bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spatial Scale Dependence of Tropical Cyclone Damage Function: Evidence From the Mainland of China
Authors: Tang Rumei , Wu Jidong , Ding Wei , Nie Juan 
Published: August 2023

AbstractTropical cyclone (TC) damage function (DF) is widely used to model TC‐event level damage and thus assess the TC risk for a country or region. The scalability of these DFs at more localized scales, such as the province scale, has not been systematically explored. We use a unique Chinese data set to examine the damage at the TC‐event scale and province scale. Our results show that the parameters and performance of TC DF are spatially dependent. For a sigmoidal DF, the parameter dependence is manifested by a flatter curve calibrated on the TC‐event scale compared to the province scale. In the case of a power‐law DF, the dependence of its parameters is evident in the statistically more significant coefficients of the explanatory variables that are aggregated to the TC‐event scale, compared to the province scale. Performance comparison results further reveal that the scale dependence of performance is related to the type of DF. Integrating hazard, exposure, and vulnerability, the power‐law DF complements the typical sigmoidal DF, producing more accurate estimates of direct economic loss and annual average damage at both the TC‐event and province scales. However, its performance, compared to that of the sigmoidal DF, is more influenced by the scale at which it is calibrated. Our findings elucidate scale‐related research questions in TC risk assessment, offer insights into the selection of DFs, and inspire the future prospect of using multiple DFs to reduce the functional uncertainty.
The Attachment Process of Negative Connecting Leader to the Lateral Surface of Downward Positive Leader in a Positive Cloud‐To‐Ground Lightning Flash
Authors: Qi Qi , Wu Bin , Lyu Weitao , Ma Ying , Chen Lyuwen , Lyu Fanchao , Gao Yan 
Published: August 2023

AbstractUsing high‐speed video cameras operating with framing rates of 20 and 50 kiloframes per second, we captured an attachment process during a positive cloud‐to‐ground flash, which demonstrates the connection of the negative connecting leader (NCL) to the lateral surface of the downward positive leader (DPL) for the first time. When the NCL was initiated, the tip of the DPL had passed the initiation position of the NCL for about 50 m. A common streamer zone (CSZ) was observed when the three‐dimensional distance between the NCL tip and the lateral surface of DPL was about 30 m. It is remarkable to note that a luminous segment (space stem/leader) with a length of about 7 m was captured within the CSZ during the attachment process. The connection between the NCL tip and the lateral surface of the DPL was caused by the development of the CSZ and its inner space leader.
Mechanistic insights into the dual role of CCAR2/DBC1 in cancer
Authors: Kim Hwa Jin , Moon Sue Jin , Kim Jeong Hoon 
Published: August 2023

AbstractCell cycle and apoptosis regulator 2 (CCAR2), also known as deleted in breast cancer 1 (DBC1), has been recently identified as a master regulator of transcriptional processes and plays diverse roles in physiology and pathophysiology, including as a regulator of apoptosis, DNA repair, metabolism, and tumorigenesis. CCAR2 functions as a coregulator of various transcription factors and a critical regulator of numerous epigenetic modifiers. Based on its ability to stimulate apoptosis by activating and stabilizing p53, CCAR2 was initially considered to be a tumor suppressor. However, an increasing number of studies have shown that CCAR2 also functions as a tumor-promoting coregulator by activating oncogenic transcription factors and regulating the enzymatic activity of epigenetic modifiers, indicating that CCAR2 may play a dual role in cancer progression by acting as a tumor suppressor and tumor promoter. Here, we review recent progress in understanding the dual tumor-suppressing and oncogenic roles of CCAR2 in cancer. We discuss CCAR2 domain structures, its interaction partners, and the molecular mechanisms by which it regulates the activities of transcription factors and epigenetic modifiers.
Phosphoinositides and intracellular calcium signaling: novel insights into phosphoinositides and calcium coupling as negative regulators of cellular signaling
Authors: Oh Byung-Chul 
Published: August 2023

