bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anyon quantum dimensions from an arbitrary ground state wave function
Authors: Liu Shang 
Published: June 2024

AbstractRealizing topological orders and topological quantum computation is a central task of modern physics. An important but notoriously hard question in this endeavor is how to diagnose topological orders that lack conventional order parameters. A breakthrough in this problem is the discovery of topological entanglement entropy, which can be used to detect nontrivial topological order from a ground state wave function, but is far from enough for fully determining the topological order. In this work, we take a key step further in this direction: We propose a simple entanglement-based protocol for extracting the quantum dimensions of all anyons from a single ground state wave function in two dimensions. The choice of the space manifold and the ground state is arbitrary. This protocol is both validated in the continuum and verified on lattices, and we anticipate it to be realizable in various quantum simulation platforms.
Acoustic ejection mass spectrometry empowers ultra-fast protein biomarker quantification
Authors: Van Puyvelde Bart , Hunter Christie L. , Zhgamadze Maxim , Savant Sudha , Wang Y. Oliver , Hoedt Esthelle , Raedschelders Koen , Pope Matt , Huynh Carissa A. , Ramanujan V. Krishnan , Tourtellotte Warren , Razavi Morteza , Anderson N. Leigh , Martens Geert , Deforce Dieter , Fu Qin , Dhaenens Maarten , Van Eyk Jennifer E. 
Published: June 2024

AbstractThe global scientific response to COVID 19 highlighted the urgent need for increased throughput and capacity in bioanalytical laboratories, especially for the precise quantification of proteins that pertain to health and disease. Acoustic ejection mass spectrometry (AEMS) represents a much-needed paradigm shift for ultra-fast biomarker screening. Here, a quantitative AEMS assays is presented, employing peptide immunocapture to enrich (i) 10 acute phase response (APR) protein markers from plasma, and (ii) SARS-CoV-2 NCAP peptides from nasopharyngeal swabs. The APR proteins were quantified in 267 plasma samples, in triplicate in 4.8 h, with %CV from 4.2% to 10.5%. SARS-CoV-2 peptides were quantified in triplicate from 145 viral swabs in 10 min. This assay represents a 15-fold speed improvement over LC-MS, with instrument stability demonstrated across 10,000 peptide measurements. The combination of speed from AEMS and selectivity from peptide immunocapture enables ultra-high throughput, reproducible quantitative biomarker screening in very large cohorts.
Additive manufacturing of an ultrastrong, deformable Al alloy with nanoscale intermetallics
Authors: Shang Anyu , Stegman Benjamin , Choy Kenyi , Niu Tongjun , Shen Chao , Shang Zhongxia , Sheng Xuanyu , Lopez Jack , Hoppenrath Luke , Zhang Bohua Peter , Wang Haiyan , Bellon Pascal , Zhang Xinghang 
Published: June 2024

AbstractLight-weight, high-strength, aluminum (Al) alloys have widespread industrial applications. However, most commercially available high-strength Al alloys, like AA 7075, are not suitable for additive manufacturing due to their high susceptibility to solidification cracking. In this work, a custom Al alloy Al92Ti2Fe2Co2Ni2 is fabricated by selective laser melting. Heterogeneous nanoscale medium-entropy intermetallic lamella form in the as-printed Al alloy. Macroscale compression tests reveal a combination of high strength, over 700 MPa, and prominent plastic deformability. Micropillar compression tests display significant back stress in all regions, and certain regions have flow stresses exceeding 900 MPa. Post-deformation analyses reveal that, in addition to abundant dislocation activities in Al matrix, complex dislocation structures and stacking faults form in monoclinic Al9Co2 type brittle intermetallics. This study shows that proper introduction of heterogeneous microstructures and nanoscale medium entropy intermetallics offer an alternative solution to the design of ultrastrong, deformable Al alloys via additive manufacturing.
Human gut microbes express functionally distinct endoglycosidases to metabolize the same N-glycan substrate
Authors: Sastre Diego E. , Sultana Nazneen , V. A. S. Navarro Marcos , Huliciak Maros , Du Jonathan , Cifuente Javier O. , Flowers Maria , Liu Xu , Lollar Pete , Trastoy Beatriz , Guerin Marcelo E. , Sundberg Eric J. 
Published: June 2024

