bluuebunny/crossref_metadata_2025_split huggingface dataset:
Rewiring the Carbon Cycle: A Theoretical Framework for Animal‐Driven Ecosystem Carbon Sequestration
Authors: Rizzuto Matteo , Leroux Shawn J. , Schmitz Oswald J. 
Published: April 2024

AbstractMost carbon cycle models do not consider animal‐mediated effects, focusing instead on carbon exchanges among plants, microbes, and the atmosphere. Yet, a growing body of empirical evidence from diverse ecosystems points to pervasive animal effects on ecosystem carbon cycling and shows that ignoring them could lead to misrepresentation of an ecosystem's carbon cycle. We develop a new theoretical framework to account for animal effects on ecosystem carbon cycling. We combine a classic ecosystem compartment modeling approach with a classic carbon model to account for carbon flux and storage among plant, animal, and soil microbial trophic compartments. We show, by way of numerical analyses of steady state conditions across three competing scenarios, that animal presence alters the dominant pathways of control over carbon storage and capture. This altered control arises via direct, consumptive effects and especially via indirect, non‐consumptive pathways by instigating faster nutrient recycling. This leads to a quantitative change in the ecosystem's carbon balance, enhancing the amount of carbon captured and stored in the ecosystem. Further, the indirect pathways appear especially important in enabling these effects because of their sensitivity to the structure of the ecosystem's food chain. The modeling shows that animals could play a larger role in ecosystem carbon cycle than previously thought. Our framework provides further guidance for empirical research aimed at quantifying animal‐mediated control of carbon cycling and to inform the development of nature‐based climate change solutions that leverage animal influence on the carbon cycle to help mitigate climate change.
Cargo specificity, regulation, and therapeutic potential of cytoplasmic dynein
Authors: Park Jin-Gyeong , Jeon Hanul , Hwang Kwang Yeon , Cha Sun-Shin , Han Rafael T. , Cho Hyesung , Lee In-Gyun 
Published: April 2024

AbstractIntracellular retrograde transport in eukaryotic cells relies exclusively on the molecular motor cytoplasmic dynein 1. Unlike its counterpart, kinesin, dynein has a single isoform, which raises questions about its cargo specificity and regulatory mechanisms. The precision of dynein-mediated cargo transport is governed by a multitude of factors, including temperature, phosphorylation, the microtubule track, and interactions with a family of activating adaptor proteins. Activating adaptors are of particular importance because they not only activate the unidirectional motility of the motor but also connect a diverse array of cargoes with the dynein motor. Therefore, it is unsurprising that dysregulation of the dynein-activating adaptor transport machinery can lead to diseases such as spinal muscular atrophy, lower extremity, and dominant. Here, we discuss dynein motor motility within cells and in in vitro, and we present several methodologies employed to track the motion of the motor. We highlight several newly identified activating adaptors and their roles in regulating dynein. Finally, we explore the potential therapeutic applications of manipulating dynein transport to address diseases linked to dynein malfunction.
Ceramide kinase-mediated C1P metabolism attenuates acute liver injury by inhibiting the interaction between KEAP1 and NRF2
Authors: Dong Wei , Li Qing , Lu Xing , Lan Jianfeng , Qiu Zhidong , Wang Xuehong , Wang Junnan , Zheng Xiaojiao , Chen Sifan , Zhang Chong , Jin Junfei 
Published: April 2024

AbstractAcute liver injury is the basis of the pathogenesis of diverse liver diseases. However, the mechanism underlying liver injury is complex and not completely understood. In our study, we revealed that CERK, which phosphorylates ceramide to produce ceramide-1-phosphate (C1P), was the sphingolipid pathway-related protein that had the most significantly upregulated expression during acute liver injury. A functional study confirmed that CERK and C1P attenuate hepatic injury both in vitro and in vivo through antioxidant effects. Mechanistic studies have shown that CERK and C1P positively regulate the protein expression of NRF2, which is a crucial protein that helps maintain redox homeostasis. Furthermore, our results indicated that C1P disrupted the interaction between NRF2 and KEAP1 by competitively binding to KEAP1, which allowed for the nuclear translocation of NRF2. In addition, pull-down assays and molecular docking analyses revealed that C1P binds to the DGR domain of KEAP1, which allows it to maintain its interaction with NRF2. Importantly, these findings were verified in human primary hepatocytes and a mouse model of hepatic ischemia‒reperfusion injury. Taken together, our findings demonstrated that CERK-mediated C1P metabolism attenuates acute liver injury via the binding of C1P to the DGR domain of KEAP1 and subsequently the release and nuclear translocation of NRF2, which activates the transcription of cytoprotective and antioxidant genes. Our study suggested that the upregulation of CERK and C1P expression may serve as a potential antioxidant strategy to alleviate acute liver injury.
Dysregulation of Wnt/β-catenin signaling contributes to intestinal inflammation through regulation of group 3 innate lymphoid cells
Authors: Hao Jiacheng , Liu Chang , Gu Zhijie , Yang Xuanming , Lan Xun , Guo Xiaohuan 
Published: April 2024

