bluuebunny/crossref_metadata_2025_split huggingface dataset:
Adaptability of prognostic prediction models for patients with acute coronary syndrome during the COVID-19 pandemic
Authors: Nishi Masahiro , Nakamura Takeshi , Yanishi Kenji , Matoba Satoaki 
Published: July 2024

BackgroundThe detrimental repercussions of the COVID-19 pandemic on the quality of care and clinical outcomes for patients with acute coronary syndrome (ACS) necessitate a rigorous re-evaluation of prognostic prediction models in the context of the pandemic environment. This study aimed to elucidate the adaptability of prediction models for 30-day mortality in patients with ACS during the pandemic periods.MethodsA total of 2041 consecutive patients with ACS were included from 32 institutions between December 2020 and April 2023. The dataset comprised patients who were admitted for ACS and underwent coronary angiography for the diagnosis during hospitalisation. The prediction accuracy of the Global Registry of Acute Coronary Events (GRACE) and a machine learning model, KOTOMI, was evaluated for 30-day mortality in patients with ST-elevation acute myocardial infarction (STEMI) and non-ST-elevation acute coronary syndrome (NSTE-ACS).ResultsThe area under the receiver operating characteristics curve (AUROC) was 0.85 (95% CI 0.81 to 0.89) in the GRACE and 0.87 (95% CI 0.82 to 0.91) in the KOTOMI for STEMI. The difference of 0.020 (95% CI −0.098–0.13) was not significant. For NSTE-ACS, the respective AUROCs were 0.82 (95% CI 0.73 to 0.91) in the GRACE and 0.83 (95% CI 0.74 to 0.91) in the KOTOMI, also demonstrating insignificant difference of 0.010 (95% CI −0.023 to 0.25). The prediction accuracy of both models had consistency in patients with STEMI and insignificant variation in patients with NSTE-ACS between the pandemic periods.ConclusionsThe prediction models maintained high accuracy for 30-day mortality of patients with ACS even in the pandemic periods, despite marginal variation observed.
Tethered IL15-IL15Rα augments antitumor activity of CD19 CAR-T cells but displays long-term toxicity in an immunocompetent lymphoma mouse model
Authors: Sánchez-Moreno Inés , Lasarte-Cia Aritz , Martín-Otal Celia , Casares Noelia , Navarro Flor , Gorraiz Marta , Sarrión Patricia , Hervas-Stubbs Sandra , Jordana Lorea , Rodriguez-Madoz Juan Roberto , San Miguel Jesús , Prosper Felipe , Lasarte Juan Jose , Lozano Teresa 
Published: July 2024

BackgroundAdoptive cell therapy using genetically modified T cells to express chimeric antigen receptors (CAR-T) has shown encouraging results, particularly in certain blood cancers. Nevertheless, over 40% of B cell malignancy patients experience a relapse after CAR-T therapy, likely due to inadequate persistence of the modified T cells in the body. IL15, known for its pro-survival and proliferative properties, has been suggested for incorporation into the fourth generation of CAR-T cells to enhance their persistence. However, the potential systemic toxicity associated with this cytokine warrants further evaluation.MethodsWe analyzed the persistence, antitumor efficacy and potential toxicity of anti-mouse CD19 CAR-T cells which express a membrane-bound IL15-IL15Rα chimeric protein (CD19/mbIL15q CAR-T), in BALB/c mice challenged with A20 tumor cells as well as in NSG mice.ResultsConventional CD19 CAR-T cells showed low persistence and poor efficacy in BALB/c mice treated with mild lymphodepletion regimens (total body irradiation (TBI) of 1 Gy). CD19/mbIL15q CAR-T exhibits prolonged persistence and enhanced in vivo efficacy, effectively eliminating established A20 B cell lymphoma. However, this CD19/mbIL15q CAR-T displays important long-term toxicities, with marked splenomegaly, weight loss, transaminase elevations, and significant inflammatory findings in some tissues. Mice survival is highly compromised after CD19/mbIL15q CAR-T cell transfer, particularly if a high TBI regimen is applied before CAR-T cell transfer.ConclusionTethered IL15-IL15Rα augments the antitumor activity of CD19 CAR-T cells but displays long-term toxicity in immunocompetent mice. Inducible systems to regulate IL15-IL15Rα expression could be considered to control this toxicity.
Impact of patient selection in clinical trials: application of ROCKET AF and ARISTOTLE criteria in GARFIELD-AF
Authors: Himmelreich Jelle C L , Virdone Saverio , Camm John , Pieper Karen , Harskamp Ralf E , Oto Ali , Jacobson Barry F , Sawhney J P S , Lim Toon Wei , Gibbs Harry , Goto Shinya , Haas Sylvia , Fox Keith A A , Jansky Petr , Verheugt Freek , Kakkar Ajay K 
Published: July 2024