AbstractBacteroidales (syn. Bacteroidetes) are prominent members of the human gastrointestinal ecosystem mainly due to their efficient glycan-degrading machinery, organized into gene clusters known as polysaccharide utilization loci (PULs). A single PUL was reported for catabolism of high-mannose (HM) N-glycan glyco-polypeptides in the gut symbiont Bacteroides thetaiotaomicron, encoding a surface endo-β-N-acetylglucosaminidase (ENGase), BT3987. Here, we discover an ENGase from the GH18 family in B. thetaiotaomicron, BT1285, encoded in a distinct PUL with its own repertoire of proteins for catabolism of the same HM N-glycan substrate as that of BT3987. We employ X-ray crystallography, electron microscopy, mass spectrometry-based activity measurements, alanine scanning mutagenesis and a broad range of biophysical methods to comprehensively define the molecular mechanism by which BT1285 recognizes and hydrolyzes HM N-glycans, revealing that the stabilities and activities of BT1285 and BT3987 were optimal in markedly different conditions. BT1285 exhibits significantly higher affinity and faster hydrolysis of poorly accessible HM N-glycans than does BT3987. We also find that two HM-processing endoglycosidases from the human gut-resident Alistipes finegoldii display condition-specific functional properties. Altogether, our data suggest that human gut microbes employ evolutionary strategies to express distinct ENGases in order to optimally metabolize the same N-glycan substrate in the gastroinstestinal tract.
Ambient air pollution and urological cancer risk: A systematic review and meta-analysis of epidemiological evidence
Authors: Li Jinhui , Deng Zhengyi , Soerensen Simon John Christoph , Kachuri Linda , Cardenas Andres , Graff Rebecca E. , Leppert John T. , Langston Marvin E. , Chung Benjamin I. 
Published: June 2024

AbstractExposure to ambient air pollution has significant adverse health effects; however, whether air pollution is associated with urological cancer is largely unknown. We conduct a systematic review and meta-analysis with epidemiological studies, showing that a 5 μg/m3 increase in PM2.5 exposure is associated with a 6%, 7%, and 9%, increased risk of overall urological, bladder, and kidney cancer, respectively; and a 10 μg/m3 increase in NO2 is linked to a 3%, 4%, and 4% higher risk of overall urological, bladder, and prostate cancer, respectively. Were these associations to reflect causal relationships, lowering PM2.5 levels to 5.8 μg/m3 could reduce the age-standardized rate of urological cancer by 1.5 ~ 27/100,000 across the 15 countries with the highest PM2.5 level from the top 30 countries with the highest urological cancer burden. Implementing global health policies that can improve air quality could potentially reduce the risk of urologic cancer and alleviate its burden.
Kinetics and mapping of Ca-driven calmodulin conformations on skeletal and cardiac muscle ryanodine receptors
Authors: Rebbeck Robyn T. , Svensson Bengt , Zhang Jingyan , Samsó Montserrat , Thomas David D. , Bers Donald M. , Cornea Razvan L. 
Published: June 2024

AbstractCalmodulin transduces [Ca2+] information regulating the rhythmic Ca2+ cycling between the sarcoplasmic reticulum and cytoplasm during contraction and relaxation in cardiac and skeletal muscle. However, the structural dynamics by which calmodulin modulates the sarcoplasmic reticulum Ca2+ release channel, the ryanodine receptor, at physiologically relevant [Ca2+] is unknown. Using fluorescence lifetime FRET, we resolve different structural states of calmodulin and Ca2+-driven shifts in the conformation of calmodulin bound to ryanodine receptor. Skeletal and cardiac ryanodine receptor isoforms show different calmodulin-ryanodine receptor conformations, as well as binding and structural kinetics with 0.2-ms resolution, which reflect different functional roles of calmodulin. These FRET methods provide insight into the physiological calmodulin-ryanodine receptor structural states, revealing additional distinct structural states that complement cryo-EM models that are based on less physiological conditions. This technology will drive future studies on pathological calmodulin-ryanodine receptor interactions and dynamics with other important ryanodine receptor bound modulators.
A bispecific antibody exhibits broad neutralization against SARS-CoV-2 Omicron variants XBB.1.16, BQ.1.1 and sarbecoviruses
Authors: Wang Yingdan , Hao Aihua , Ji Ping , Ma Yunping , Zhang Zhaoyong , Chen Jiali , Mao Qiyu , Xiong Xinyi , Rehati Palizhati , Wang Yajie , Wang Yanqun , Wen Yumei , Lu Lu , Chen Zhenguo , Zhao Jincun , Wu Fan , Huang Jinghe , Sun Lei 
Published: June 2024

