bluuebunny/crossref_metadata_2025_split huggingface dataset:
Raman time-delay in attosecond transient absorption of strong-field created krypton vacancy
Authors: Wang Li , Bai Guangru , Wang Xiaowei , Zhao Jing , Gao Cheng , Wang Jiacan , Xiao Fan , Tao Wenkai , Song Pan , Qiu Qianyu , Liu Jinlei , Zhao Zengxiu 
Published: March 2024

AbstractStrong field ionization injects a transient vacancy in the atom which is entangled to the outgoing photoelectron. When the electron is finally detached, the ion is populated at different excited states with part of coherence information lost. The preserved coherence of matter after interacting with intense short pulses has important consequences on the subsequent nonequilibrium evolution and energy relaxation. Here we employ attosecond transient absorption spectroscopy to measure the time-delay of resonant transitions of krypton vacancy during their creation. We have observed that the absorptions by the two spin-orbit split states are modulated at different paces when varying the time-delay between the near-infrared pumping pulse and the attosecond probing pulse. It is shown that the coupling of the ions with the remaining field leads to a suppression of ionic coherence. Comparison between theory and experiments uncovers that coherent Raman coupling induces time-delay between the resonant absorptions, which provides insight into laser-ion interactions enriching attosecond chronoscopy.
Modeling Si/SiGe quantum dot variability induced by interface disorder reconstructed from multiperspective microscopy
Authors: Peña Luis Fabián , Koepke Justine C. , Dycus Joseph Houston , Mounce Andrew , Baczewski Andrew D. , Jacobson N. Tobias , Bussmann Ezra 
Published: March 2024

AbstractSiGe heteroepitaxial growth yields pristine host material for quantum dot qubits, but residual interface disorder can lead to qubit-to-qubit variability that might pose an obstacle to reliable SiGe-based quantum computing. By convolving data from scanning tunneling microscopy and high-angle annular dark field scanning transmission electron microscopy, we reconstruct 3D interfacial atomic structure and employ an atomistic multi-valley effective mass theory to quantify qubit spectral variability. The results indicate (1) appreciable valley splitting (VS) variability of ~50% owing to alloy disorder and (2) roughness-induced double-dot detuning bias energy variability of order 1–10 meV depending on well thickness. For measured intermixing, atomic steps have negligible influence on VS, and uncorrelated roughness causes spatially fluctuating energy biases in double-dot detunings potentially incorrectly attributed to charge disorder. Our approach yields atomic structure spanning orders of magnitude larger areas than post-growth microscopy or tomography alone, enabling more holistic predictions of disorder-induced qubit variability.
Exploiting sulfonated covalent organic frameworks to fabricate long-lasting stability and chlorine-resistant thin-film nanocomposite nanofiltration membrane
Authors: Meng Wenqiao , Xue Qiang , Zhu Jinyuan , Zhang Kaisong 
Published: March 2024

AbstractIncorporating hydrophilic and charged porous nanofillers to prepare high-performance thin film nanocomposite (TFN) nanofiltration (NF) membranes is an effective method to achieve efficient water treatment. In this study, we synthesize the sulfonated covalent organic framework nanosheets (S-CONs) with higher hydrophilicity and electronegativity by immobilizing sulfonic acid groups (–SO3H) on TpPa-1 nanosheets. The S-CONs are incorporated in the PA layer by interfacial polymerization (IP) reaction. The results indicated that the S-CONs could modulate the hydrophilicity, thickness, and electronegativity of TFN-NF membranes. At the optimal addition of S-CONs (0.006 g), the pure water permeance increases to 8.84 $${\rm{L}}\cdot{\rm{m}}^{-2}\cdot{\rm{h}}^{-1}\cdot{\rm{bar}}^{-1}$$

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, which is about 1.75 times than the TFC membrane, with a high Na2SO4 rejection reaching 98.97%. The improvement of the separation performance mainly results from the reduction of PA layer thickness (from ~178.00–198.00 to ~100.00–128.00 nm) and the increase of surface electronegativity (from −20.37 to −44.41 mV at pH = 7.00). More interestingly, the amide bond formed between the S-CONs and TMC improved the chlorine resistance of the membranes. This study reveals the potential of using functionalized 2D CONs as nanofillers to modify TFC membranes for efficient nanofiltration.
High-threshold and low-overhead fault-tolerant quantum memory
Authors: Bravyi Sergey , Cross Andrew W. , Gambetta Jay M. , Maslov Dmitri , Rall Patrick , Yoder Theodore J. 
Published: March 2024