AbstractRORγt+ group 3 innate lymphoid cells (ILC3s) are essential for intestinal homeostasis. Dysregulation of ILC3s has been found in the gut of patients with inflammatory bowel disease and colorectal cancer, yet the specific mechanisms still require more investigation. Here we observe increased β-catenin in intestinal ILC3s from inflammatory bowel disease and colon cancer patients compared with healthy donors. In contrast to promoting RORγt expression in T cells, activation of Wnt/β-catenin signaling in ILC3s suppresses RORγt expression, inhibits its proliferation and function, and leads to a deficiency of ILC3s and subsequent intestinal inflammation in mice. Activated β-catenin and its interacting transcription factor, TCF-1, cannot directly suppress RORγt expression, but rather alters global chromatin accessibility and inhibits JunB expression, which is essential for RORγt expression in ILC3s. Together, our findings suggest that dysregulated Wnt/β-catenin signaling impairs intestinal ILC3s through TCF-1/JunB/RORγt regulation, further disrupting intestinal homeostasis, and promoting inflammation and cancer.
Intrathecal delivery of adipose-derived mesenchymal stem cells in traumatic spinal cord injury: Phase I trial
Authors: Bydon Mohamad , Qu Wenchun , Moinuddin F. M. , Hunt Christine L. , Garlanger Kristin L. , Reeves Ronald K. , Windebank Anthony J. , Zhao Kristin D. , Jarrah Ryan , Trammell Brandon C. , El Sammak Sally , Michalopoulos Giorgos D. , Katsos Konstantinos , Graepel Stephen P. , Seidel-Miller Kimberly L. , Beck Lisa A. , Laughlin Ruple S. , Dietz Allan B. 
Published: April 2024

Abstract
Intrathecal delivery of autologous culture-expanded adipose tissue-derived mesenchymal stem cells (AD-MSC) could be utilized to treat traumatic spinal cord injury (SCI). This Phase I trial (ClinicalTrials.gov: NCT03308565) included 10 patients with American Spinal Injury Association Impairment Scale (AIS) grade A or B at the time of injury. The study’s primary outcome was the safety profile, as captured by the nature and frequency of adverse events. Secondary outcomes included changes in sensory and motor scores, imaging, cerebrospinal fluid markers, and somatosensory evoked potentials. The manufacturing and delivery of the regimen were successful for all patients. The most commonly reported adverse events were headache and musculoskeletal pain, observed in 8 patients. No serious AEs were observed. At final follow-up, seven patients demonstrated improvement in AIS grade from the time of injection. In conclusion, the study met the primary endpoint, demonstrating that AD-MSC harvesting and administration were well-tolerated in patients with traumatic SCI.
A negative feedback loop between TET2 and leptin in adipocyte regulates body weight
Authors: Zeng Qin , Song Jianfeng , Sun Xiaoxiao , Wang Dandan , Liao Xiyan , Ding Yujin , Hu Wanyu , Jiao Yayi , Mai Wuqian , Aini Wufuer , Wang Fanqi , Zhou Hui , Xie Limin , Mei Ying , Tang Yuan , Xie Zhiguo , Wu Haijing , Liu Wei , Deng Tuo 
Published: April 2024

