bluuebunny/crossref_metadata_2025_split huggingface dataset:
On the Role of Ripple Secondary Crest on Nearbed Hydrodynamics
Authors: Jin C. , Gong Z. , San Juan J. E. , Tinoco R. O. , Coco G. 
Published: January 2025

AbstractRipples are ubiquitous in sandy beds and their geometry plays an important role in determining seabed roughness and intensifying near‐bed turbulence. Ripple geometry in natural settings often deviates from equilibrium configurations. To understand how such nonequilibrium geometry and structures impact near‐bottom hydrodynamics and hydraulic roughness, we performed laboratory experiments examining the effect of two different types of ripple configurations. We employed two distinct fixed 3D‐printed ripple morphologies, uniform ripples and ripples with superimposed secondary crests, and replicated natural conditions by adhering sand grains, matching in size to the ripple scale, onto their surfaces. Our results show that the introduction of secondary crest disrupts the flow over not only the modified ripple but also over its neighbors. Secondary crests induce a thicker boundary layer than regular ripples. Velocities over the upstream side of secondary crest show substantial deviation from the regular ripple baseline case, while the downstream side experiences a lower effect. The shear velocity at the crest of ripples with a secondary feature is significantly higher, indicating an increased capacity for sediment transport and bedform evolution. The turbulent kinetic energy over ripples with secondary crests is twice as high as that over regular ripples. Our results further affirm that the hydraulic roughness is a function of not only the height and wavelength of the ripples, but also of specific structures and ripple geometry.
Effects of Hot Versus Dry Vapor Pressure Deficit on Ecosystem Carbon and Water Fluxes
Authors: Johnston Miriam R. , Barnes Mallory L. , Preisler Yakir , Smith William K. , Biederman Joel A. , Scott Russell L. , Williams A. Park , Dannenberg Matthew P. 
Published: January 2025

AbstractVapor pressure deficit (VPD) has increased and will likely continue increasing, with wide‐ranging effects on ecosystems. Future VPD increases will largely be driven by warming, yet most experiments examining VPD effects on plants have done so by changing humidity. Here, we used meteorological data and carbon and water fluxes measured at 26 climatically‐diverse eddy covariance sites to quantify the extent to which VPD has been driven by variation in air temperature versus humidity. We fit generalized additive models (GAMs) at each site to quantify effects of hotter (and wetter) and cooler (and drier) versus typical VPD on ecosystem‐scale fluxes of carbon and water. We found that VPD has occurred under diverse combinations of temperature and humidity: >50% of a site's daytime growing season temperature range and >35% of its relative humidity range have often combined to define a particular VPD. We found moderate evidence that hotter versus drier VPD of the same magnitude differentially affect gross primary productivity (GPP), net ecosystem productivity (NEP), and latent heat flux (LE): Selected GPP and NEP GAMs at about half of sites and LE GAMs at about a third of sites included a VPD‐temperature interaction. The magnitude of the interaction varied, but was generally 29%–57% of the effect attributable solely to VPD. The direction of the interaction also varied, but hot VPD was commonly associated with higher carbon fluxes. These effects were not strongly modified by soil moisture. Overall, results emphasize the relevance of VPD‐temperature interactions at a critical time of rapid VPD increase.
A safe haven for cancer cells: tumor plus stroma control by DYRK1B
Authors: Ems Miriam , Brichkina Anna , Lauth Matthias 
Published: January 2025