AbstractThe accumulation of physical errors1–3 prevents the execution of large-scale algorithms in current quantum computers. Quantum error correction4 promises a solution by encoding k logical qubits onto a larger number n of physical qubits, such that the physical errors are suppressed enough to allow running a desired computation with tolerable fidelity. Quantum error correction becomes practically realizable once the physical error rate is below a threshold value that depends on the choice of quantum code, syndrome measurement circuit and decoding algorithm5. We present an end-to-end quantum error correction protocol that implements fault-tolerant memory on the basis of a family of low-density parity-check codes6. Our approach achieves an error threshold of 0.7% for the standard circuit-based noise model, on par with the surface code7–10 that for 20 years was the leading code in terms of error threshold. The syndrome measurement cycle for a length-n code in our family requires n ancillary qubits and a depth-8 circuit with CNOT gates, qubit initializations and measurements. The required qubit connectivity is a degree-6 graph composed of two edge-disjoint planar subgraphs. In particular, we show that 12 logical qubits can be preserved for nearly 1 million syndrome cycles using 288 physical qubits in total, assuming the physical error rate of 0.1%, whereas the surface code would require nearly 3,000 physical qubits to achieve said performance. Our findings bring demonstrations of a low-overhead fault-tolerant quantum memory within the reach of near-term quantum processors.
Five million years of Antarctic Circumpolar Current strength variability
Authors: Lamy Frank , Winckler Gisela , Arz Helge W. , Farmer Jesse R. , Gottschalk Julia , Lembke-Jene Lester , Middleton Jennifer L. , van der Does Michèlle , Tiedemann Ralf , Alvarez Zarikian Carlos , Basak Chandranath , Brombacher Anieke , Dumm Levin , Esper Oliver M. , Herbert Lisa C. , Iwasaki Shinya , Kreps Gaston , Lawson Vera J. , Lo Li , Malinverno Elisa , Martinez-Garcia Alfredo , Michel Elisabeth , Moretti Simone , Moy Christopher M. , Ravelo Ana Christina , Riesselman Christina R. , Saavedra-Pellitero Mariem , Sadatzki Henrik , Seo Inah , Singh Raj K. , Smith Rebecca A. , Souza Alexandre L. , Stoner Joseph S. , Toyos Maria , de Oliveira Igor M. Venancio P. , Wan Sui , Wu Shuzhuang , Zhao Xiangyu 
Published: March 2024

AbstractThe Antarctic Circumpolar Current (ACC) represents the world’s largest ocean-current system and affects global ocean circulation, climate and Antarctic ice-sheet stability1–3. Today, ACC dynamics are controlled by atmospheric forcing, oceanic density gradients and eddy activity4. Whereas palaeoceanographic reconstructions exhibit regional heterogeneity in ACC position and strength over Pleistocene glacial–interglacial cycles5–8, the long-term evolution of the ACC is poorly known. Here we document changes in ACC strength from sediment cores in the Pacific Southern Ocean. We find no linear long-term trend in ACC flow since 5.3 million years ago (Ma), in contrast to global cooling9 and increasing global ice volume10. Instead, we observe a reversal on a million-year timescale, from increasing ACC strength during Pliocene global cooling to a subsequent decrease with further Early Pleistocene cooling. This shift in the ACC regime coincided with a Southern Ocean reconfiguration that altered the sensitivity of the ACC to atmospheric and oceanic forcings11–13. We find ACC strength changes to be closely linked to 400,000-year eccentricity cycles, probably originating from modulation of precessional changes in the South Pacific jet stream linked to tropical Pacific temperature variability14. A persistent link between weaker ACC flow, equatorward-shifted opal deposition and reduced atmospheric CO2 during glacial periods first emerged during the Mid-Pleistocene Transition (MPT). The strongest ACC flow occurred during warmer-than-present intervals of the Plio-Pleistocene, providing evidence of potentially increasing ACC flow with future climate warming.
Formation of memory assemblies through the DNA-sensing TLR9 pathway
Authors: Jovasevic Vladimir , Wood Elizabeth M. , Cicvaric Ana , Zhang Hui , Petrovic Zorica , Carboncino Anna , Parker Kendra K. , Bassett Thomas E. , Moltesen Maria , Yamawaki Naoki , Login Hande , Kalucka Joanna , Sananbenesi Farahnaz , Zhang Xusheng , Fischer Andre , Radulovic Jelena 
Published: March 2024