AbstractIntracellular calcium (Ca2+) and phosphoinositides (PIPs) are crucial for regulating cellular activities such as metabolism and cell survival. Cells maintain precise intracellular Ca2+ and PIP levels via the actions of a complex system of Ca2+ channels, transporters, Ca2+ ATPases, and signaling effectors, including specific lipid kinases, phosphatases, and phospholipases. Recent research has shed light on the complex interplay between Ca2+ and PIP signaling, suggesting that elevated intracellular Ca2+ levels negatively regulate PIP signaling by inhibiting the membrane localization of PIP-binding proteins carrying specific domains, such as the pleckstrin homology (PH) and Ca2+-independent C2 domains. This dysregulation is often associated with cancer and metabolic diseases. PIPs recruit various proteins with PH domains to the plasma membrane in response to growth hormones, which activate signaling pathways regulating metabolism, cell survival, and growth. However, abnormal PIP signaling in cancer cells triggers consistent membrane localization and activation of PIP-binding proteins. In the context of obesity, an excessive intracellular Ca2+ level prevents the membrane localization of the PIP-binding proteins AKT, IRS1, and PLCδ via Ca2+-PIPs, contributing to insulin resistance and other metabolic diseases. Furthermore, an excessive intracellular Ca2+ level can cause functional defects in subcellular organelles such as the endoplasmic reticulum (ER), lysosomes, and mitochondria, causing metabolic diseases. This review explores how intracellular Ca2+ overload negatively regulates the membrane localization of PIP-binding proteins.
Electrical programmable multilevel nonvolatile photonic random-access memory
Authors: Meng Jiawei , Gui Yaliang , Nouri Behrouz Movahhed , Ma Xiaoxuan , Zhang Yifei , Popescu Cosmin-Constantin , Kang Myungkoo , Miscuglio Mario , Peserico Nicola , Richardson Kathleen , Hu Juejun , Dalir Hamed , Sorger Volker J. 
Published: August 2023

AbstractPhotonic Random-Access Memories (P-RAM) are an essential component for the on-chip non-von Neumann photonic computing by eliminating optoelectronic conversion losses in data links. Emerging Phase-Change Materials (PCMs) have been showed multilevel memory capability, but demonstrations still yield relatively high optical loss and require cumbersome WRITE-ERASE approaches increasing power consumption and system package challenges. Here we demonstrate a multistate electrically programmed low-loss nonvolatile photonic memory based on a broadband transparent phase-change material (Ge2Sb2Se5, GSSe) with ultralow absorption in the amorphous state. A zero-static-power and electrically programmed multi-bit P-RAM is demonstrated on a silicon-on-insulator platform, featuring efficient amplitude modulation up to 0.2 dB/μm and an ultralow insertion loss of total 0.12 dB for a 4-bit memory showing a 100× improved signal to loss ratio compared to other phase-change-materials based photonic memories. We further optimize the positioning of dual microheaters validating performance tradeoffs. Experimentally we demonstrate a half-a-million cyclability test showcasing the robust approach of this material and device. Low-loss photonic retention-of-state adds a key feature for photonic functional and programmable circuits impacting many applications including neural networks, LiDAR, and sensors for example.
Delayed step-by-step decompression with DSF alleviates skeletal muscle crush injury by inhibiting NLRP3/CASP-1/GSDMD pathway
Authors: Li Ning , Wang Xinyue , Wang Yuru , Wang Pengtao , Sun Na , Chen Jiale , Han Lu , Li Zizheng , Fan Haojun , Gong Yanhua 
Published: August 2023

AbstractCrush injury (CI) is a common disease in earthquake and traffic accidents. It refers to long-term compression that induces ischemia and hypoxia injury of skeletal muscle rich parts, leading to rupture of muscle cells and release of contents into the blood circulation. Crush syndrome (CS) is the systemic manifestation of severe, traumatic muscle injury. CI rescue faces a dilemma. Ischemic reperfusion due to decompression is a double-edged sword for the injured. Death often occurs when the injured are glad to be rescued. Programmed cell death (PCD) predominates in muscle CI or ischemia-reperfusion injury. However, the function and mechanism of pyroptosis and apoptosis in the pathogenesis of skeletal muscle injury in CI remain elusive. Here, we identified that pyroptosis and apoptosis occur independently of each other and are regulated differently in the injured mice’s skeletal muscle of CI. While in vitro model, we found that glucose-deprived ischemic myoblast cells could occur pyroptosis. However, the cell damage degree was reduced if the oxygen was further deprived. Then, we confirmed that delayed step-by-step decompression of CI mice could significantly reduce skeletal muscle injury by substantially inhibiting NLRP3/Casp-1/GSDMD pyroptosis pathway but not altering the Casp-3/PARP apoptosis pathway. Moreover, pyroptotic inhibitor DSF therapy alone, or the combination of delayed step-by-step decompression and pyroptotic inhibitor therapy, significantly alleviated muscle injury of CI mice. The new physical stress relief and drug intervention method proposed in this study put forward new ideas and directions for rescuing patients with CI, even CS-associated acute kidney injury (CS-AKI).
VAPB-mediated ER-targeting stabilizes IRS-1 signalosomes to regulate insulin/IGF signaling
Authors: Gao Xiu Kui , Sheng Zu Kang , Lu Ye Hong , Sun Yu Ting , Rao Xi Sheng , Shi Lin Jing , Cong Xiao Xia , Chen Xiao , Wu Hao Bo , Huang Man , Zheng Qiang , Guo Jian-sheng , Jiang Liang Jun , Zheng Li Ling , Zhou Yi Ting 
Published: August 2023