BackgroundThe extent to which differences in results from Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation (ARISTOTLE) and Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial (ROCKET) atrial fibrillation (AF)—the landmark trials for the approval of apixaban and rivaroxaban, respectively, for non-valvular AF—were influenced by differences in their protocols is debated. The potential influence of selection criteria on trial results was assessed by emulating these trials in data from the Global Anticoagulant Registry in the Field (GARFIELD)-AF registry.MethodsVitamin K antagonist (VKA) and non-vitamin K oral antagonist (NOAC) users from GARFIELD-AF were selected according to eligibility for the original ARISTOTLE or ROCKET AF trials. A propensity score overlap weighted Cox model was used to emulate trial randomisation between treatment groups. Adjusted HRs for stroke or systemic embolism (SE) within 2 years of enrolment were calculated for each NOAC versus VKA.ResultsAmong patients on apixaban, rivaroxaban and VKA, 2570, 3560 and 8005 were eligible for ARISTOTLE, respectively, and 1612, 2005 and 4368, respectively, for ROCKET AF. When selecting for ARISTOTLE criteria, apixaban users had significantly lower stroke/SE risk versus VKA (HR 0.57; 95% CI 0.34 to 0.94) while no reduction was observed with rivaroxaban (HR 0.98; 95% CI 0.68 to 1.40). When selecting for ROCKET AF criteria, safety and efficacy versus VKA were similar across the NOACs.ConclusionApixaban and rivaroxaban showed similar results versus VKA in high-risk patients selected according to ROCKET AF criteria, whereas differences emerged when selecting for the more inclusive ARISTOTLE criteria. Our results highlight the importance of trial selection criteria in interpreting trial results and underline the problems faced in comparing treatments across rather than within clinical trials.
Effects of shape/phase transition regions on neutron capture cross sections
Authors: Couture A. , Cakirli R. B. , Casten R. F. 
Published: July 2024

AbstractA recent study found a new, purely empirical correlation between two-neutron separation energies and neutron capture cross sections in keV neutron energy regimes. In shape/phase transition regimes, such as that near A= 150, S$$_{2n}$$

2
n

values show an anomaly—a flattening of the normal near linear decrease with neutron number. This paper addresses two questions: (1) Using this new correlation, is this anomaly in S$$_{2n}$$

2
n

values sizeable enough to produce an observable effect in capture cross sections? and (2) Can the correlation be used to quantitatively reproduce the cross sections in the transition region? It is found that the answer to both questions is in the affirmative. Possible relations to the r-process are briefly discussed.
Framed DDF operators and the general solution to Virasoro constraints
Authors: Biswas Dripto , Pesando Igor 
Published: July 2024

AbstractWe define the framed DDF operators by introducing the concept of local frames in the usual formulation of DDF operators. In doing so it is possible to completely decouple the DDF operators from the associated tachyon and show that they are good zero-dimensional conformal operators. These framed DDFs allow for an explicit covariant formulation of the general solution of the Virasoro constraints both on-shell and off-shell which depends on a unique set of tangent space lightcone polarizations. This is possible since the frame allows us to embed the $$SO(D-2)$$

S
O
(
D
-
2
)

lightcone physical polarizations into the $$SO(1,D-1)$$

S
O
(
1
,
D
-
1
)

covariant ones in the most general way. The solution to the Virasoro constraints is not in the gauge that is usually used since the states obtained from DDF operators are generically the sum of terms which are partially transverse due to the presence of a projector but not traceless and terms which are partially traceless but not transverse. We then show that different embeddings are connected by states generated by improved Brower operators both on shell and off shell. Brower states are null on-shell and equivalent to BRST exact states. Therefore on shell one embedding is sufficient to compute all amplitudes except the ones with vanishing momentum. Off-shell a change of frame cannot be obtained by null states but only by Brower states. Improved Brower operators generate a gauge invariance associated with local frame rotations, which replaces the usual gauge invariance generated by Virasoro operators or BRST. To check the identification, we verify the matching of the expectation value of the second Casimir of the Poincaré group for some lightcone states with the corresponding covariant states built using the framed DDFs.
Nonlocal QED and lepton g-2 anomalies
Authors: Li Hang , Wang P. 
Published: July 2024