AbstractAs hippocampal neurons respond to diverse types of information1, a subset assembles into microcircuits representing a memory2. Those neurons typically undergo energy-intensive molecular adaptations, occasionally resulting in transient DNA damage3–5. Here we found discrete clusters of excitatory hippocampal CA1 neurons with persistent double-stranded DNA (dsDNA) breaks, nuclear envelope ruptures and perinuclear release of histone and dsDNA fragments hours after learning. Following these early events, some neurons acquired an inflammatory phenotype involving activation of TLR9 signalling and accumulation of centrosomal DNA damage repair complexes6. Neuron-specific knockdown of Tlr9 impaired memory while blunting contextual fear conditioning-induced changes of gene expression in specific clusters of excitatory CA1 neurons. Notably, TLR9 had an essential role in centrosome function, including DNA damage repair, ciliogenesis and build-up of perineuronal nets. We demonstrate a novel cascade of learning-induced molecular events in discrete neuronal clusters undergoing dsDNA damage and TLR9-mediated repair, resulting in their recruitment to memory circuits. With compromised TLR9 function, this fundamental memory mechanism becomes a gateway to genomic instability and cognitive impairments implicated in accelerated senescence, psychiatric disorders and neurodegenerative disorders. Maintaining the integrity of TLR9 inflammatory signalling thus emerges as a promising preventive strategy for neurocognitive deficits.
Revealing uncertainty in the status of biodiversity change
Authors: Johnson T. F. , Beckerman A. P. , Childs D. Z. , Webb T. J. , Evans K. L. , Griffiths C. A. , Capdevila P. , Clements C. F. , Besson M. , Gregory R. D. , Thomas G. H. , Delmas E. , Freckleton R. P. 
Published: March 2024

AbstractBiodiversity faces unprecedented threats from rapid global change1. Signals of biodiversity change come from time-series abundance datasets for thousands of species over large geographic and temporal scales. Analyses of these biodiversity datasets have pointed to varied trends in abundance, including increases and decreases. However, these analyses have not fully accounted for spatial, temporal and phylogenetic structures in the data. Here, using a new statistical framework, we show across ten high-profile biodiversity datasets2–11 that increases and decreases under existing approaches vanish once spatial, temporal and phylogenetic structures are accounted for. This is a consequence of existing approaches severely underestimating trend uncertainty and sometimes misestimating the trend direction. Under our revised average abundance trends that appropriately recognize uncertainty, we failed to observe a single increasing or decreasing trend at 95% credible intervals in our ten datasets. This emphasizes how little is known about biodiversity change across vast spatial and taxonomic scales. Despite this uncertainty at vast scales, we reveal improved local-scale prediction accuracy by accounting for spatial, temporal and phylogenetic structures. Improved prediction offers hope of estimating biodiversity change at policy-relevant scales, guiding adaptive conservation responses.
CGRP sensory neurons promote tissue healing via neutrophils and macrophages
Authors: Lu Yen-Zhen , Nayer Bhavana , Singh Shailendra Kumar , Alshoubaki Yasmin K. , Yuan Elle , Park Anthony J. , Maruyama Kenta , Akira Shizuo , Martino Mikaël M. 
Published: March 2024

Abstract
The immune system has a critical role in orchestrating tissue healing. As a result, regenerative strategies that control immune components have proved effective1,2. This is particularly relevant when immune dysregulation that results from conditions such as diabetes or advanced age impairs tissue healing following injury2,3. Nociceptive sensory neurons have a crucial role as immunoregulators and exert both protective and harmful effects depending on the context4–12. However, how neuro–immune interactions affect tissue repair and regeneration following acute injury is unclear. Here we show that ablation of the NaV1.8 nociceptor impairs skin wound repair and muscle regeneration after acute tissue injury. Nociceptor endings grow into injured skin and muscle tissues and signal to immune cells through the neuropeptide calcitonin gene-related peptide (CGRP) during the healing process. CGRP acts via receptor activity-modifying protein 1 (RAMP1) on neutrophils, monocytes and macrophages to inhibit recruitment, accelerate death, enhance efferocytosis and polarize macrophages towards a pro-repair phenotype. The effects of CGRP on neutrophils and macrophages are mediated via thrombospondin-1 release and its subsequent autocrine and/or paracrine effects. In mice without nociceptors and diabetic mice with peripheral neuropathies, delivery of an engineered version of CGRP accelerated wound healing and promoted muscle regeneration. Harnessing neuro–immune interactions has potential to treat non-healing tissues in which dysregulated neuro–immune interactions impair tissue healing.
Climate velocities and species tracking in global mountain regions
Authors: Chan Wei-Ping , Lenoir Jonathan , Mai Guan-Shuo , Kuo Hung-Chi , Chen I-Ching , Shen Sheng-Feng 
Published: March 2024

