bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of Stress‐Driven Melt Segregation on Melt Orientation, Melt Connectivity and Anisotropic Permeability
Authors: Bader James , Zhu Wenlu , Montési Laurent , Qi Chao , Cordonnier Benoit , Kohlstedt David , Warren Jessica 
Published: March 2024

AbstractStress‐driven melt segregation may have important geochemical and geophysical effects but remains a poorly understood process. Few constraints exist on the permeability and distribution of melt in deformed partially molten rocks. Here, we characterize the 3D melt network and resulting permeability of an experimentally deformed partially molten rock containing several melt‐rich bands based on an X‐ray microtomography data set. Melt fractions range from 0.08 to 0.28 in the ∼20‐μm‐thick melt‐rich bands, and from 0.02 to 0.07 in the intervening ∼30‐μm‐thick regions. We simulated melt flow through subvolumes extracted from the reconstructed rock at five length scales ranging from the grain scale (3 μm) to the minimum length required to fully encompass two melt‐rich bands (64 μm). At grain scale, few subvolumes contain interconnected melt, and permeability is isotropic. As the length scale increases, more subvolumes contain melt that is interconnected parallel to the melt bands, but connectivity diminishes in the direction perpendicular to them. Even if melt is connected in all directions, permeability is lower perpendicular to the bands, in agreement with the elongation of melt pockets. Permeability parallel to the bands is proportional to melt fraction to the power of an exponent that increases from ∼2 to 5 with increasing length scale. The permeability in directions parallel to the bands is comparable to that for an isotropic partially molten rock. However, no flow is possible perpendicular to the bands over distances similar to the band spacing. Melt connectivity limits sample scale melt flow to the plane of the melt‐rich bands.
Comment on “Comparison of the Efficiencies of the Prognostic Generalized Complementary Functions on Evaporation Estimation” by Wang, L., et al., Published in Journal of Geophysical Research: Atmospheres
Authors: Szilagyi Jozsef 
Published: March 2024

AbstractSurprising significant underperformance of the polynomial complementary relationship (PCR) of evaporation (Szilagyi et al., 2017, https://doi.org/10.1002/2016jd025611) by Wang et al. (2023, https://doi.org/10.1029/2023jd038683) is caused by the (a) station‐by‐station application of a grid‐based estimation procedure of the Priestley‐Taylor parameter (α) value, and (b) choice of the wind function. Application of the Rome wind function in the Penman equation together with either a well‐chosen single (constant) α or α as a function of the wet‐environment air temperature, should result in much improved evaporation estimates by the PCR in line with previous studies.
Topological Dirac-vortex microcavity laser for robust on-chip optoelectronics
Authors: Wu Yuanpeng , Mi Zetian 
Published: March 2024

AbstractDirac-vortex microcavity laser based on InAs/InGaAs quantum dots have been experimentally realized on silicon substrate. The topological laser features a large spectral range and high robustness against variations such as cavity size.
Less common phenotypes of myelin oligodendrocyte glycoprotein antibody-related diseases in children deserve more attention
Authors: Wang Xiao-yu , Jiang Yan , Wu Peng , Ma Jian-nan , Yuan Ping , Li Xiu-juan , Jiang Li 
Published: March 2024

Abstract
Background
To facilitate the identification of less common clinical phenotypes of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) in children.

Methods
We retrospectively reviewed medical records of 236 patients with MOGAD. The following phenotypes were considered to be typical for MOGAD: ADEM, ON, TM, and NMOSD. Less common onset clinical phenotypes were screened out; their clinical and magnetic resonance imaging (MRI), diagnosis, treatment, and prognosis were summarized and analyzed.

Results
16 cases (6.8%) presented as cortical encephalitis, with convulsions, headache, and fever as the main symptoms. 15 cases were misdiagnosed in the early period. 13 cases (5.5%) showed the overlapping syndrome of MOGAD and anti-N-methyl-D aspartate receptor encephalitis (MNOS), with seizures (92.3%) being the most common clinical symptom. 11 cases (84.6%) showed relapses. The cerebral leukodystrophy-like phenotype was present in seven cases (3.0%), with a recurrence rate of 50%. Isolated seizures without any findings on MRI phenotype was present in three cases (1.3%), with the only clinical symptom being seizures of focal origin. Three cases (1.3%) of aseptic meningitis phenotype presented with prolonged fever.

