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Solvation sheath reorganization enables fast ion transfer kinetics in lithium-ion battery
Dopaminergic processes predict temporal distortions in event memory
Abstract Our memories do not simply keep time — they distort it, stretching and compressing the past to reflect the structure of experience. Here, we combined functional magnetic resonance imaging (fMRI; n = 32) with eye-tracking ( n = 28) to test whether activation of the dopaminergic system, known to influence encoding and time perception, expands mnemonic representations of time between contextually distinct events. Participants encoded item sequences while listening to tones that typically repeated over time, but occasionally changed, creating salient event boundaries. We found that tone switches significantly activated the ventral tegmental area (VTA), and the magnitude of these responses predicted greater time dilation between item pairs spanning those switches. At a longer timescale, increased blinking also predicted greater time dilation in memory, but only for boundary-spanning item pairs. Together, these findings suggest that dopaminergic processes are sensitive to event structure and contribute to distortions of remembered time that may help segment continuous experience into distinct episodic memories.
Passivating pinholes for large-area and high-efficiency silicon solar cells with tunnel oxide passivated contact
Ferroelectricity-modulated asymmetric van der Waals heterostructure for ultralow-power neuromorphic synapse and logic-in-memory operations
MFF budding from mitochondria regulates melanosome size and maturation
Vacuum-induced interfacial compaction for scalable fabrication of high-performance organic solar cells
Control of lysosome function by the GTPase-activating protein TBC1D9B and its binding partner TMEM55B
Abstract Lysosomes are highly dynamic organelles that serve antagonistic functions as terminal catabolic stations for the degradation of macromolecules and as central metabolic decision centers for anabolic growth signaling. Lysosome dysfunction is implicated in various human diseases. The physiological roles of lysosomes are linked to the control of lysosome position and dynamics via the activity of the kinesin-activating small GTPase ARL8. How the activity of ARL8 is regulated remains poorly understood. Here, we identify the GTPase-activating Tre-2/Bub2/Cdc16 (TBC) domain protein TBC1D9B as a critical negative regulator of ARL8B function. We demonstrate that TBC1D9B is associated with the lysosomal membrane protein TMEM55B, directly binds to ARL8B-GTP, and stimulates its GTPase activity. Knockout of TBC1D9B or its binding partner TMEM55B causes lysosome dispersion, defective autophagic flux, and impairs the adaptive degradative response of cells to limiting nutrient supply. These lysosomal phenotypes of TBC1D9B loss are occluded by concomitant depletion of ARL8 in cells. Collectively, our data unravel a key role for TBC1D9B in controlling lysosome function by serving as a negative regulator of ARL8 activity.
Global literature review and survey of implementation constraints on natural climate solutions
Abstract Natural Climate Solutions – protection, restoration, and improved management of lands and waters that reduce greenhouse gasses – have large climate change mitigation potential. However, lack of comprehensive information on implementation challenges hinders the adoption of Natural Climate Solutions and the delivery of near-term mitigation. Using a global survey of Natural Climate Solutions projects and a systematic review of recent studies, we map 46 constraints in eight categories, yielding 15,572 geo-referenced pathway-constraint observations from 501 studies and projects in 137 countries covering 20 of 22 United Nations subregions. Social-behavioral, Knowledge, and Government-Organizational are the most-reported constraint categories, and lack of policy coordination or implementation capacity the most-observed constraint and most frequently top-ranking constraint for pathways and subregions. Despite broad congruence, top constraint and category rankings vary among subregions and pathways, respectively. We find that projects generally encounter diverse sets of challenges. Without enabling efforts, near-term mitigation from Natural Climate Solutions may remain well below its biophysical potential.
DIS3 mutations enhance AID-driven translocations during B-cell activation, promoting transformation to multiple myeloma
Abstract DIS3, a key nuclear RNA-degrading enzyme, is essential for immunoglobulin class switch recombination (CSR), promoting activation-induced cytidine deaminase (AID) activity on both DNA strands to induce double-strand DNA breaks. During somatic hypermutation, AID-dependent lesions predominantly occur on the non-template DNA strand. Dominant mutations impairing DIS3 exoribonucleolytic activity are common in multiple myeloma (MM), but their role in carcinogenesis remains unclear. Here we show, using a knock-in mouse model, that the clinically relevant DIS3 G766R variant causes chromosomal translocations in B-cells, characterized by aberrant AID activity signatures. The mice develop pristane-induced plasmacytomas, modeling early-stage MM. In clinical MM samples, DIS3 mutations correlate with IGH translocations and AID-driven lesions in driver genes. Mechanistically, mutated DIS3 accumulates on chromatin-bound RNA, particularly at aberrant AID target sites, promoting mutations on both DNA strands. This results in increased AID-dependent double-strand DNA breaks, fostering microhomology-mediated oncogenic rearrangements. Translocations occur specifically during CSR, which remains functionally intact. The DIS3 G766R mutation does not disrupt chromatin architecture in activated B cells but exploits spatial proximity to permanently juxtapose enhancers and proto-oncogenes, facilitating transformation. Thus, gain-of-function DIS3 mutations enhance AID promiscuity, driving IGH translocations and MM development without broadly affecting B-cell physiology.