AbstractThe scaffold protein IRS-1 is an essential node in insulin/IGF signaling. It has long been recognized that the stability of IRS-1 is dependent on its endomembrane targeting. However, how IRS-1 targets the intracellular membrane, and what type of intracellular membrane is actually targeted, remains poorly understood. Here, we found that the phase separation-mediated IRS-1 puncta attached to endoplasmic reticulum (ER). VAPB, an ER-anchored protein that mediates tethers between ER and membranes of other organelles, was identified as a direct interacting partner of IRS-1. VAPB mainly binds active IRS-1 because IGF-1 enhanced the VAPB-IRS-1 association and replacing of the nine tyrosine residues of YXXM motifs disrupted the VAPB-IRS-1 association. We further delineated that the Y745 and Y746 residues in the FFAT-like motif of IRS-1 mediated the association with VAPB. Notably, VAPB targeted IRS-1 to the ER and subsequently maintained its stability. Consistently, ablation of VAPB in mice led to downregulation of IRS-1, suppression of insulin signaling, and glucose intolerance. The amyotrophic lateral sclerosis (ALS)-derived VAPB P56S mutant also impaired IRS-1 stability by interfering with the ER-tethering of IRS-1. Our findings thus revealed a previously unappreciated condensate-membrane contact (CMC), by which VAPB stabilizes the membraneless IRS-1 signalosome through targeting it to ER membrane.
Hexanary blends: a strategy towards thermally stable organic photovoltaics
Authors: Paleti Sri Harish Kumar , Hultmark Sandra , Han Jianhua , Wen Yuanfan , Xu Han , Chen Si , Järsvall Emmy , Jalan Ishita , Villalva Diego Rosas , Sharma Anirudh , Khan Jafar. I. , Moons Ellen , Li Ruipeng , Yu Liyang , Gorenflot Julien , Laquai Frédéric , Müller Christian , Baran Derya 
Published: August 2023

AbstractNon-fullerene based organic solar cells display a high initial power conversion efficiency but continue to suffer from poor thermal stability, especially in case of devices with thick active layers. Mixing of five structurally similar acceptors with similar electron affinities, and blending with a donor polymer is explored, yielding devices with a power conversion efficiency of up to 17.6%. The hexanary device performance is unaffected by thermal annealing of the bulk-heterojunction active layer for at least 23 days at 130 °C in the dark and an inert atmosphere. Moreover, hexanary blends offer a high degree of thermal stability for an active layer thickness of up to 390 nm, which is advantageous for high-throughput processing of organic solar cells. Here, a generic strategy based on multi-component acceptor mixtures is presented that permits to considerably improve the thermal stability of non-fullerene based devices and thus paves the way for large-area organic solar cells.
Robust phenotyping of highly multiplexed tissue imaging data using pixel-level clustering
Authors: Liu Candace C. , Greenwald Noah F. , Kong Alex , McCaffrey Erin F. , Leow Ke Xuan , Mrdjen Dunja , Cannon Bryan J. , Rumberger Josef Lorenz , Varra Sricharan Reddy , Angelo Michael 
Published: August 2023