Conclusion
40/236 (16.9%) of children with MOGAD had less common phenotypes. Less common clinical phenotypes of pediatric MOGAD are susceptible to misdiagnosis and deserve more attention.

Impact

This is the first comprehensive analysis and summary of all less commonl clinical phenotypes of MOGAD in children, while previous studies have only focused on a specific phenotype or case reports.

We analyzed the characteristics of MOGAD in children and further revealed the reasons why these less common clinical phenotypes are prone to misdiagnosis and deserve more attention.

Our research on treatment has shown that early detection of MOG antibodies and early treatment are of great significance for improving the prognosis of these patients.
Effects of hemodynamic alterations and oxygen saturation on cerebral perfusion in congenital heart disease
Authors: De Silvestro Alexandra , Natalucci Giancarlo , Feldmann Maria , Hagmann Cornelia , Nguyen Thi Dao , Coraj Seline , Jakab Andras , Kottke Raimund , Latal Beatrice , Knirsch Walter , Tuura Ruth 
Published: March 2024

Abstract
Background
Patients with severe congenital heart disease (CHD) are at risk for neurodevelopmental impairment. An abnormal cerebral blood supply caused by the altered cardiac physiology may limit optimal brain development. The aim of this study was to evaluate the effect of a systemic-to-pulmonary shunt, aortic arch obstruction and arterial oxygen saturation on cerebral perfusion in patients with severe CHD.

Methods
Patients with severe CHD requiring cardiac surgery within the first six weeks of life, who underwent pre- and/or postoperative brain magnetic resonance imaging (MRI), and healthy controls with one postnatal scan were included. Cerebral perfusion in deep and cortical gray matter was assessed by pseudocontinuous arterial spin labeling MRI.

Results
We included 59 CHD and 23 healthy control scans. The presence of a systemic-to-pulmonary shunt was associated with decreased perfusion in cortical (p = 0.003), but not in deep gray matter (p = 0.031). No evidence for an effect of aortic arch obstruction and arterial oxygen saturation on cerebral perfusion was found. After adjusting for hemodynamic and oxygen saturation parameters, deep (p = 0.018) and cortical (p = 0.012) gray matter perfusion was increased in patients with CHD compared to controls.

Conclusion
We detected regional differences in compensation to the cerebral steal effect in patients with severe CHD.

Impact

Patients with severe congenital heart disease (CHD) have altered postnatal brain hemodynamics.

A systemic-to-pulmonary shunt was associated with decreased perfusion in cortical gray matter but preserved perfusion in deep gray matter, pointing towards regional differences in compensation to the cerebral steal effect.

No effects of aortic arch obstruction and arterial oxygenation on cerebral perfusion were seen.

Cerebral perfusion was increased in patients with CHD compared to healthy controls after adjusting for hemodynamic alterations and oxygen saturation.

To improve neuroprotection and neurodevelopmental outcomes, it is important to increase our understanding of the factors influencing cerebral perfusion in neonates with severe CHD.
Management of neurogenic bladder in patients with spinal cord injuries/disorders and end stage renal disease: a case series
Authors: Chaggar Rajbir , Goetz Lance L. , Adler Jordan , Bhuiyan Mohammed B. A. , McAvoy Sean , Tubbs Jeffrey 
Published: March 2024

Abstract
Introduction
Patients with spinal cord injuries/disorders (SCI/D) often suffer from bladder dysfunction, commonly referred to as neurogenic bladder or neurogenic lower urinary tract dysfunction (NLUTD). Standard urologic evaluation and management help to minimize complications such as vesicoureteral reflux, urinary tract infection, and nephrolithiasis. However, we have further encountered patients with more complex issues, such as chronic kidney disease (CKD), end-stage renal disease (ESRD), bilateral nephrectomies, and urinary diversion/augmentation surgeries. Of particular interest, there is a lack of standardized guidance for bladder management in SCI/D patients with ESRD. These patients are at high risk for urological complications and would benefit from codified bladder management strategies.

Case presentation
In this article, we present eleven unique cases of NLUTD with associated ESRD and discuss recommendations utilizing simple and commonly available clinical interventions.