Abstract
The development of resistance remains one of the biggest challenges in clinical cancer patient care and it comprises all treatment modalities from chemotherapy to targeted or immune therapy. In solid malignancies, drug resistance is the result of adaptive processes occurring in cancer cells or the surrounding tumor microenvironment (TME). Future therapy attempts will therefore benefit from targeting both, tumor and stroma compartments and drug targets which affect both sides will be highly appreciated. In this review, we describe a seemingly paradoxical oncogenic mediator with this potential: The dual-specificity tyrosine-phosphorylation regulated kinase 1B (DYRK1B). DYRK1B promotes proliferative quiescence and yet is overexpressed or amplified in many hyperproliferative malignancies including ovarian cancer and pancreatic cancer. In particular the latter disease is a paradigmatic example for a therapy-recalcitrant and highly stroma-rich cancer entity. Here, recent evidence suggests that DYRK1B exerts its oncogenic features by installing a protective niche for cancer cells by directly affecting cancer cells but also the TME. Specifically, DYRK1B not only fosters cell-intrinsic processes like cell survival, chemoresistance, and disease recurrence, but it also upregulates TME and cancer cell-protective innate immune checkpoints and down-modulates anti-tumoral macrophage functionality. In this article, we outline the well-established cell-autonomous roles of DYRK1B and extend its importance to the TME and the control of the tumor immune stroma. In summary, DYRK1B appears as a single novel key player creating a safe haven for cancer cells by acting cell-intrinsically and—extrinsically, leading to the promotion of cancer cell survival, chemoresistance, and relapse. Thus, DYRK1B appears as an attractive drug target for future therapeutic approaches.
Extracellular vesicles from pancreatic cancer and its tumour microenvironment promote increased Schwann cell migration
Authors: Wong Fang Cheng , Merker Sebastian R. , Bauer Lisa , Han Yi , Le Van Manh Hung , Wenzel Carina , Böthig Lukas , Heiduk Max , Drobisch Pascal , Rao Venkatesh Sadananda , Malekian Farzaneh , Mansourkiaei Ana , Sperling Christian , Polster Heike , Pecqueux Mathieu , Istvanffy Rouzanna , Ye Linhan , Kong Bo , Aust Daniela E. , Baretton Gustavo , Seifert Lena , Seifert Adrian M. , Weitz Jürgen , Demir Ihsan Ekin , Kahlert Christoph 
Published: January 2025

Abstract

Background
Pancreatic ductal adenocarcinoma (PDAC) exhibits a high frequency of neural invasion (NI). Schwann cells (SCs) have been shown to be reprogrammed to facilitate cancer cell migration and invasion into nerves. Since extracellular vesicles (EVs) affect the tumour microenvironment and promote metastasis, the present study analysed the involvement of EVs from pancreatic cancer cells and their microenvironment in altering SC phenotype as part of the early events in the process of NI.

Methods
EVs were isolated from human/murine PDAC cells, pancreatic stellate cells (PSCs), human tissues and plasma to perform a novel 3D migration assay, qRT-PCR and western blot. Kaplan–Meier and Cox regression analyses were employed to evaluate the clinical potential of plasma EV-derived candidate from 165 PDAC patients.

Results
The EVs from PDAC cells, PSCs derived from human tumour tissues, other cell types in the tumour microenvironment from tumour tissues and circulating plasma act as drivers of a pro-migratory phenotype of SCs by inducing dedifferentiation in SCs. Notably, p75NTR expression was upregulated in the plasma-derived EVs from patients with NI (Pn1) relative to those without NI (Pn0). High expression of plasma-derived EV p75NTR correlated with reduced overall survival and was identified as an independent prognostic factor.

Conclusions
These findings suggest that EV-mediated SC migration underlies the interactions contributing to PDAC-associated NI with implications for improved outcome and therapeutic strategy.
Ferroptosis triggers mitochondrial fragmentation via Drp1 activation
Authors: Pedrera Lohans , Prieto Clemente Laura , Dahlhaus Alina , Lotfipour Nasudivar Sara , Tishina Sofya , Olmo González Daniel , Stroh Jenny , Yapici Fatma Isil , Singh Randhwaj Pratap , Grotehans Nils , Langer Thomas , García-Sáez Ana J. , von Karstedt Silvia 
Published: January 2025