AbstractTen-eleven translocation (TET) 2 is an enzyme that catalyzes DNA demethylation to regulate gene expression by oxidizing 5-methylcytosine to 5-hydroxymethylcytosine, functioning as an essential epigenetic regulator in various biological processes. However, the regulation and function of TET2 in adipocytes during obesity are poorly understood. In this study, we demonstrate that leptin, a key adipokine in mammalian energy homeostasis regulation, suppresses adipocyte TET2 levels via JAK2-STAT3 signaling. Adipocyte Tet2 deficiency protects against high-fat diet-induced weight gain by reducing leptin levels and further improving leptin sensitivity in obese male mice. By interacting with C/EBPα, adipocyte TET2 increases the hydroxymethylcytosine levels of the leptin gene promoter, thereby promoting leptin gene expression. A decrease in adipose TET2 is associated with obesity-related hyperleptinemia in humans. Inhibition of TET2 suppresses the production of leptin in mature human adipocytes. Our findings support the existence of a negative feedback loop between TET2 and leptin in adipocytes and reveal a compensatory mechanism for the body to counteract the metabolic dysfunction caused by obesity.
Intelligent wireless power transfer via a 2-bit compact reconfigurable transmissive-metasurface-based router
Authors: Li Wenzhi , Yu Qiyue , Qiu Jing Hui , Qi Jiaran 
Published: April 2024

AbstractWith the rapid development of the Internet of Things, numerous devices have been deployed in complex environments for environmental monitoring and information transmission, which brings new power supply challenges. Wireless power transfer is a promising solution since it enables power delivery without cables, providing well-behaved flexibility for power supplies. Here we propose a compact wireless power transfer framework. The core components of the proposed framework include a plane-wave feeder and a transmissive 2-bit reconfigurable metasurface-based beam generator, which constitute a reconfigurable power router. The combined profile of the feeder and the beam generator is 0.8 wavelengths. In collaboration with a deep-learning-driven environment sensor, the router enables object detection and localization, and intelligent wireless power transfer to power-consuming targets, especially in dynamic multitarget environments. Experiments also show that the router is capable of simultaneous wireless power and information transfer. Due to the merits of low cost and compact size, the proposed framework may boost the commercialization of metasurface-based wireless power transfer routers.
Defect-induced triple synergistic modulation in copper for superior electrochemical ammonia production across broad nitrate concentrations
Authors: Zhang Bocheng , Dai Zechuan , Chen Yanxu , Cheng Mingyu , Zhang Huaikun , Feng Pingyi , Ke Buqi , Zhang Yangyang , Zhang Genqiang 
Published: April 2024

AbstractNitrate can be electrochemically degraded to produce ammonia while treating sewage while it remains grand challenge to simultaneously realize high Faradaic efficiency and production rate over wide-range concentrations in real wastewater. Herein, we report the defect-rich Cu nanowire array electrode generated by in-situ electrochemical reduction, exhibiting superior performance in the electrochemical nitrate reduction reaction benefitting from the triple synergistic modulation. Notably, the defect-rich Cu nanowire array electrode delivers current density ranging from 50 to 1100 mA cm−2 across wide nitrate concentrations (1–100 mM) with Faradaic efficiency over 90%. Operando Synchrotron radiation Fourier Transform Infrared Spectroscopy and theoretical calculations revealed that the defective Cu sites can simultaneously enhance nitrate adsorption, promote water dissociation and suppress hydrogen evolution. A two-electrode system integrating nitrate reduction reaction in industrial wastewater with glycerol oxidation reaction achieves current density of 550 mA cm−2 at −1.4 V with 99.9% ammonia selectivity and 99.9% nitrate conversion with 100 h stability, demonstrating outstanding practicability.
Native-state proteomics of Parvalbumin interneurons identifies unique molecular signatures and vulnerabilities to early Alzheimer’s pathology
Authors: Kumar Prateek , Goettemoeller Annie M. , Espinosa-Garcia Claudia , Tobin Brendan R. , Tfaily Ali , Nelson Ruth S. , Natu Aditya , Dammer Eric B. , Santiago Juliet V. , Malepati Sneha , Cheng Lihong , Xiao Hailian , Duong Duc D. , Seyfried Nicholas T. , Wood Levi B. , Rowan Matthew J. M. , Rangaraju Srikant 
Published: April 2024

AbstractDysfunction in fast-spiking parvalbumin interneurons (PV-INs) may represent an early pathophysiological perturbation in Alzheimer’s Disease (AD). Defining early proteomic alterations in PV-INs can provide key biological and translationally-relevant insights. We used cell-type-specific in-vivo biotinylation of proteins (CIBOP) coupled with mass spectrometry to obtain native-state PV-IN proteomes. PV-IN proteomic signatures include high metabolic and translational activity, with over-representation of AD-risk and cognitive resilience-related proteins. In bulk proteomes, PV-IN proteins were associated with cognitive decline in humans, and with progressive neuropathology in humans and the 5xFAD mouse model of Aβ pathology. PV-IN CIBOP in early stages of Aβ pathology revealed signatures of increased mitochondria and metabolism, synaptic and cytoskeletal disruption and decreased mTOR signaling, not apparent in whole-brain proteomes. Furthermore, we demonstrated pre-synaptic defects in PV-to-excitatory neurotransmission, validating our proteomic findings. Overall, in this study we present native-state proteomes of PV-INs, revealing molecular insights into their unique roles in cognitive resiliency and AD pathogenesis.
The Miocene primate Pliobates is a pliopithecoid
Authors: Bouchet Florian , Zanolli Clément , Urciuoli Alessandro , Almécija Sergio , Fortuny Josep , Robles Josep M. , Beaudet Amélie , Moyà-Solà Salvador , Alba David M. 
Published: April 2024