Discussion
The inherently small population size of SCI/D patients with NLUTD and ESRD makes detailing a large sample size case series difficult. Future studies must aim to include a larger sample size as able, however, to better determine standardized protocols for chronic bladder management in SCI/D patients with NLUTD and ESRD. Experiences from this small case series are offered for consideration.
Hot metacognition: poorer metacognitive efficiency following acute but not traumatic stress
Authors: Smith Alicia J. , Bisby James A. , Dercon Quentin , Bevan Anna , Kigar Stacey L. , Lynall Mary-Ellen , Dalgleish Tim , Hitchcock Caitlin , Nord Camilla L. 
Published: March 2024

AbstractAberrations to metacognition—the ability to reflect on and evaluate self-performance—are a feature of poor mental health. Theoretical models of post-traumatic stress disorder propose that following severe stress or trauma, maladaptive metacognitive evaluations and appraisals of the event drive the development of symptoms. Empirical research is required in order to reveal whether disruptions to metacognition cause or contribute to symptom development in line with theoretical accounts, or are simply a consequence of ongoing psychopathology. In two experiments, using hierarchical Bayesian modelling of metacognition measured in a memory recognition task, we assessed whether distortions to metacognition occur at a state-level after an acute stress induction, and/or at a trait-level in a sample of individuals experiencing intrusive memories following traumatic stress. Results from experiment 1, an in-person laboratory-based experiment, demonstrated that heightened psychological responses to the stress induction were associated with poorer metacognitive efficiency, despite there being no overall change in metacognitive efficiency from pre- to post-stress (N = 27). Conversely, in experiment 2, an online experiment using the same metamemory task, we did not find evidence of metacognitive alterations in a transdiagnostic sample of patients with intrusive memory symptomatology following traumatic stress (N = 36, compared to 44 matched controls). Our results indicate a relationship between state-level psychological responses to stress and metacognitive alterations. The lack of evidence for pre- to post-stress differences in metamemory illustrates the importance for future studies to reveal the direction of this relationship, and consequently the duration of stress-associated metacognitive impairments and their impact on mental health.
Metabolic remodeling by the PD-L1 inhibitor BMS-202 significantly inhibits cell malignancy in human glioblastoma
Authors: Yang Xueou , Wang Wenjun , Ji Tianhai 
Published: March 2024

AbstractRecently, crystallographic studies have demonstrated that BMS-202, a small-molecule compound characterized by a methoxy-1-pyridine chemical structure, exhibits a high affinity to PD-L1 dimerization. However, its roles and mechanisms in glioblastoma (GBM) remain unclear. The objective of this study is to investigate the antitumor activity of BMS-202 and its underlying mechanisms in GBM using multi-omics and bioinformatics techniques, along with a majority of in vitro and in vivo experiments, including CCK-8 assays, flow cytometry, co-immunoprecipitation, siRNA transfection, PCR, western blotting, cell migration/invasion assays and xenografts therapeutic assays. Our findings indicate that BMS-202 apparently inhibits the proliferation of GBM cells both in vitro and in vivo. Besides, it functionally blocks cell migration and invasion in vitro. Mechanistically, it reduces the expression of PD-L1 on the surface of GBM cells and interrupts the PD-L1-AKT-BCAT1 axis independent of mTOR signaling. Taken together, we conclude that BMS-202 is a promising therapeutic candidate for patients with GBM by remodeling their cell metabolism regimen, thus leading to better survival.
Cancer associated fibroblasts-derived SULF1 promotes gastric cancer metastasis and CDDP resistance through the TGFBR3-mediated TGF-β signaling pathway
Authors: Fang Xingchao , Chen Damin , Yang Xinyu , Cao Xiaogang , Cheng Quan , Liu Kanghui , Xu Peng , Wang Yanjuan , Xu Jiafeng , Zhao Siguo , Yan Zhengyuan 
Published: March 2024

AbstractSULF1 has been implicated in a number of malignancies. The function of SULF1 in gastric cancer is disputed. The objective of this study was to examine the role and underlying molecular mechanisms of SULF1 in the context of gastric cancer. We found that the expression of SULF1 was increased in gastric cancer, especially in cancer-associated fibroblasts. The overexpression of SULF1 was found to be significantly correlated with unfavorable prognosis among individuals diagnosed with gastric cancer. Functionally, cancer-associated fibroblasts-derived SULF1 served as a oncogenic molecule which facilitated gastric cancer cells metastasis and CDDP resistance. Mechanistically, SULF1 regulated the communication between gastric cancer cells and cancer-associated fibroblasts in tumor microenvironment as a signaling molecule. Cancer-associated fibroblasts-secreted SULF1 interfered with the interaction between TGF-β1 and TGFBR3 by combining with TGFBR3 on gastric cancer cell membrane, subsequently activated TGF-β signaling pathway. In conclusion, our findings have presented novel approaches for potential treatment and prognosis prediction in individuals diagnosed with gastric cancer through the targeting of the CAFs-SULF1-TGFBR3-TGF-β1 signaling axis.
Targeting cell death pathways in intestinal ischemia-reperfusion injury: a comprehensive review
Authors: Wang Fei , Huang Huiming , Wei Xuejiao , Tan Peng , Wang Zhuguo , Hu Zhongdong 
Published: March 2024