Abstract
Constitutive mitochondrial dynamics ensure quality control and metabolic fitness of cells, and their dysregulation has been implicated in various human diseases. The large GTPase Dynamin-related protein 1 (Drp1) is intimately involved in mediating constitutive mitochondrial fission and has been implicated in mitochondrial cell death pathways. During ferroptosis, a recently identified type of regulated necrosis driven by excessive lipid peroxidation, mitochondrial fragmentation has been observed. Yet, how this is regulated and whether it is involved in ferroptotic cell death has remained unexplored. Here, we provide evidence that Drp1 is activated upon experimental induction of ferroptosis and promotes cell death execution and mitochondrial fragmentation. Using time-lapse microscopy, we found that ferroptosis induced mitochondrial fragmentation and loss of mitochondrial membrane potential, but not mitochondrial outer membrane permeabilization. Importantly, Drp1 accelerated ferroptotic cell death kinetics. Notably, this function was mediated by the regulation of mitochondrial dynamics, as overexpression of Mitofusin 2 phenocopied the effect of Drp1 deficiency in delaying ferroptosis cell death kinetics. Mechanistically, we found that Drp1 is phosphorylated and activated after induction of ferroptosis and that it translocates to mitochondria. Further activation at mitochondria through the phosphatase PGAM5 promoted ferroptotic cell death. Remarkably, Drp1 depletion delayed mitochondrial and plasma membrane lipid peroxidation. These data provide evidence for a functional role of Drp1 activation and mitochondrial fragmentation in the acceleration of ferroptotic cell death, with important implications for targeting mitochondrial dynamics in diseases associated with ferroptosis.
Positive feedback loop involving AMPK and CLYBL acetylation links metabolic rewiring and inflammatory responses
Authors: Wang Wenke , Wu Boquan , Hao Mingjun , Chen Sichong , Cong Ruiting , Wu Wenjie , Wang Pengbo , Zhang Qiaoyi , Jia Pengyu , Song Yuequn , Liu Bo , Qu Siyao , Pei Jian-Fei , Li Da , Zhang Naijin 
Published: January 2025

Abstract
Metabolic rewiring underlies effective macrophages defense to respond disease microenvironment. However, the underlying mechanisms driving metabolic rewiring to enhance macrophage effector functions remain unclear. Here, we demonstrated that the metabolic reprogramming in inflammatory macrophages depended on the acetylation of CLYBL, a citramalyl-CoA lyase, at lysine 154 (K154), and blocking CLYBL-K154 acetylation restricted the release of pro-inflammatory factors. Mechanistically, we found a crucial AMPK-CLYBL acetylation positive feedback loop, triggered by toll-like receptors (TLRs), involving AMPK hypophosphorylation and CLYBL hyperacetylation. The deacetylase enzyme SIRT2 acted as the bridge between AMPK phosphorylation and CLYBL acetylation, thereby regulating macrophage polarization and the release of pro-inflammatory cytokines. Furthermore, CLYBL hypoacetylation decreased monocyte infiltration, thereby alleviating cardiac remodeling. These findings suggest that the AMPK-CLYBL acetylation positive feedback loop serves as a metabolic switch driving inflammatory response and inhibiting CLYBL-K154 acetylation may offer a promising therapeutic strategy for inflammatory response-related disorders.
IDO1 inhibits ferroptosis by regulating FTO-mediated m6A methylation and SLC7A11 mRNA stability during glioblastoma progression
Authors: Tian Qianting , Dan Guixue , Wang Xuyan , Zhu Jiamei , Chen Chaochun , Tang Dekun , Wang Ziming , Chen Dan , Lei Shan , Yang Chao , Wang Houmei , Guo Bing , Jin Bangming , Chen Tengxiang , Tang Lei 
Published: January 2025

Abstract
Indoleamine 2, 3-dioxygenase 1 (IDO1) has been recognized as an enzyme involved in tryptophan catabolism with immunosuppressive ability. This study determined to investigate the impact of IDO1 on glioblastoma multiforme (GBM) cells. Here, we showed that the expression of IDO1 was markedly increased in patients with glioma and associated with GBM progression. IDO1 overexpression suppressed ferroptotic cell death, reduced ROS and lipid peroxide generation in GBM cells. IDO1 expression increased the SLC7A11 mRNA stability through FTO-dependent m6A methylation. Mechanistically, IDO1 promoted the AhR expression and nuclear translocation, thus facilitating AhR recruitment at the promoter regions of FTO gene and negatively regulating its transcription. These findings demonstrate that IDO1 facilitates GBM progression by inhibiting SLC7A11-dependent ferroptosis through an IDO1-AhR-FTO axis-mediated m6A methylation mechanism.
Assessment of corneal vessels activity through the ‘Barcode sign’ of corneal OCT
Authors: Elzawahry Farida Omar , Sahay Prity , Said Dalia , Dua Harminder Singh 
Published: January 2025

Abstract

Background/objectives
Anterior segment optical Coherence Tomography (AS-OCT) is used extensively in imaging the cornea in health and disease. Our objective was to analyse and monitor corneal vascularisation (CVas) through the corresponding back-shadows visible on AS-OCT.