Synergistic surface modification of Cu with schiff-base networks for high selectivity and durability in CO2-to-C2H4 electroreduction
Chlorine radical-mediated electrochemical propylene epoxidation from seawater
Ultraflexible photoelectrical impedance tomography-based imager for 3-axis robotic tactile sensing
Frazzled/DCC directs spatial progenitor integration ensuring steady-state intestinal turnover
Abstract Adult epithelial organs undergo continual steady-state turnover that is achieved by tight coupling of stem cell production with replacement of worn-out epithelial cells by local intercellular signalling 1,2 . Like many eukaryotic epithelia, absorptive enterocytes (EC) of the adult Drosophila midgut are arranged in a hexagonal, honeycomb-like pattern. On tricellular nexuses of EC, intestinal stem cells (ISC) are scattered in a way so that around two thirds of EC can be renewed directly by adjacent ISC. However, the mechanism for replacement of the remaining third of remotely located EC is unknown. Here, we show that a conserved axonal guidance cue directs enteroblasts (EB), the immediate ISC daughters, to selectively replace worn-out adjacent and remote EC with identical frequency. Worn-out EC express Netrin-B ligands that attract Frazzled/DCC-receptor dependent EB protrusions and subsequent EB migration towards the Netrin-B expressing EC. Our newly developed ‘Hamelin’ assay confirms Frazzled-dependent EB migration towards Netrin-B sources and hints to invasive progenitor behaviour as midgut progenitors cross the organ boundary into the hindgut. Together, we establish spatially directed EB migration and integration as essential for intestinal homeostasis and provide first mechanistic support for recent findings resuscitating conserved Netrins and Frazzled/DCC-signalling as therapeutic target in metastasis.
Cortical representation of multidimensional handwriting movement and implications for neuroprostheses
Comparison of state-of-the-art error-correction coding for sequence-based DNA data storage
Abstract Many codecs with different error-correction approaches have been implemented for DNA data storage to date. However, no studies have systematically benchmarked codec implementations to establish their current state-of-the-art. Here, we use in silico and in vitro experiments to compare the performance of six representative codecs from literature. In isolation, these codecs can tolerate error rates up to 14% and a sequence loss of 65%. Under realistic conditions, we further establish that storage densities as high as 117 EB g −1 are feasible using existing codecs and current synthesis and sequencing technologies. Verifying our results experimentally, we demonstrate data storage at 43 EB g −1 using synthesis by material deposition and 13 EB g −1 using electrochemical synthesis, employing existing codecs from literature. Besides closing in on the physical limits of DNA data storage, this study thus demonstrates the maturity of error-correction coding, defines its current state-of-the-art, and establishes best practices for codec benchmarking.
Unpacking sources of transmission in HIV prevention trials with deep-sequence pathogen data
Abstract To develop effective HIV prevention strategies to guide public health policy the main sources of infection in HIV prevention studies must be identified. Accordingly, we devised a statistical approach that estimates the relative contribution of different sources of infection in community-randomized trials of infectious disease prevention using deep- (or next generation) sequenced pathogen data. We applied this approach to the Botswana Combination Prevention Project (BCPP) and estimated that 90% [95% Confidence Interval (CI): 80–94] of new infections in communities that received combination prevention (including universal HIV test-and-treat) originated from individuals residing in communities outside the trial area. We estimate from our model that the relative benefit of providing the BCPP intervention to all communities nationwide would be a 59% [3–87] reduction in transmissions to recipients in trial communities, exceeding the 30% reduction observed when providing the BCPP intervention to trial communities only. Our results suggest that the impact of the BCPP trial intervention was curtailed by sources of transmission outside the trial area and could be considerably larger if applied nationally. We recommend that the impact of sources of transmission beyond the reach of the intervention be considered when designing and evaluating interventions to inform public health programs.