AbstractIntestinal ischemia-reperfusion (I/R) is a multifaceted pathological process, and there is a lack of clear treatment for intestinal I/R injury. During intestinal I/R, oxidative stress and inflammation triggered by cells can trigger a variety of cell death mechanisms, including apoptosis, autophagy, pyroptosis, ferroptosis, and necrosis. These cell death processes can send a danger signal for the body to be damaged and prevent intestinal I/R injury. Therefore, identifying key regulatory molecules or markers of these cell death mechanisms when intestinal I/R injury occurs may provide valuable information for the treatment of intestinal I/R injury. This paper reviews the regulatory molecules and potential markers that may be involved in regulating cell death during intestinal I/R and elaborates on the cell death mechanism of intestinal I/R injury at the molecular level to provide a theoretical basis for discovering new molecules or markers regulating cell death during intestinal I/R injury and provides ideas for drug development for the treatment of intestinal I/R injury.
Enhancing the fairness of AI prediction models by Quasi-Pareto improvement among heterogeneous thyroid nodule population
Authors: Yao Siqiong , Dai Fang , Sun Peng , Zhang Weituo , Qian Biyun , Lu Hui 
Published: March 2024

AbstractArtificial Intelligence (AI) models for medical diagnosis often face challenges of generalizability and fairness. We highlighted the algorithmic unfairness in a large thyroid ultrasound dataset with significant diagnostic performance disparities across subgroups linked causally to sample size imbalances. To address this, we introduced the Quasi-Pareto Improvement (QPI) approach and a deep learning implementation (QP-Net) combining multi-task learning and domain adaptation to improve model performance among disadvantaged subgroups without compromising overall population performance. On the thyroid ultrasound dataset, our method significantly mitigated the area under curve (AUC) disparity for three less-prevalent subgroups by 0.213, 0.112, and 0.173 while maintaining the AUC for dominant subgroups; we also further confirmed the generalizability of our approach on two public datasets: the ISIC2019 skin disease dataset and the CheXpert chest radiograph dataset. Here we show the QPI approach to be widely applicable in promoting AI for equitable healthcare outcomes.
Hardware implementation of memristor-based artificial neural networks
Authors: Aguirre Fernando , Sebastian Abu , Le Gallo Manuel , Song Wenhao , Wang Tong , Yang J. Joshua , Lu Wei , Chang Meng-Fan , Ielmini Daniele , Yang Yuchao , Mehonic Adnan , Kenyon Anthony , Villena Marco A. , Roldán Juan B. , Wu Yuting , Hsu Hung-Hsi , Raghavan Nagarajan , Suñé Jordi , Miranda Enrique , Eltawil Ahmed , Setti Gianluca , Smagulova Kamilya , Salama Khaled N. , Krestinskaya Olga , Yan Xiaobing , Ang Kah-Wee , Jain Samarth , Li Sifan , Alharbi Osamah , Pazos Sebastian , Lanza Mario 
Published: March 2024

AbstractArtificial Intelligence (AI) is currently experiencing a bloom driven by deep learning (DL) techniques, which rely on networks of connected simple computing units operating in parallel. The low communication bandwidth between memory and processing units in conventional von Neumann machines does not support the requirements of emerging applications that rely extensively on large sets of data. More recent computing paradigms, such as high parallelization and near-memory computing, help alleviate the data communication bottleneck to some extent, but paradigm- shifting concepts are required. Memristors, a novel beyond-complementary metal-oxide-semiconductor (CMOS) technology, are a promising choice for memory devices due to their unique intrinsic device-level properties, enabling both storing and computing with a small, massively-parallel footprint at low power. Theoretically, this directly translates to a major boost in energy efficiency and computational throughput, but various practical challenges remain. In this work we review the latest efforts for achieving hardware-based memristive artificial neural networks (ANNs), describing with detail the working principia of each block and the different design alternatives with their own advantages and disadvantages, as well as the tools required for accurate estimation of performance metrics. Ultimately, we aim to provide a comprehensive protocol of the materials and methods involved in memristive neural networks to those aiming to start working in this field and the experts looking for a holistic approach.
Trans-lesion synthesis and mismatch repair pathway crosstalk defines chemoresistance and hypermutation mechanisms in glioblastoma
Authors: Cheng Xing , An Jing , Lou Jitong , Gu Qisheng , Ding Weimin , Droby Gaith Nabil , Wang Yilin , Wang Chenghao , Gao Yanzhe , Anand Jay Ramanlal , Shelton Abigail , Satterlee Andrew Benson , Mann Breanna , Hsiao Yun-Chung , Liu Chih-Wei , Lu Kun , Hingtgen Shawn , Wang Jiguang , Liu Zhaoliang , Miller C. Ryan , Wu Di , Vaziri Cyrus , Yang Yang 
Published: March 2024