Subjects/Methods
AS-OCT scans were obtained from 26 consecutive patients (eyes) with CVas of different aetiologies. AS-OCT horizontal line scans showing the back shadows cast by the vessels were analysed and correlated with findings seen on slit lamp examination. Vessels were graded clinically as active, partially regressed, and regressed. The density of back shadow in the patient samples before and after treatment was analysed using Image-J software.

Results
AS-OCT demonstrated a dense back shadow in all the 26 active vessels studied. When multiple vessels were present, the barcode sign was apparent. The back shadows absent in 22 (84.62%) at the regressed (healed) stage. The intensity of the backshadow had reduced in regressing vessels 4 (15.38%). The integrated density of the backshadow on AS-OCT in the active stage (pre-treatment) and corresponding healed (post-treatment, partially regressed or ghost vessels) scans was statistically significantly different (P < 0.0001).

Conclusion
This study demonstrates that AS-OCT provides additional important information in patients with CVas enabling distinction between active and regressing/regressed vessels. Semiquantitative assessment can be made by measuring the integrated density of the back shadows produced by the vessels.
Silicon-based all-solid-state batteries operating free from external pressure
Authors: Zhang Zhiyong , Zhang Xiuli , Liu Yan , Lan Chaofei , Han Xiang , Pei Shanpeng , Luo Linshan , Su Pengfei , Zhang Ziqi , Liu Jingjing , Gong Zhengliang , Li Cheng , Lin Guangyang , Li Cheng , Huang Wei , Wang Ming-Sheng , Chen Songyan 
Published: January 2025

Abstract
Silicon-based all-solid-state batteries offer high energy density and safety but face significant application challenges due to the requirement of high external pressure. In this study, a Li21Si5/Si–Li21Si5 double-layered anode is developed for all-solid-state batteries operating free from external pressure. Under the cold-pressed sintering of Li21Si5 alloys, the anode forms a top layer (Li21Si5 layer) with mixed ionic/electronic conduction and a bottom layer (Si–Li21Si5 layer) containing a three-dimensional continuous conductive network. The resultant uniform electric field at the anode|SSE interface eliminates the need for high external pressure and simultaneously enables a twofold enhancement of the lithium-ion flux at the anode interface. Such an efficient ionic/electronic transport system also facilitates the uniform release of cycling expansion stresses from the Si particles and stabilizes bulk-phase and interfacial structure of anode. Consequently, the Li21Si5/Si–Li21Si5 anode exhibited a critical current density of 10 mA cm−2 at 45 °C with a capacity of 10 mAh cm−2. And the Li21Si5/Si–Li21Si5|Li6PS5Cl|Li3InCl6|LCO cell achieve an high initial Coulombic efficiency of (97 ± 0.7)% with areal capacity of 2.8 mAh cm−2 at 0.25 mA cm−2, as well as a low expansion rate of 14.5% after 1000 cycles at 2.5 mA cm−2.
Genetic variation in IL-4 activated tissue resident macrophages determines strain-specific synergistic responses to LPS epigenetically
Authors: Zhao Mingming , Jankovic Dragana , Link Verena M. , Souza Camila Oliveira Silva , Hornick Katherine M. , Oyesola Oyebola , Belkaid Yasmine , Lack Justin , Loke Png 
Published: January 2025

Abstract
How macrophages in the tissue environment integrate multiple stimuli depends on the genetic background of the host, but this is still poorly understood. We investigate IL-4 activation of male C57BL/6 and BALB/c strain specific in vivo tissue-resident macrophages (TRMs) from the peritoneal cavity. C57BL/6 TRMs are more transcriptionally responsive to IL-4 stimulation, with induced genes associated with more super enhancers, induced enhancers, and topologically associating domains (TAD) boundaries. IL-4-directed epigenomic remodeling reveals C57BL/6 specific enrichment of NF-κB, IRF, and STAT motifs. Additionally, IL-4-activated C57BL/6 TRMs demonstrate an augmented synergistic response upon in vitro lipopolysaccharide (LPS) exposure, despite naïve BALB/c TRMs displaying a more robust transcriptional response to LPS. Single-cell RNA sequencing (scRNA-seq) analysis of mixed bone marrow chimeras indicates that transcriptional differences and synergy are cell intrinsic within the same tissue environment. Hence, genetic variation alters IL-4-induced cell intrinsic epigenetic reprogramming resulting in strain specific synergistic responses to LPS exposure.
Mechanisms of RCD-1 pore formation and membrane bending
Authors: Ren Keli , Farrell James Daniel , Li Yueyue , Guo Xinrui , Xie Ruipei , Liu Xin , Kang Qiaozhen , Fan Qihui , Ye Fangfu , Ding Jingjin , Jiao Fang 
Published: January 2025