AbstractQuantum electrodynamics is generally extended to a nonlocal QED by introducing the correlation functions. The gauge link is introduced to guarantee that the nonlocal QED is locally U(1) gauge invariant. The corresponding Feynman rules as well as the proof of Ward–Takahashi identity are presented. As an example, the anomalous magnetic moments of leptons are studied in nonlocal QED. At one-loop level, besides the ordinary diagrams, there are many additional Feynman diagrams which are generated from the gauge link. It shows the nonlocal QED can provide a reasonable explanation for lepton $$g-2$$

g
-
2

anomalies.
Time-periodic electrokinetic analysis of a micropolar fluid flow through hydrophobic microannulus
Authors: Faltas M. S. , El-Sapa Shreen 
Published: July 2024

Abstract
The oscillating aspects of pressure-driven micropolar fluid flow through a hydrophobic cylindrical microannulus under the influence of electroosmotic flow are analytically studied. The study is based on a linearized Poisson–Boltzmann equation and the micropolar model of Eringen for microstructure fluids. An analytical solution is obtained for the distributions of electroosmotic flow velocity and microrotation as functions of radial distance, periodic time, and relevant parameters. The findings of the present study demonstrate that, unlike the decrease in flow rate resulting from the micropolarity of fluid particles, velocity slip and spin velocity slip, when contrasted with Newtonian fluids, act as a counteractive mechanism that tends to enhance the flow rate. Additionally, the findings indicate that a square plug-like profile in electroosmotic velocity amplitude is observed when the electric oscillating parameter is low and the electrokinetic width is large, for both Newtonian and micropolar fluids. Moreover, in cases where there is a wide gap between the cylindrical walls and a high-frequency parameter, the electroosmotic velocity and microrotation amplitudes tend to approach zero at the center of the microannulus across all ranges of micropolarity and zeta potential parameters. Furthermore, it has been observed that the amplitude of microrotation strength rises as slip and spin slip parameters increase. Across the entire spectrum of micropolarity, the zeta potential ratio influences both the dimension and direction of the electroosmotic velocity profiles within the electric double layer near the two cylindrical walls of the microannulus. The study emphasizes the physical quantities by presenting graphs for various values of the pertinent parameters juxtaposing them with existing data in the literature and comparing them with the Newtonian fluids.

Graphic abstract
Toward biodefence: a framework for the mitigation of malicious threats to livestock production enterprises in Australia
Authors: Evans Deborah , Coole Michael , Brooks David J. 
Published: July 2024

AbstractBiosecurity underpins the Australian agricultural sector, estimated to be worth $51 billion in exports and trade, $50 billion in tourism, $5.7 trillion in environmental assets, and more than 1.6 million jobs. Given the value to the Australian economy and the potential consequences of a deliberately introduced biological agent, measures to prevent malicious biosecurity threats are critical for national security. Using the framework of Situational Crime Prevention (SCP), the study examined recommended biosecurity practices for cattle production enterprises in Australia and explored the extent to which the Australian biosecurity framework is underpinned by preventative security. The study found the existing biosecurity framework has limited theoretical security underpinning and is constituted by practices primarily aimed at preventing naturally occurring and accidental threats, rather than an active preventative security approach at the farming level to mitigate threats of a malicious or deliberate nature. These findings identify a deficit in Australia’s national security approach to biosecurity in cattle production enterprises, establishing a need for biosecurity recommendations at an industry and primary production level to embed security theory and principles to account for malicious actors in alignment with international biodefence strategy. Subsequently, the study demonstrated how security theory can be applied to biosecurity and the agricultural sector more broadly and developed an SCP framework toward biodefence of agriculture, converging biosecurity and security as a bilateral approach to mitigating naturally occurring, accidental, and deliberate biosecurity threats.
Do Not Forget the Granulocytic Compartment’s Role in T cell–Mediated Antitumor Immunity
Authors: Gaipl Udo S. 
Published: July 2024