AbstractAlmost all Glioblastoma (GBM) are either intrinsically resistant to the chemotherapeutical drug temozolomide (TMZ) or acquire therapy-induced mutations that cause chemoresistance and recurrence. The genome maintenance mechanisms responsible for GBM chemoresistance and hypermutation are unknown. We show that the E3 ubiquitin ligase RAD18 (a proximal regulator of TLS) is activated in a Mismatch repair (MMR)-dependent manner in TMZ-treated GBM cells, promoting post-replicative gap-filling and survival. An unbiased CRISPR screen provides an aerial map of RAD18-interacting DNA damage response (DDR) pathways deployed by GBM to tolerate TMZ genotoxicity. Analysis of mutation signatures from TMZ-treated GBM reveals a role for RAD18 in error-free bypass of O6mG (the most toxic TMZ-induced lesion), and error-prone bypass of other TMZ-induced lesions. Our analyses of recurrent GBM patient samples establishes a correlation between low RAD18 expression and hypermutation. Taken together we define molecular underpinnings for the hallmark tumorigenic phenotypes of TMZ-treated GBM.
Dynamic mechanostereochemical switching of a co-conformationally flexible [2]catenane controlled by specific ionic guests
Authors: Yao Yueliang , Tse Yuen Cheong , Lai Samuel Kin-Man , Shi Yixiang , Low Kam-Hung , Au-Yeung Ho Yu 
Published: March 2024

AbstractResponsive synthetic receptors for adaptive recognition of different ionic guests in a competitive environment are valuable molecular tools for not only ion sensing and transport, but also the development of ion-responsive smart materials and related technologies. By virtue of the mechanical chelation and ability to undergo large-amplitude co-conformational changes, described herein is the discovery of a chameleon-like [2]catenane that selectively binds copper(I) or sulfate ions and its associated co-conformational mechanostereochemical switching. This work highlights not only the advantages and versatility of catenane as a molecular skeleton in receptor design, but also its potential in constructing complex responsive systems with multiple inputs and outputs.
Structural basis for the modulation of MRP2 activity by phosphorylation and drugs
Authors: Mazza Tiziano , Roumeliotis Theodoros I. , Garitta Elena , Drew David , Rashid S. Tamir , Indiveri Cesare , Choudhary Jyoti S. , Linton Kenneth J. , Beis Konstantinos 
Published: March 2024

AbstractMultidrug resistance-associated protein 2 (MRP2/ABCC2) is a polyspecific efflux transporter of organic anions expressed in hepatocyte canalicular membranes. MRP2 dysfunction, in Dubin-Johnson syndrome or by off-target inhibition, for example by the uricosuric drug probenecid, elevates circulating bilirubin glucuronide and is a cause of jaundice. Here, we determine the cryo-EM structure of rat Mrp2 (rMrp2) in an autoinhibited state and in complex with probenecid. The autoinhibited state exhibits an unusual conformation for this class of transporter in which the regulatory domain is folded within the transmembrane domain cavity. In vitro phosphorylation, mass spectrometry and transport assays show that phosphorylation of the regulatory domain relieves this autoinhibition and enhances rMrp2 transport activity. The in vitro data is confirmed in human hepatocyte-like cells, in which inhibition of endogenous kinases also reduces human MRP2 transport activity. The drug-bound state reveals two probenecid binding sites that suggest a dynamic interplay with autoinhibition. Mapping of the Dubin-Johnson mutations onto the rodent structure indicates that many may interfere with the transition between conformational states.