bluuebunny/crossref_metadata_2025_split huggingface dataset:
2.5‐D Local Hybrid Simulations of Discontinuity‐Driven Compressional Boundaries Under Various Magnetic Field Geometries
Authors: Vu Andrew , Liu Terry Z. , Angelopoulos Vassilis , Zhang Hui 
Published: May 2024

AbstractIn the ion foreshock, there are many foreshock transients driven by back streaming foreshock ions. When the foreshock ions interact with tangential discontinuities (TDs), hot flow anomalies form if the foreshock ion‐driven current decreases field strength at TDs, but the opposite situation has been paid little attention. Using 2.5‐D local hybrid simulations, we show that a compressional boundary with enhanced field strength and density can form. We examine how the foreshock ions interact with TDs under various magnetic field geometries to drive currents that lead to compressional boundaries. The current driven by the foreshock ions should peak on its initial side of a TD so that the enhanced field strength at the TD in turn increases this current by keeping more foreshock ions on their initial side. Which side the current peaks can be determined by whether the foreshock ions initially cross the TD and/or how their velocity is projected into the local perpendicular direction. Additionally, the foreshock ion‐driven currents from two sides could compete, and whether a compressional boundary forms is determined by the net current profile. Because such compressive structures in the foreshock can drive magneto sheath jets and cause many geoeffects, it is necessary to fully understand their formation.
Compartmentalization of Axial Seamount's Magma Reservoir Inferred by Analytical and Numerical Deformation Modeling With Realistic Geometry
Authors: Slead S. R. , Wei M. , Nooner S. L. , Chadwick W. W. , Caress D. W. , Beeson J. 
Published: May 2024

AbstractAxial Seamount is a submarine volcano on the Juan de Fuca Ridge with enhanced magma supply from the Cobb hotspot. We compare several deformation model configurations to explore how the spatial component of Axial's deformation time series relates to magma reservoir geometry imaged by multi‐channel seismic (MCS) surveys. To constrain the models, we use vertical displacements from seafloor pressure sensors and repeat autonomous underwater vehicle (AUV) bathymetric surveys between 2016 and 2020. We show that implementing the MCS‐derived 3D main magma reservoir (MMR) geometry with uniform pressure in a finite element model with uniform elastic host rock properties poorly fits the geodetic data. To test the hypothesis that there is compartmentalization within the MMR that results in heterogeneous pressure distribution, we compare analytical models using various horizontal sill configurations constrained by the MMR geometry. Using distributed pressure sources significantly improves the Root Mean Square Error (RMSE) between the inflation data and the models by an order of magnitude. The RMSE between the AUV data and the models is not improved as much, likely due to larger uncertainty of the AUV data. The models estimate the volume change for the 2016–2020 inter‐eruptive inflation period to be between 0.054 and 0.060 km3 and suggest that the MMR is compartmentalized, with most magma accumulating in sill‐like bodies embedded in crystal mush along the western‐central edge of the MMR. The results reveal the complexity of Axial's plumbing system and demonstrate the utility of integrating geodetic data and seismic imagery to gain insights into magma storage at active volcanoes.
Modeling Interactive Effects of Manganese Bioavailability, Nitrogen Deposition, and Warming on Soil Carbon Storage
Authors: Sulman Benjamin N. , Herndon Elizabeth M. 
Published: May 2024