Antitumor immune responses are predominantly mediated by CD8+ cytotoxic T cells (CTLs). But immune-modulatory factors in the tumor microenvironment determine the effectiveness of these responses. In this issue, Wei and colleagues report a new role for CTL-derived IL3 in stimulating basophilic granulocytes to produce IL4, which, in turn, activates, reprograms, and stabilizes CTLs. These findings stress the importance of the crosstalk between the innate and adaptive immune systems to elicit efficient antitumor immunity.See related article by Wei et al., p. 822 (3).
Skin thickness effects on failure mechanisms in foam infilled composite sandwich structures
Authors: Malekinejad Hossein , Farrokhabadi Amin , Rahimi Gholam Hossein , Carbas Ricardo , Marques Eduardo AS , da Silva Lucas 
Published: July 2024

Sandwich structures are often prone to catastrophic failure due to premature separation between the core and skin layers. Geometric parameters, such as the thickness of the skin and core, along with the materials used in their manufacturing, directly influence the resistance to separation between the skin and core. This study explores how variations in skin thickness affect both failure modes and maximum load capacity in sandwich structures, utilizing both experimental testing and numerical simulations. Specimens were categorized as intact and pre-debonded samples. Each specimen featured four different skin thicknesses (3, 6, 8, and 10 layers of composite laminated skins, with corresponding thicknesses of 0.68, 1.33, 1.73, and 2.1 mm respectively). The specimens incorporated a foam-filled square corrugated core and underwent 3-point bending tests. Results revealed a significant shift in the failure mode: initially observed as upper skin fracture (V-shaped failure), it transitioned to separation between skins and cores with increased skin thickness, particularly in the presence of pre-debonding. Notably, the predominant failure mode did not involve separation between the skin and core in specimens without a pre-existing crack. Furthermore, numerical simulations effectively demonstrated the accurate capture of failure modes and loads using the Hashin and cohesive zone model (CZM).
Developing a lightweight corrugated sandwich panel based on tea oil camellia shell: correlation of experimental and numerical performance
Authors: Choupani Chaydarreh Kamran , Tan Jingyi , Zhou Yonghui , Li Yongtao , Hu Chuanshuang 
Published: July 2024

AbstractThis study presents an experimental and numerical comparison between the mechanical performance of a lightweight corrugated sandwich panel based on the tea oil camellia shell (TOCS). Hence, TOCS was mixed in two groups with Poplar particles and fibers. After that, in the experimental part, the conventional mechanical tests, including the 3-point bending test, flatwise compression, dowel bearing, and screw resistance, and in the numerical part, finite element analysis (FEA), including the normal, maximum principal, and equivalent (von Mises) stress by Ansys Mechanical software carried out. The specimens for experimental and numerical tests were prepared in transverse and longitudinal directions. Before that, the engineering data (shear modulus, Young's modulus, and Poisson's ratio) for improving the FEA simulation were obtained from TOCS-based flat panels fabricated with a mixture of Poplar particles and fibers. The results of FEA are used to compare the mechanical behavior and failure mechanism with the results of experimental tests. According to the mean values of bending stiffness and maximum bending moment, sandwich panels made with 100% particles demonstrated an advantage in both directions. Nevertheless, the compression strength and screw resistance showed the same trend, but the dowel bearing showed higher values for panels made with fibers. The observed results of equivalent (von Mises) stress indicated a coloration with the results of failure mechanisms.
Impairment of α-tubulin and F-actin interactions of GJB3 induces aneuploidy in urothelial cells and promotes bladder cancer cell invasion
Authors: Liu Junnan , Wang Xue , Jiang Wencheng , Azoitei Anca , Eiseler Tim , Eckstein Markus , Hartmann Arndt , Stilgenbauer Stephan , Elati Mohamed , Hohwieler Meike , Kleger Alexander , John Axel , Wezel Felix , Zengerling Friedemann , Bolenz Christian , Günes Cagatay 
Published: July 2024

Abstract
Background
We have previously identified an unsuspected role for GJB3 showing that the deficiency of this connexin protein induces aneuploidy in human and murine cells and accelerates cell transformation as well as tumor formation in xenograft models. The molecular mechanisms by which loss of GJB3 leads to aneuploidy and cancer initiation and progression remain unsolved.