AbstractWhile technologies for multiplexed imaging have provided an unprecedented understanding of tissue composition in health and disease, interpreting this data remains a significant computational challenge. To understand the spatial organization of tissue and how it relates to disease processes, imaging studies typically focus on cell-level phenotypes. However, images can capture biologically important objects that are outside of cells, such as the extracellular matrix. Here, we describe a pipeline, Pixie, that achieves robust and quantitative annotation of pixel-level features using unsupervised clustering and show its application across a variety of biological contexts and multiplexed imaging platforms. Furthermore, current cell phenotyping strategies that rely on unsupervised clustering can be labor intensive and require large amounts of manual cluster adjustments. We demonstrate how pixel clusters that lie within cells can be used to improve cell annotations. We comprehensively evaluate pre-processing steps and parameter choices to optimize clustering performance and quantify the reproducibility of our method. Importantly, Pixie is open source and easily customizable through a user-friendly interface.
Patrilocality and hunter-gatherer-related ancestry of populations in East-Central Europe during the Middle Bronze Age
Authors: Chyleński Maciej , Makarowicz Przemysław , Juras Anna , Krzewińska Maja , Pospieszny Łukasz , Ehler Edvard , Breszka Agnieszka , Górski Jacek , Taras Halina , Szczepanek Anita , Polańska Marta , Włodarczak Piotr , Lasota-Kuś Anna , Wójcik Irena , Romaniszyn Jan , Szmyt Marzena , Kośko Aleksander , Ignaczak Marcin , Sadowski Sylwester , Matoga Andrzej , Grossman Anna , Ilchyshyn Vasyl , Yahodinska Maryna O. , Romańska Adriana , Tunia Krzysztof , Przybyła Marcin , Grygiel Ryszard , Szostek Krzysztof , Dabert Miroslawa , Götherström Anders , Jakobsson Mattias , Malmström Helena 
Published: August 2023

AbstractThe demographic history of East-Central Europe after the Neolithic period remains poorly explored, despite this region being on the confluence of various ecological zones and cultural entities. Here, the descendants of societies associated with steppe pastoralists form Early Bronze Age were followed by Middle Bronze Age populations displaying unique characteristics. Particularly, the predominance of collective burials, the scale of which, was previously seen only in the Neolithic. The extent to which this re-emergence of older traditions is a result of genetic shift or social changes in the MBA is a subject of debate. Here by analysing 91 newly generated genomes from Bronze Age individuals from present Poland and Ukraine, we discovered that Middle Bronze Age populations were formed by an additional admixture event involving a population with relatively high proportions of genetic component associated with European hunter-gatherers and that their social structure was based on, primarily patrilocal, multigenerational kin-groups.
Genetic inhibition of CARD9 accelerates the development of atherosclerosis in mice through CD36 dependent-defective autophagy
Authors: Zhang Yujiao , Vandestienne Marie , Lavillegrand Jean-Rémi , Joffre Jeremie , Santos-Zas Icia , Lavelle Aonghus , Zhong Xiaodan , Le Goff Wilfried , Guérin Maryse , Al-Rifai Rida , Laurans Ludivine , Bruneval Patrick , Guérin Coralie , Diedisheim Marc , Migaud Melanie , Puel Anne , Lanternier Fanny , Casanova Jean-Laurent , Cochain Clément , Zernecke Alma , Saliba Antoine-Emmanuel , Mokry Michal , Silvestre Jean-Sebastien , Tedgui Alain , Mallat Ziad , Taleb Soraya , Lenoir Olivia , Vindis Cécile , Camus Stéphane M. , Sokol Harry , Ait-Oufella Hafid 
Published: August 2023

AbstractCaspase recruitment-domain containing protein 9 (CARD9) is a key signaling pathway in macrophages but its role in atherosclerosis is still poorly understood. Global deletion of Card9 in Apoe-/- mice as well as hematopoietic deletion in Ldlr-/- mice increases atherosclerosis. The acceleration of atherosclerosis is also observed in Apoe-/-Rag2-/-Card9-/- mice, ruling out a role for the adaptive immune system in the vascular phenotype of Card9 deficient mice. Card9 deficiency alters macrophage phenotype through CD36 overexpression with increased IL-1β production, increased lipid uptake, higher cell death susceptibility and defective autophagy. Rapamycin or metformin, two autophagy inducers, abolish intracellular lipid overload, restore macrophage survival and autophagy flux in vitro and finally abolish the pro-atherogenic effects of Card9 deficiency in vivo. Transcriptomic analysis of human CARD9-deficient monocytes confirms the pathogenic signature identified in murine models. In summary, CARD9 is a key protective pathway in atherosclerosis, modulating macrophage CD36-dependent inflammatory responses, lipid uptake and autophagy.
Machine-learning-assisted material discovery of oxygen-rich highly porous carbon active materials for aqueous supercapacitors
Authors: Wang Tao , Pan Runtong , Martins Murillo L. , Cui Jinlei , Huang Zhennan , Thapaliya Bishnu P. , Do-Thanh Chi-Linh , Zhou Musen , Fan Juntian , Yang Zhenzhen , Chi Miaofang , Kobayashi Takeshi , Wu Jianzhong , Mamontov Eugene , Dai Sheng 
Published: August 2023