AbstractMountain ranges contain high concentrations of endemic species and are indispensable refugia for lowland species that are facing anthropogenic climate change1,2. Forecasting biodiversity redistribution hinges on assessing whether species can track shifting isotherms as the climate warms3,4. However, a global analysis of the velocities of isotherm shifts along elevation gradients is hindered by the scarcity of weather stations in mountainous regions5. Here we address this issue by mapping the lapse rate of temperature (LRT) across mountain regions globally, both by using satellite data (SLRT) and by using the laws of thermodynamics to account for water vapour6 (that is, the moist adiabatic lapse rate (MALRT)). By dividing the rate of surface warming from 1971 to 2020 by either the SLRT or the MALRT, we provide maps of vertical isotherm shift velocities. We identify 17 mountain regions with exceptionally high vertical isotherm shift velocities (greater than 11.67 m per year for the SLRT; greater than 8.25 m per year for the MALRT), predominantly in dry areas but also in wet regions with shallow lapse rates; for example, northern Sumatra, the Brazilian highlands and southern Africa. By linking these velocities to the velocities of species range shifts, we report instances of close tracking in mountains with lower climate velocities. However, many species lag behind, suggesting that range shift dynamics would persist even if we managed to curb climate-change trajectories. Our findings are key for devising global conservation strategies, particularly in the 17 high-velocity mountain regions that we have identified.
Xenografted human microglia display diverse transcriptomic states in response to Alzheimer’s disease-related amyloid-β pathology
Authors: Mancuso Renzo , Fattorelli Nicola , Martinez-Muriana Anna , Davis Emma , Wolfs Leen , Van Den Daele Johanna , Geric Ivana , Premereur Jessie , Polanco Paula , Bijnens Baukje , Preman Pranav , Serneels Lutgarde , Poovathingal Suresh , Balusu Sriram , Verfaillie Catherine , Fiers Mark , De Strooper Bart 
Published: March 2024

AbstractMicroglia are central players in Alzheimer’s disease pathology but analyzing microglial states in human brain samples is challenging due to genetic diversity, postmortem delay and admixture of pathologies. To circumvent these issues, here we generated 138,577 single-cell expression profiles of human stem cell-derived microglia xenotransplanted in the brain of the AppNL-G-F model of amyloid pathology and wild-type controls. Xenografted human microglia adopt a disease-associated profile similar to that seen in mouse microglia, but display a more pronounced human leukocyte antigen or HLA state, likely related to antigen presentation in response to amyloid plaques. The human microglial response also involves a pro-inflammatory cytokine/chemokine cytokine response microglia or CRM response to oligomeric Aβ oligomers. Genetic deletion of TREM2 or APOE as well as APOE polymorphisms and TREM2R47H expression in the transplanted microglia modulate these responses differentially. The expression of other Alzheimer’s disease risk genes is differentially regulated across the distinct cell states elicited in response to amyloid pathology. Thus, we have identified multiple transcriptomic cell states adopted by human microglia in a multipronged response to Alzheimer’s disease-related pathology, which should be taken into account in translational studies.
A dataset of thermal preferences for Mediterranean demersal and benthic macrofauna
Authors: Valente Salvatore , Colloca Francesco 
Published: March 2024

AbstractClimate change is swiftly reshaping marine ecosystems, affecting different biological levels. Changes in thermal conditions profoundly influence ectotherms’ growth, behaviour, and functions, making knowledge of species’ thermal preferences (TP) crucial for understanding their responses to ongoing warming. However, obtaining this data is challenging due to limited studies, especially for deep-sea demersal and bottom-dwelling species. Here, we present the MedFaunaTP dataset, a collection of survey-based TPs for 939 Mediterranean species of fish, crustaceans, molluscs, echinoderms, cnidarians, and tunicates calculated using species abundance data obtained from the international bottom-trawl survey in the Mediterranean (MEDITS) and bottom temperature data derived from the Copernicus Monitoring Environment Marine Service. MEDITS estimates are based on species biomass indices from 27587 sampling stations, collected from 1994 to 2020, covering the northern Mediterranean Sea and spanning depths from 10 to 800 m. The MedFaunaTP dataset may serves as a valuable resource for understanding and addressing marine ecosystem ecological, conservation, and management challenges in the context of climate change and associated global warming.
miR-889-3p targeting BMPR2 promotes the development of retinoblastoma via JNK/MAPK/ERK signaling
Authors: Gao Yuan , Du Pei 
Published: March 2024