Methods
GJB3 expression levels were determined by RT-qPCR and Western blot. The consequences of GJB3 knockdown on genome instability were assessed by metaphase chromosome counting, multinucleation of cells, by micronuclei formation and by the determination of spindle orientation. Interactions of GJB3 with α-tubulin and F-actin was analyzed by immunoprecipitation and immunocytochemistry. Consequences of GJB3 deficiency on microtubule and actin dynamics were measured by live cell imaging and fluorescence recovery after photobleaching experiments, respectively. Immunohistochemistry was used to determine GJB3 levels on human and murine bladder cancer tissue sections. Bladder cancer in mice was chemically induced by BBN-treatment.

Results
We find that GJB3 is highly expressed in the ureter and bladder epithelium, but it is downregulated in invasive bladder cancer cell lines and during tumor progression in both human and mouse bladder cancer. Downregulation of GJB3 expression leads to aneuploidy and genomic instability in karyotypically stable urothelial cells and experimental modulation of GJB3 levels alters the migration and invasive capacity of bladder cancer cell lines. Importantly, GJB3 interacts both with α-tubulin and F-actin. The impairment of these interactions alters the dynamics of these cytoskeletal components and leads to defective spindle orientation.

Conclusion
We conclude that deregulated microtubule and actin dynamics have an impact on proper chromosome separation and tumor cell invasion and migration. Consequently, these observations indicate a possible role for GJB3 in the onset and spreading of bladder cancer and demonstrate a molecular link between enhanced aneuploidy and invasive capacity cancer cells during tumor cell dissemination.

Graphical Abstract
RUNX1, FUS, and ELAVL1-induced circPTPN22 promote gastric cancer cell proliferation, migration, and invasion through miR-6788-5p/PAK1 axis-mediated autophagy
Authors: Ma Shuo , Xu Yanhua , Qin Xinyue , Tao Mei , Gu Xinliang , Shen Lei , Chen Yinhao , Zheng Ming , Qin Shiyi , Wu Guoqiu , Ju Shaoqing 
Published: July 2024

Abstract
Background
An increasing number of studies have demonstrated the association of circular RNAs (circRNAs) with the pathological processes of various diseases and their involvement in the onset and progression of multiple cancers. Nevertheless, the functional roles and underlying mechanisms of circRNAs in the autophagy regulation of gastric cancer (GC) have not been fully elucidated.

Methods
We used transmission electron microscopy and the mRFP-GFP-LC3 dual fluorescent autophagy indicator to investigate autophagy regulation. The cell counting kit-8 assay, colony formation assay, 5-ethynyl-2′-deoxyuridine incorporation assay, Transwell assay, and Western blot assay were conducted to confirm circPTPN22’s influence on GC progression. Dual luciferase reporter assays validated the binding between circPTPN22 and miR-6788-5p, as well as miR-6788-5p and p21-activated kinase-1 (PAK1). Functional rescue experiments assessed whether circPTPN22 modulates PAK1 expression by competitively binding miR-6788-5p, affecting autophagy and other biological processes in GC cells. We investigated the impact of circPTPN22 on in vivo GC tumors using a nude mouse xenograft model. Bioinformatics tools predicted upstream regulatory transcription factors and binding proteins of circPTPN22, while chromatin immunoprecipitation and ribonucleoprotein immunoprecipitation assays confirmed the binding status.

Results
Upregulation of circPTPN22 in GC has been shown to inhibit autophagy and promote cell proliferation, migration, and invasion. Mechanistically, circPTPN22 directly binds to miR-6788-5p, subsequently regulating the expression of PAK1, which activates protein kinase B (Akt) and extracellular signal-regulated kinase (Erk) phosphorylation. This modulation ultimately affects autophagy levels in GC cells. Additionally, runt-related transcription factor 1 (RUNX1) negatively regulates circPTPN22 expression, while RNA-binding proteins such as FUS (fused in sarcoma) and ELAVL1 (recombinant ELAV-like protein 1) positively regulate its expression. Inhibition of the autophagy pathway can increase FUS expression, further upregulating circPTPN22 in GC cells, thereby exacerbating the progression of GC.

Conclusion
Under the regulation of the transcription factor RUNX1 and RNA-binding proteins FUS and ELAVL1, circPTPN22 activates the phosphorylation of Akt and Erk through the miR-6788-5p/PAK1 axis, thereby modulating autophagy in GC cells. Inhibition of autophagy increases FUS, which in turn upregulates circPTPN22, forming a positive feedback loop that ultimately accelerates the progression of GC.