AbstractThe systematic status of the small-bodied catarrhine primate Pliobates cataloniae, from the Miocene (11.6 Ma) of Spain, is controversial because it displays a mosaic of primitive and derived features compared with extant hominoids (apes and humans). Cladistic analyses have recovered Pliobates as either a stem hominoid or as a pliopithecoid stem catarrhine (i.e., preceding the cercopithecoid–hominoid divergence). Here, we describe additional dental remains of P. cataloniae from another locality that display unambiguous synapomorphies of crouzeliid pliopithecoids. Our cladistic analyses support a close phylogenetic link with poorly-known small crouzeliids from Europe based on (cranio)dental characters but recover pliopithecoids as stem hominoids when postcranial characters are included. We conclude that Pliobates is a derived stem catarrhine that shows postcranial convergences with modern apes in the elbow and wrist joints—thus clarifying pliopithecoid evolution and illustrating the plausibility of independent acquisition of postcranial similarities between hylobatids and hominids.
Deuteration-enhanced neutron contrasts to probe amorphous domain sizes in organic photovoltaic bulk heterojunction films
Authors: Cai Guilong , Li Yuhao , Fu Yuang , Yang Hua , Mei Le , Nie Zhaoyang , Li Tengfei , Liu Heng , Ke Yubin , Wang Xun-Li , Brédas Jean-Luc , Tang Man-Chung , Chen Xiankai , Zhan Xiaowei , Lu Xinhui 
Published: March 2024

AbstractAn organic photovoltaic bulk heterojunction comprises of a mixture of donor and acceptor materials, forming a semi-crystalline thin film with both crystalline and amorphous domains. Domain sizes critically impact the device performance; however, conventional X-ray scattering techniques cannot detect the contrast between donor and acceptor materials within the amorphous intermixing regions. In this study, we employ neutron scattering and targeted deuteration of acceptor materials to enhance the scattering contrast by nearly one order of magnitude. Remarkably, the PM6:deuterated Y6 system reveals a new length scale, indicating short-range aggregation of Y6 molecules in the amorphous intermixing regions. All-atom molecular dynamics simulations confirm that this short-range aggregation is an inherent morphological advantage of Y6 which effectively assists charge extraction and suppresses charge recombination as shown by capacitance spectroscopy. Our findings uncover the amorphous nanomorphology of organic photovoltaic thin films, providing crucial insights into the morphology-driven device performance.
Loss-of-function mutation in PRMT9 causes abnormal synapse development by dysregulation of RNA alternative splicing
Authors: Shen Lei , Ma Xiaokuang , Wang Yuanyuan , Wang Zhihao , Zhang Yi , Pham Hoang Quoc Hai , Tao Xiaoqun , Cui Yuehua , Wei Jing , Lin Dimitri , Abeywanada Tharindumala , Hardikar Swanand , Halabelian Levon , Smith Noah , Chen Taiping , Barsyte-Lovejoy Dalia , Qiu Shenfeng , Xing Yi , Yang Yanzhong 
Published: April 2024