AbstractManganese (Mn) is a redox‐active micronutrient that has been shown to accelerate plant litter decomposition; however, the effect of Mn‐promoted decomposition on soil C storage is unclear. We present a novel biogeochemical model simulating how Mn bioavailability influences soil organic C (SOC) stocks in a soil profile (<50 cm) within a temperate forest. In our model, foliar Mn increased in response to increasing soluble Mn released through Mn‐oxide (birnessite) dissolution in mineral soil layers. The ensuing Mn enrichment in leaf litter redistributed Mn to the surface forest floor layer, promoted enzymatic oxidation of lignin, and decreased SOC stocks. Total SOC loss was partially mitigated by accumulation of lignin‐oxidation products as mineral‐associated organic C. We also explored how Mn‐driven changes to C storage interacted with effects of N deposition and warming. Nitrogen enrichment inhibited Mn‐dependent lignin degradation, increasing SOC stocks and weakening their dependence on Mn bioavailability. Warming stimulated decomposition and reduced C stocks but was less effective at low Mn bioavailability. Our model results suggest that SOC stocks are sensitive to Mn bioavailability because increased plant uptake redistributes Mn to surface soils where it can enhance litter decomposition. Based on our simulations, we predict that Mn becomes limiting to litter decomposition where Mn is poorly soluble. Depletion of bioavailable Mn or other cofactors that are critical to decomposition could limit the response of organic C stocks to warming over time, but quantitative projections of the role of Mn bioavailability in regulating decomposition requires additional measurements to constrain model uncertainties.
Dipolarizing Flux Bundles and Magnetic Flux Transport
Authors: Lui A. T. Y. 
Published: May 2024

AbstractAn important feature intimately related to substorm process is the development of dipolarization in the near‐Earth region. A common concept is that it arises from magnetic flux transported by dipolarizing flux bundles generated by magnetic reconnection in the mid‐tail region. This concept is based on assuming the validity of the frozen‐in‐field condition for dipolarizing flux bundles. The frozen‐in‐field condition of this structure is critically evaluated from observations and by theoretical consideration. It is shown that this structure cannot transport sufficient magnetic flux to the near‐Earth region that is required from observations for substorms.
Spatial Features of the Delayed Ionospheric Response During Low and High Solar Activity
Authors: Schmölter Erik , Dühnen Hanna , Berdermann Jens , Vaishnav Rajesh , Jacobi Christoph 
Published: May 2024

AbstractThe ionospheric response to solar 27‐day signatures has complex temporal and spatial variations, which are driven by short‐ and long‐term changes of the solar activity among other processes (e.g., geomagnetic activity). A delay between these solar and ionospheric signatures occurs due to accumulation of plasma, which depends on the rates of photoionization, photodissociation and recombination in the upper atmosphere. The balance of these processes changes significantly at different solar activity levels. Therefore the present study investigates the delayed ionospheric response during low and high solar activity. For that purpose, global as well as latitude‐ and longitude‐dependent total electron content (TEC) is analyzed via superposed epoch analysis (SEA). Different results based on the solar proxy F10.7 and solar extreme ultraviolet (EUV) irradiance measurements are presented to discuss findings of preceding studies and to provide a first wavelength‐dependent analysis of the spatial features. The SEA shows a good correlation between solar activity level and delayed ionospheric response with particular strong enhancements of the delay at mid‐latitudes. Increased delays are also observed for morning and evening hours. Thus, the present study confirms the correlation of delayed ionospheric response and solar activity level as indicated in preceding studies, and also quantifies the temporal and spatial variations with commonly used data sets. This in turn allows a better understanding of the processes that cause the delayed ionospheric response.
Timing and risk factors associated with acute kidney injury in infants with necrotizing enterocolitis
Authors: Lingasubramanian Geethanjali , Hum Christina Eva , Hunter Krystal , Mehta Rajeev , Bhandari Vineet 
Published: May 2024

Abstract
Objective
To evaluate the prevalence, onset, risk factors, and mortality associated with acute kidney injury (AKI) in infants with necrotizing enterocolitis (NEC).

Design/Methods
Retrospective study at 2 centers in infants with NEC, with/without AKI. AKI assessed by serum creatinine and urine output. Statistical tests used included t, Mann-Whitney U, Chi-square, and Fisher Exact tests.

Results
Among 80 eligible infants with NEC, 56 (70%) had AKI. Median onset of NEC was day 15, with median AKI onset two days (IQR, –5.75 to 0) prior to NEC onset. Vasopressors were significantly more likely to be used in infants with NEC and AKI (p = 0.009). Increased mortality (p = 0.01) was noted in infants with NEC and AKI.

