic cell by modulating the presynaptic action potential (AP) amplitude. As a consequence, synaptic transmission is facilitated at cortical synapses when the presynaptic spike is produced by synchronous inputs. Using dual soma-axon recordings, imaging, and modeling, we show that this facilitation results from enhanced AP amplitude in the axon due to minimized inactivation of axonal sodium channels. Quantifying local circuit activity and using network modeling, we found that spikes induced by synchronous inputs produced a larger effect on network activity than spikes induced by asynchronous inputs. Therefore, this input synchrony-dependent facilitation may constitute a powerful mechanism, regulating synaptic transmission at proximal synapses.Bioinformatic and functional data link integrin-mediated cell adhesion to cellular senescence; however, the significance of and molecular mechanisms behind these connections are unknown. We now report that the focal adhesion-localized βPAK-interacting exchange factor (βPIX)-G protein-coupled receptor kinase interacting protein (GIT) complex controls cellular senescence in vitro and in vivo. βPIX and GIT levels decline with age. βPIX knockdown induces cellular senescence, which was prevented by reexpression. Loss of βPIX induced calpain cleavage of the endocytic adapter amphiphysin 1 to suppress clathrin-mediated endocytosis (CME); direct competition of GIT1/2 for the calpain-binding site on paxillin mediates this effect. Decreased CME and thus integrin endocytosis induced abnormal integrin signaling, with elevated reactive oxygen species production. Blocking integrin signaling inhibited senescence in human fibroblasts and mouse lungs in vivo. These results reveal a central role for integrin signaling in cellular senescence, potentially identifying a new therapeutic direction.
My Website: https://www.selleckchem.com/products/plerixafor.html
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