AbstractThe Omicron subvariants BQ.1.1, XBB.1.5, and XBB.1.16 of SARS-CoV-2 are known for their adeptness at evading immune responses. Here, we isolate a neutralizing antibody, 7F3, with the capacity to neutralize all tested SARS-CoV-2 variants, including BQ.1.1, XBB.1.5, and XBB.1.16. 7F3 targets the receptor-binding motif (RBM) region and exhibits broad binding to a panel of 37 RBD mutant proteins. We develop the IgG-like bispecific antibody G7-Fc using 7F3 and the cross-neutralizing antibody GW01. G7-Fc demonstrates robust neutralizing activity against all 28 tested SARS-CoV-2 variants and sarbecoviruses, providing potent prophylaxis and therapeutic efficacy against XBB.1 infection in both K18-ACE and BALB/c female mice. Cryo-EM structure analysis of the G7-Fc in complex with the Omicron XBB spike (S) trimer reveals a trimer-dimer conformation, with G7-Fc synergistically targeting two distinct RBD epitopes and blocking ACE2 binding. Comparative analysis of 7F3 and LY-CoV1404 epitopes highlights a distinct and highly conserved epitope in the RBM region bound by 7F3, facilitating neutralization of the immune-evasive Omicron variant XBB.1.16. G7-Fc holds promise as a potential prophylactic countermeasure against SARS-CoV-2, particularly against circulating and emerging variants.
Fusaric acid mediates the assembly of disease-suppressive rhizosphere microbiota via induced shifts in plant root exudates
Authors: Jin Xue , Jia Huiting , Ran Lingyi , Wu Fengzhi , Liu Junjie , Schlaeppi Klaus , Dini-Andreote Francisco , Wei Zhong , Zhou Xingang 
Published: June 2024

AbstractThe plant health status is determined by the interplay of plant-pathogen-microbiota in the rhizosphere. Here, we investigate this tripartite system focusing on the pathogenFusarium oxysporumf. sp.lycopersici(FOL) and tomato plants as a model system. First, we explore differences in tomato genotype resistance to FOL potentially associated with the differential recruitment of plant-protective rhizosphere taxa. Second, we show the production of fusaric acid by FOL to trigger systemic changes in the rhizosphere microbiota. Specifically, we show this molecule to have opposite effects on the recruitment of rhizosphere disease-suppressive taxa in the resistant and susceptible genotypes. Last, we elucidate that FOL and fusaric acid induce changes in the tomato root exudation with direct effects on the recruitment of specific disease-suppressive taxa. Our study unravels a mechanism mediating plant rhizosphere assembly and disease suppression by integrating plant physiological responses to microbial-mediated mechanisms in the rhizosphere.
Functional group tolerant hydrogen borrowing C-alkylation
Authors: Bailey Elliot P. , Donohoe Timothy J. , Smith Martin D. 
Published: June 2024

AbstractHydrogen borrowing is an attractive and sustainable strategy for carbon–carbon bond formation that enables alcohols to be used as alkylating reagents in place of alkyl halides. However, despite intensive efforts, limited functional group tolerance is observed in this methodology, which we hypothesize is due to the high temperatures and harsh basic conditions often employed. Here we demonstrate that room temperature and functional group tolerant hydrogen borrowing can be achieved with a simple iridium catalyst in the presence of substoichiometric base without an excess of reagents. Achieving high yields necessitates the application of anaerobic conditions to counteract the oxygen sensitivity of the catalytic iridium hydride intermediate, which otherwise leads to catalyst degradation. Substrates containing heteroatoms capable of complexing the catalyst exhibit limited room temperature reactivity, but the application of moderately higher temperatures enables extension to a broad range of medicinally relevant nitrogen rich heterocycles. These newly developed conditions allow alcohols possessing functional groups that were previously incompatible with hydrogen borrowing reactions to be employed.
G6PD and ACSL3 are synthetic lethal partners of NF2 in Schwann cells
Authors: Kyrkou Athena , Valla Robert , Zhang Yao , Ambrosi Giulia , Laier Stephanie , Müller-Decker Karin , Boutros Michael , Teleman Aurelio A. 
Published: June 2024

AbstractNeurofibromatosis Type II (NFII) is a genetic condition caused by loss of the NF2 gene, resulting in activation of the YAP/TAZ pathway and recurrent Schwann cell tumors, as well as meningiomas and ependymomas. Unfortunately, few pharmacological options are available for NFII. Here, we undertake a genome-wide CRISPR/Cas9 screen to search for synthetic-lethal genes that, when inhibited, cause death of NF2 mutant Schwann cells but not NF2 wildtype cells. We identify ACSL3 and G6PD as two synthetic-lethal partners for NF2, both involved in lipid biogenesis and cellular redox. We find that NF2 mutant Schwann cells are more oxidized than control cells, in part due to reduced expression of genes involved in NADPH generation such as ME1. Since G6PD and ME1 redundantly generate cytosolic NADPH, lack of either one is compatible with cell viability, but not down-regulation of both. Since genetic deficiency for G6PD is tolerated in the human population, G6PD could be a good pharmacological target for NFII.
A versatile automated pipeline for quantifying virus infectivity by label-free light microscopy and artificial intelligence
Authors: Petkidis Anthony , Andriasyan Vardan , Murer Luca , Volle Romain , Greber Urs F. 
Published: June 2024