Abstract
Regulator of cell death-1 (RCD-1) governs the heteroallelic expression of RCD-1-1 and RCD-1-2, a pair of fungal gasdermin (GSDM)-like proteins, which prevent cytoplasmic mixing during allorecognition and safeguard against mycoparasitism, genome exploitation, and deleterious cytoplasmic elements (e.g., senescence plasmids) by effecting a form of cytolytic cell death. However, the underlying mechanisms by which RCD-1 acts on the cell membrane remain elusive. Here, we demonstrate that RCD-1 binds acidic lipid membranes, forms pores, and induces membrane bending. Using atomic force microscopy (AFM) and AlphaFold, we show that RCD-1-1 and RCD-1-2 form heterodimers that further self-assemble into ~14.5 nm-wide transmembrane pores (~10 heterodimers). Moreover, through AFM force spectroscopy and micropipette aspiration, we reveal that RCD-1 proteins bend membranes with low bending moduli. This combined action of pore formation and membrane deformation may constitute a conserved mechanism within the broader GSDM family.
Multidimensional library for the improved identification of per- and polyfluoroalkyl substances (PFAS)
Authors: Joseph Kara M. , Boatman Anna K. , Dodds James N. , Kirkwood-Donelson Kaylie I. , Ryan Jack P. , Zhang Jian , Thiessen Paul A. , Bolton Evan E. , Valdiviezo Alan , Sapozhnikova Yelena , Rusyn Ivan , Schymanski Emma L. , Baker Erin S. 
Published: January 2025

Abstract
As the occurrence of human diseases and conditions increase, questions continue to arise about their linkages to chemical exposure, especially for per-and polyfluoroalkyl substances (PFAS). Currently, many chemicals of concern have limited experimental information available for their use in analytical assessments. Here, we aim to increase this knowledge by providing the scientific community with multidimensional characteristics for 175 PFAS and their resulting 281 ion types. Using a platform coupling reversed-phase liquid chromatography (RPLC), electrospray ionization (ESI) or atmospheric pressure chemical ionization (APCI), drift tube ion mobility spectrometry (IMS), and mass spectrometry (MS), the retention times, collision cross section (CCS) values, and m/z ratios were determined for all analytes and assembled into an openly available multidimensional dataset. This information will provide the scientific community with essential characteristics to expand analytical assessments of PFAS and augment machine learning training sets for discovering new PFAS.
Impact of single versus dual arterial supply on perfusion and function in finger replantation after complex hand injuries
Authors: Tamulevicius Martynas , Steinbach Malte David , Bucher Florian , Dastagir Nadjib , Obed Doha , Vogt Peter M. , Dastagir Khaled 
Published: January 2025

Abstract
Finger amputations following complex hand injuries (CHI) pose a significant challenge in hand surgery due to severe tissue trauma and neurovascular damage, necessitating precise arterial repair. While restoring arterial perfusion is critical, it remains unclear whether reconstructing both proper palmar digital arteries is required for optimal outcomes. This study evaluates whether restoring one or both arteries in finger replantation after complex injuries impacts perfusion and overall outcomes. In this retrospective, cross-sectional, follow-up study, we investigated patients with finger amputations following CHI admitted to the high-volume regional hand trauma center between January 2013 and December 2020. Perfusion has been assessed using FLIR thermal imaging and laser speckle contrast analysis. Functional outcomes and quality of life scores were measured using standardized questionnaires. Sensory assessments, along with pain and grip strength measurements were also conducted. A total of 31 patients were included in the study. Thermal imaging showed a significantly higher finger surface temperature in patients with two-artery reconstruction. Laser speckle contrast analysis confirmed better perfusion, though not statistically significant. Functional and quality-of-life scores were similar across groups, except for significantly improved temperature sensation in the two-artery group. In conclusion, reconstructing both arteries in finger replantation following CHI isn’t essential for good outcomes if one artery provides adequate perfusion, but dual reconstruction may improve perfusion and temperature sensation.