Conclusions
The onset of AKI mostly precedes NEC onset, with moderate to severe AKI more prevalent than the milder form in infants with NEC. These infants are significantly more likely to be hemodynamically unstable and have increased mortality.
Shorter long-term post-transplant life expectancy may be due to prior chemotherapy for the underlying disease: analysis of 3012 patients with acute myeloid leukemia enrolled on 9 consecutive ECOG-ACRIN trials
Authors: Ganzel C. , Wang Y. , Roopcharan K. , Sun Z. , Rowe J. M. , Fernandez H. F. , Paietta E. M. , Luger S. M. , Lazarus H. M. , Cripe L. D. , Douer D. , Wiernik P. H. , Tallman M. S. , Litzow M. R. 
Published: May 2024

AbstractSeveral studies reported that patients with acute myeloid leukemia (AML) who remain in long-term remission after allogeneic or autologous transplant have a shorter life expectancy, compared to the general population. However, little is known about the life expectancy of adult long-term survivors of AML who were treated with chemotherapy alone without a transplant and there have been no comparisons with survival among the general population. The current study indicates that the life expectancy of AML patients who achieved and maintained CR for at least 3 years is shorter than expected for age in the US population. This was observed also in patients who did not undergo a transplant including those who have not relapsed during the entire long follow-up period. Thus, late relapse does not explain why patients without transplants have a shortened life expectancy. Taken together, these data strongly suggest that prior chemotherapy for the underlying AML is at least a major contributing factor for the known shortened life expectancy post-transplant.
The OGT–c-Myc–PDK2 axis rewires the TCA cycle and promotes colorectal tumor growth
Authors: Wang Huijuan , Sun Jie , Sun Haofan , Wang Yifei , Lin Bingyi , Wu Liming , Qin Weijie , Zhu Qiang , Yi Wen 
Published: May 2024

AbstractDeregulated glucose metabolism termed the “Warburg effect” is a fundamental feature of cancers, including the colorectal cancer. This is typically characterized with an increased rate of glycolysis, and a concomitant reduced rate of the tricarboxylic acid (TCA) cycle metabolism as compared to the normal cells. How the TCA cycle is manipulated in cancer cells remains unknown. Here, we show that O-linked N-acetylglucosamine (O-GlcNAc) regulates the TCA cycle in colorectal cancer cells. Depletion of OGT, the sole transferase of O-GlcNAc, significantly increases the TCA cycle metabolism in colorectal cancer cells. Mechanistically, OGT-catalyzed O-GlcNAc modification of c-Myc at serine 415 (S415) increases c-Myc stability, which transcriptionally upregulates the expression of pyruvate dehydrogenase kinase 2 (PDK2). PDK2 phosphorylates pyruvate dehydrogenase (PDH) to inhibit the activity of mitochondrial pyruvate dehydrogenase complex, which reduces mitochondrial pyruvate metabolism, suppresses reactive oxygen species production, and promotes xenograft tumor growth. Furthermore, c-Myc S415 glycosylation levels positively correlate with PDK2 expression levels in clinical colorectal tumor tissues. This study highlights the OGT–c-Myc–PDK2 axis as a key mechanism linking oncoprotein activation with deregulated glucose metabolism in colorectal cancer.
How do I manage functional visual loss
Authors: Ramsay Neil , McKee Justin , Al-Ani Gillian , Stone Jon 
Published: May 2024