AbstractVirus infectivity is traditionally determined by endpoint titration in cell cultures, and requires complex processing steps and human annotation. Here we developed an artificial intelligence (AI)-powered automated framework for ready detection of virus-induced cytopathic effect (DVICE). DVICE uses the convolutional neural network EfficientNet-B0 and transmitted light microscopy images of infected cell cultures, including coronavirus, influenza virus, rhinovirus, herpes simplex virus, vaccinia virus, and adenovirus. DVICE robustly measures virus-induced cytopathic effects (CPE), as shown by class activation mapping. Leave-one-out cross-validation in different cell types demonstrates high accuracy for different viruses, including SARS-CoV-2 in human saliva. Strikingly, DVICE exhibits virus class specificity, as shown with adenovirus, herpesvirus, rhinovirus, vaccinia virus, and SARS-CoV-2. In sum, DVICE provides unbiased infectivity scores of infectious agents causing CPE, and can be adapted to laboratory diagnostics, drug screening, serum neutralization or clinical samples.
Unpredictable benefits of social information can lead to the evolution of individual differences in social learning
Authors: van den Berg Pieter , Vu TuongVan , Molleman Lucas 
Published: June 2024

AbstractHuman ecological success is often attributed to our capacity for social learning, which facilitates the spread of adaptive behaviours through populations. All humans rely on social learning to acquire culture, but there is substantial variation across societies, between individuals and over developmental time. However, it is unclear why these differences exist. Here, we present an evolutionary model showing that individual variation in social learning can emerge if the benefits of social learning are unpredictable. Unpredictability selects for flexible developmental programmes that allow individuals to update their reliance on social learning based on previous experiences. This developmental flexibility, in turn, causes some individuals in a population to end up consistently relying more heavily on social learning than others. We demonstrate this core evolutionary mechanism across three scenarios of increasing complexity, investigating the impact of different sources of uncertainty about the usefulness of social learning. Our results show how evolution can shape how individuals learn to learn from others, with potentially profound effects on cultural diversity.
Intra-islet α-cell Gs signaling promotes glucagon release
Authors: Liu Liu , El Kimberley , Dattaroy Diptadip , Barella Luiz F. , Cui Yinghong , Gray Sarah M. , Guedikian Carla , Chen Min , Weinstein Lee S. , Knuth Emily , Jin Erli , Merrins Matthew J. , Roman Jeffrey , Kaestner Klaus H. , Doliba Nicolai , Campbell Jonathan E. , Wess Jürgen 
Published: June 2024

AbstractGlucagon, a hormone released from pancreatic α-cells, is critical for maintaining euglycemia and plays a key role in the pathophysiology of diabetes. To stimulate the development of new classes of therapeutic agents targeting glucagon release, key α-cell signaling pathways that regulate glucagon secretion need to be identified. Here, we focused on the potential importance of α-cell Gs signaling on modulating α-cell function. Studies with α-cell-specific mouse models showed that activation of α-cell Gs signaling causes a marked increase in glucagon secretion. We also found that intra-islet adenosine plays an unexpected autocrine/paracrine role in promoting glucagon release via activation of α−cell Gs-coupled A2A adenosine receptors. Studies with α-cell-specific Gαs knockout mice showed that α-cell Gs also plays an essential role in stimulating the activity of the Gcg gene, thus ensuring proper islet glucagon content. Our data suggest that α-cell enriched Gs-coupled receptors represent potential targets for modulating α-cell function for therapeutic purposes.
Resilient, environment tolerant and biocompatible electroluminescent devices with enhanced luminance based on compliant and self-adhesive electrodes
Authors: Lu Ya , Chen Yuanyuan , Sun Haoyu , Deng Fang , Mei Changtong , Xu Xinwu , Wu Qinglin , Xiao Huining , Yue Yiying , Han Jingquan 
Published: June 2024