AbstractProtein arginine methyltransferase 9 (PRMT9) is a recently identified member of the PRMT family, yet its biological function remains largely unknown. Here, by characterizing an intellectual disability associated PRMT9 mutation (G189R) and establishing a Prmt9 conditional knockout (cKO) mouse model, we uncover an important function of PRMT9 in neuronal development. The G189R mutation abolishes PRMT9 methyltransferase activity and reduces its protein stability. Knockout of Prmt9 in hippocampal neurons causes alternative splicing of ~1900 genes, which likely accounts for the aberrant synapse development and impaired learning and memory in the Prmt9 cKO mice. Mechanistically, we discover a methylation-sensitive protein–RNA interaction between the arginine 508 (R508) of the splicing factor 3B subunit 2 (SF3B2), the site that is exclusively methylated by PRMT9, and the pre-mRNA anchoring site, a cis-regulatory element that is critical for RNA splicing. Additionally, using human and mouse cell lines, as well as an SF3B2 arginine methylation-deficient mouse model, we provide strong evidence that SF3B2 is the primary methylation substrate of PRMT9, thus highlighting the conserved function of the PRMT9/SF3B2 axis in regulating pre-mRNA splicing.
Hyperbolic metamaterial empowered controllable photonic Weyl nodal line semimetals
Authors: Hu Shengyu , Guo Zhiwei , Liu Wenwei , Chen Shuqi , Chen Hong 
Published: March 2024

AbstractMotivated by unique topological semimetals in condensed matter physics, we propose an effective Hamiltonian with four degrees of freedom to describe evolutions of photonic double Weyl nodal line semimetals in one-dimensional hyper-crystals, which supports the energy bands translating or rotating independently in the form of Weyl quasiparticles. Especially, owing to the unit cells without inversion symmetry, a pair of reflection-phase singularities carrying opposite topological charges emerge near each nodal line, and result in a unique bilateral drumhead surface state. After reducing radiation leakages and absorption losses, these two singularities gather together gradually, and form a quasi-bound state in the continuum (quasi-BIC) ring at the nodal line ultimately. Our work not only reports the first realization of controllable photonics Weyl nodal line semimetals, establishes a bridge between two independent topological concepts−BICs and Weyl semimetals, but also heralds new possibilities for unconventional device applications, such as dual-mode schemes for highly sensitive sensing and switching.
The thylakoid proton antiporter KEA3 regulates photosynthesis in response to the chloroplast energy status
Authors: Uflewski Michał , Rindfleisch Tobias , Korkmaz Kübra , Tietz Enrico , Mielke Sarah , Correa Galvis Viviana , Dünschede Beatrix , Luzarowski Marcin , Skirycz Aleksandra , Schwarzländer Markus , Strand Deserah D. , Hertle Alexander P. , Schünemann Danja , Walther Dirk , Thalhammer Anja , Wolff Martin , Armbruster Ute 
Published: March 2024

AbstractPlant photosynthesis contains two functional modules, the light-driven reactions in the thylakoid membrane and the carbon-fixing reactions in the chloroplast stroma. In nature, light availability for photosynthesis often undergoes massive and rapid fluctuations. Efficient and productive use of such variable light supply requires an instant crosstalk and rapid synchronization of both functional modules. Here, we show that this communication involves the stromal exposed C-terminus of the thylakoid K+-exchange antiporter KEA3, which regulates the ΔpH across the thylakoid membrane and therefore pH-dependent photoprotection. By combining in silico, in vitro, and in vivo approaches, we demonstrate that the KEA3 C-terminus senses the energy state of the chloroplast in a pH-dependent manner and regulates transport activity in response. Together our data pinpoint a regulatory feedback loop by which the stromal energy state orchestrates light capture and photoprotection via multi-level regulation of KEA3.
Genetic associations of protein-coding variants in venous thromboembolism
Authors: He Xiao-Yu , Wu Bang-Sheng , Yang Liu , Guo Yu , Deng Yue-Ting , Li Ze-Yu , Fei Chen-Jie , Liu Wei-Shi , Ge Yi-Jun , Kang Jujiao , Feng Jianfeng , Cheng Wei , Dong Qiang , Yu Jin-Tai 
Published: April 2024

AbstractPrevious genetic studies of venous thromboembolism (VTE) have been largely limited to common variants, leaving the genetic determinants relatively incomplete. We performed an exome-wide association study of VTE among 14,723 cases and 334,315 controls. Fourteen known and four novel genes (SRSF6, PHPT1, CGN, and MAP3K2) were identified through protein-coding variants, with broad replication in the FinnGen cohort. Most genes we discovered exhibited the potential to predict future VTE events in longitudinal analysis. Notably, we provide evidence for the additive contribution of rare coding variants to known genome-wide polygenic risk in shaping VTE risk. The identified genes were enriched in pathways affecting coagulation and platelet activation, along with liver-specific expression. The pleiotropic effects of these genes indicated the potential involvement of coagulation factors, blood cell traits, liver function, and immunometabolic processes in VTE pathogenesis. In conclusion, our study unveils the valuable contribution of protein-coding variants in VTE etiology and sheds new light on its risk stratification.