AbstractMicroRNAs (miRNAs) are vital regulators of tumor pathogenesis, including that of retinoblastoma (Rb). This study investigated the functions and mechanisms of action of miR-889-3p in Rb. BMPR2 and miR-889-3p levels were assessed by quantitative reverse transcription PCR (qRT-PCR) or western blotting. Through several cell function tests, the effects of miR-889-3p and BMPR2 on cell proliferation, migration, and JNK/MAPK/ERK signaling were evaluated. The interaction between miR-889-3p and BMPR2 was investigated using a luciferase reporter assay. In vivo tumor development was investigated using a xenograft test. The association between miR-889-3p and BMPR2 expression was identified using Pearson’s correlation analysis. miR-889-3p was increased in Rb cells, and miR-889-3p knockdown inhibited Rb cell proliferation, migration, and phosphorylation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and ERK1/2 in vitro, as well as tumor growth in vivo. Further, they were inversely associated in Rb tissues and miR-889-3p may directly attached to the 3′-UTR of BMPR2 mRNA. Finally, the inhibition of BMPR2 inverted the negative effects of the miR-889-3p inhibitor on migration, proliferation, and activation of JNK, p38 MAPK, and ERK1/2 in Rb cells. Our results indicate that miR-889-3p, which targets BMPR2 and promotes Rb growth by controlling the JNK/MAPK/ERK pathway, is an oncogene in Rb. These results suggested that the miR-889-3p/BMPR2 axis may be a new therapeutic target for Rb.
Association of maternal leukocyte, monocyte, and neutrophil counts with hypertensive disorders of pregnancy: the Japan Environment and Children’s Study (JECS)
Authors: Ishiyama Shiori , Mochizuki Kazuki , Shinohara Ryoji , Miyake Kunio , Kushima Megumi , Kojima Reiji , Horiuchi Sayaka , Otawa Sanae , Yui Hideki , Ooka Tadao , Akiyama Yuka , Yokomichi Hiroshi , Yamagata Zentaro ,   The Japan Environment and Children’s Study Group, Kamijima Michihiro , Yamazaki Shin , Ohya Yukihiro , Kishi Reiko , Yaegashi Nobuo , Hashimoto Koichi , Mori Chisato , Ito Shuichi , Yamagata Zentaro , Inadera Hidekuni , Nakayama Takeo , Sobue Tomotaka , Shima Masayuki , Kageyama Seiji , Suganuma Narufumi , Ohga Shoichi , Katoh Takahiko 
Published: March 2024

AbstractHypertensive disorders of pregnancy (HDP) increase the risk of preterm births and cesarean delivery. This study aimed to investigate whether maternal blood leukocyte, monocyte, or neutrophil counts in the first trimester are related to the development of HDP. Data were collected from the Japan Environment and Children’s Study, a large birth cohort study (n = 38,194) that recruited pregnant women in 15 Regional Centers across Japan (from January 2011 to March 2014). The odds ratios (ORs) for mild/severe HDP according to the cut-off value of leukocyte/neutrophil/monocyte counts by the receiver operating characteristic curve showed high ORs. Furthermore, pregnant women with the highest quartiles of leukocyte and monocyte counts had higher adjusted ORs (aORs) for mild (leukocyte: aOR = 1.27, 95% confidence interval [CI]: 1.02–1.58; monocyte: aOR = 1.30, 95% CI 1.04–1.63) and severe HDP (leukocyte: aOR = 1.51, 95% CI 1.08–2.13; monocyte: aOR = 1.44, 95% CI 1.03–2.01) compared with those with the lowest quartiles of those counts. In addition, pregnant women with the highest neutrophil counts had higher aOR for mild HDP (aOR = 1.26, 95% CI 1.02–1.56) compared with those with the lowest count. In conclusion, high leukocyte and monocyte counts in the first trimester are associated with the development of HDP. Thus, they may be used to predict subsequent HDP.