AbstractElectroluminescent (EL) devices are of great significance for expanding the application range of optoelectronics. However, the realization of EL devices with environment-tolerance, stretchability, mechanical cycling stability, self-adhesion, biocompatibility, and high dielectric constant still remains a challenge. Herein, a type of EL device with enhanced comprehensive performances composing of a chlorinated barium titanate/phosphor/polydimethylsiloxane (Cl-BT/phosphor/PDMS) luminescent layer sandwiched between two silver nanowire-cellulose nanocrystal with II crystalline allomorph/Triton X-100 modified polydimethylsiloxane (AgNW-CNC II/TX-PDMS) electrodes fabricated through a full solution-processing strategy is proposed. Environmentally-friendly CNC II with high transmittance acts as an antioxidant, dispersant and film-former for AgNWs. The hydrophilic modification of TX to PDMS imparts the electrodes with self-adhesion, high stretchability, as well as strong interfacial bonding between TX-PDMS and AgNW-CNC II. The electrodes achieve skin-like modulus by adjusting TX content, endowing the EL devices with a high compliance (186 kPa of Young’s modulus). The luminescent layer with Cl-BT exhibits a high dielectric constant (19) and luminance (up to 72 cd m−2). The assembled EL device with excellent cyclic stability (luminance retention 85% after 400 cycles), durability (luminance retention >94% after 400 min) and stretchability (88% luminance at 200% strain) can work properly at broad temperatures (−20 ~ 70 °C) and underwater. This biocompatible and self-adhesive EL device demonstrates great potential for implantable biomedical devices and wearable displays under harsh environments.
Excitation/inhibition imbalance in schizophrenia: a meta-analysis of inhibitory and excitatory TMS-EMG paradigms
Authors: Lányi Orsolya , Koleszár Boróka , Schulze Wenning Alexander , Balogh David , Engh Marie Anne , Horváth András Attila , Fehérvari Péter , Hegyi Péter , Molnár Zsolt , Unoka Zsolt , Csukly Gábor 
Published: June 2024

AbstractCortical excitation-inhibition (E/I) imbalance is a potential model for the pathophysiology of schizophrenia. Previous research using transcranial magnetic stimulation (TMS) and electromyography (EMG) has suggested inhibitory deficits in schizophrenia. In this meta-analysis we assessed the reliability and clinical potential of TMS-EMG paradigms in schizophrenia following the methodological recommendations of the PRISMA guideline and the Cochrane Handbook. The search was conducted in three databases in November 2022. Included articles reported Short-Interval Intracortical Inhibition (SICI), Intracortical Facilitation (ICF), Long-Interval Intracortical Inhibition (LICI) and Cortical Silent Period (CSP) in patients with schizophrenia and healthy controls. Meta-analyses were conducted using a random-effects model. Subgroup analysis and meta-regressions were used to assess heterogeneity. Results of 36 studies revealed a robust inhibitory deficit in schizophrenia with a significant decrease in SICI (Cohen’s d: 0.62). A trend-level association was found between SICI and antipsychotic medication. Our findings support the E/I imbalance hypothesis in schizophrenia and suggest that SICI may be a potential pathophysiological characteristic of the disorder.
Decoding the hallmarks of allograft dysfunction with a comprehensive pan-organ transcriptomic atlas
Authors: Robertson Harry , Kim Hani Jieun , Li Jennifer , Robertson Nicholas , Robertson Paul , Jimenez-Vera Elvira , Ameen Farhan , Tran Andy , Trinh Katie , O’Connell Philip J. , Yang Jean Y. H. , Rogers Natasha M. , Patrick Ellis 
Published: June 2024

AbstractThe pathogenesis of allograft (dys)function has been increasingly studied using ‘omics’-based technologies, but the focus on individual organs has created knowledge gaps that neither unify nor distinguish pathological mechanisms across allografts. Here we present a comprehensive study of human pan-organ allograft dysfunction, analyzing 150 datasets with more than 12,000 samples across four commonly transplanted solid organs (heart, lung, liver and kidney, n = 1,160, 1,241, 1,216 and 8,853 samples, respectively) that we leveraged to explore transcriptomic differences among allograft dysfunction (delayed graft function, acute rejection and fibrosis), tolerance and stable graft function. We identified genes that correlated robustly with allograft dysfunction across heart, lung, liver and kidney transplantation. Furthermore, we developed a transfer learning omics prediction framework that, by borrowing information across organs, demonstrated superior classifications compared to models trained on single organs. These findings were validated using a single-center prospective kidney transplant cohort study (a collective 329 samples across two timepoints), providing insights supporting the potential clinical utility of our approach. Our study establishes the capacity for machine learning models to learn across organs and presents a transcriptomic transplant resource that can be employed to develop pan-organ biomarkers of allograft dysfunction.