AbstractPorous carbons are the active materials of choice for supercapacitor applications because of their power capability, long-term cycle stability, and wide operating temperatures. However, the development of carbon active materials with improved physicochemical and electrochemical properties is generally carried out via time-consuming and cost-ineffective experimental processes. In this regard, machine-learning technology provides a data-driven approach to examine previously reported research works to find the critical features for developing ideal carbon materials for supercapacitors. Here, we report the design of a machine-learning-derived activation strategy that uses sodium amide and cross-linked polymer precursors to synthesize highly porous carbons (i.e., with specific surface areas > 4000 m2/g). Tuning the pore size and oxygen content of the carbonaceous materials, we report a highly porous carbon-base electrode with 0.7 mg/cm2 of electrode mass loading that exhibits a high specific capacitance of 610 F/g in 1 M H2SO4. This result approaches the specific capacitance of a porous carbon electrode predicted by the machine learning approach. We also investigate the charge storage mechanism and electrolyte transport properties via step potential electrochemical spectroscopy and quasielastic neutron scattering measurements.
Quadrupolar excitons and hybridized interlayer Mott insulator in a trilayer moiré superlattice
Authors: Lian Zhen , Chen Dongxue , Ma Lei , Meng Yuze , Su Ying , Yan Li , Huang Xiong , Wu Qiran , Chen Xinyue , Blei Mark , Taniguchi Takashi , Watanabe Kenji , Tongay Sefaattin , Zhang Chuanwei , Cui Yong-Tao , Shi Su-Fei 
Published: August 2023

AbstractTransition metal dichalcogenide (TMDC) moiré superlattices, owing to the moiré flatbands and strong correlation, can host periodic electron crystals and fascinating correlated physics. The TMDC heterojunctions in the type-II alignment also enable long-lived interlayer excitons that are promising for correlated bosonic states, while the interaction is dictated by the asymmetry of the heterojunction. Here we demonstrate a new excitonic state, quadrupolar exciton, in a symmetric WSe2-WS2-WSe2trilayer moiré superlattice. The quadrupolar excitons exhibit a quadratic dependence on the electric field, distinctively different from the linear Stark shift of the dipolar excitons in heterobilayers. This quadrupolar exciton stems from the hybridization of WSe2valence moiré flatbands. The same mechanism also gives rise to an interlayer Mott insulator state, in which the two WSe2layers share one hole laterally confined in one moiré unit cell. In contrast, the hole occupation probability in each layer can be continuously tuned via an out-of-plane electric field, reaching 100% in the top or bottom WSe2under a large electric field, accompanying the transition from quadrupolar excitons to dipolar excitons. Our work demonstrates a trilayer moiré system as a new exciting playground for realizing novel correlated states and engineering quantum phase transitions.
Cullin-associated and neddylation-dissociated protein 1 (CAND1) alleviates NAFLD by reducing ubiquitinated degradation of ACAA2
Authors: Huang Xiang , Liu Xin , Li Xingda , Zhang Yang , Gao Jianjun , Yang Ying , Jiang Yuan , Gao Haiyu , Sun Chongsong , Xuan Lina , Zhao Lexin , Song Jiahui , Bao Hairong , Zhou Zhiwen , Li Shangxuan , Zhang Xiaofang , Lu Yanjie , Zhong Xiangyu , Yang Baofeng , Pan Zhenwei 
Published: August 2023

AbstractNonalcoholic fatty liver disease (NAFLD) is the most common liver disorder with high morbidity and mortality. The current study aims to explore the role of Cullin-associated and neddylation-dissociated protein 1 (CAND1) in the development of NAFLD and the underlying mechanisms. CAND1 is reduced in the liver of NAFLD male patients and high fat diet (HFD)-fed male mice. CAND1 alleviates palmitate (PA) induced lipid accumulation in vitro. Hepatocyte-specific knockout of CAND1 exacerbates HFD-induced liver injury in HFD-fed male mice, while hepatocyte-specific knockin of CAND1 ameliorates these pathological changes. Mechanistically, deficiency of CAND1 enhances the assembly of Cullin1, F-box only protein 42 (FBXO42) and acetyl-CoA acyltransferase 2 (ACAA2) complexes, and thus promotes the ubiquitinated degradation of ACAA2. ACAA2 overexpression abolishes the exacerbated effects of CAND1 deficiency on NAFLD. Additionally, androgen receptor binds to the −187 to −2000 promoter region of CAND1. Collectively, CAND1 mitigates NAFLD by inhibiting Cullin1/FBXO42 mediated ACAA2 degradation.