AbstractFunctional visual loss is a subtype of functional neurological disorder (FND) and is a common cause of visual impairment seen in both general and neuro-ophthalmological practice. Ophthalmologists can generally diagnose functional visual loss reasonably confidently but often find it harder to know what to say to the patient, how to approach, or even whether to attempt, treatment. There is little evidence-based treatment despite studies showing up to 60% of adults having impactful symptoms on long-term follow-up. The last 20 years has seen large changes in how we understand, approach, and manage FND more widely. In this article, we set out our practical approach to managing functional visual loss which includes : 1) Make a positive diagnosis based on investigations that demonstrate normal vision in the presence of subjectively impaired vision, not just because tests or ocular exam is normal; 2) Explain and label the condition with an emphasis on these positive diagnostic features, not reassurance; 3) Consider eye or brain comorbidities such as migraine, idiopathic intracranial hypertension or amblyopia; 4) Consider working with an orthoptist using diagnostic tests in a positive way to highlight the possibility of better vision; 5) Develop simple treatment strategies for photophobia; 6) Consider psychological factors and comorbidity as part of assessment and therapy, but keep a broader view of aetiology and don’t use this to make a diagnosis; 7) Other treatment modalities including hypnotherapy, transcranial magnetic stimulation and more advanced forms of visual feedback are promising candidates for functional visual loss treatment in the future.
Distinct µ-opioid ensembles trigger positive and negative fentanyl reinforcement
Authors: Chaudun Fabrice , Python Laurena , Liu Yu , Hiver Agnes , Cand Jennifer , Kieffer Brigitte L. , Valjent Emmanuel , Lüscher Christian 
Published: May 2024

AbstractFentanyl is a powerful painkiller that elicits euphoria and positive reinforcement1. Fentanyl also leads to dependence, defined by the aversive withdrawal syndrome, which fuels negative reinforcement2,3 (that is, individuals retake the drug to avoid withdrawal). Positive and negative reinforcement maintain opioid consumption, which leads to addiction in one-fourth of users, the largest fraction for all addictive drugs4. Among the opioid receptors, µ-opioid receptors have a key role5, yet the induction loci of circuit adaptations that eventually lead to addiction remain unknown. Here we injected mice with fentanyl to acutely inhibit γ-aminobutyric acid-expressing neurons in the ventral tegmental area (VTA), causing disinhibition of dopamine neurons, which eventually increased dopamine in the nucleus accumbens. Knockdown of µ-opioid receptors in VTA abolished dopamine transients and positive reinforcement, but withdrawal remained unchanged. We identified neurons expressing µ-opioid receptors in the central amygdala (CeA) whose activity was enhanced during withdrawal. Knockdown of µ-opioid receptors in CeA eliminated aversive symptoms, suggesting that they mediate negative reinforcement. Thus, optogenetic stimulation caused place aversion, and mice readily learned to press a lever to pause optogenetic stimulation of CeA neurons that express µ-opioid receptors. Our study parses the neuronal populations that trigger positive and negative reinforcement in VTA and CeA, respectively. We lay out the circuit organization to develop interventions for reducing fentanyl addiction and facilitating rehabilitation.
Molecular mechanism of choline and ethanolamine transport in humans
Authors: Ri Keiken , Weng Tsai-Hsuan , Claveras Cabezudo Ainara , Jösting Wiebke , Zhang Yu , Bazzone Andre , Leong Nancy C. P. , Welsch Sonja , Doty Raymond T. , Gursu Gonca , Lim Tiffany Jia Ying , Schmidt Sarah Luise , Abkowitz Janis L. , Hummer Gerhard , Wu Di , Nguyen Long N. , Safarian Schara 
Published: May 2024

AbstractHuman feline leukaemia virus subgroup C receptor-related proteins 1 and 2 (FLVCR1 and FLVCR2) are members of the major facilitator superfamily1. Their dysfunction is linked to several clinical disorders, including PCARP, HSAN and Fowler syndrome2–7. Earlier studies concluded that FLVCR1 may function as a haem exporter8–12, whereas FLVCR2 was suggested to act as a haem importer13, yet conclusive biochemical and detailed molecular evidence remained elusive for the function of both transporters14–16. Here, we show that FLVCR1 and FLVCR2 facilitate the transport of choline and ethanolamine across the plasma membrane, using a concentration-driven substrate translocation process. Through structural and computational analyses, we have identified distinct conformational states of FLVCRs and unravelled the coordination chemistry underlying their substrate interactions. Fully conserved tryptophan and tyrosine residues form the binding pocket of both transporters and confer selectivity for choline and ethanolamine through cation–π interactions. Our findings clarify the mechanisms of choline and ethanolamine transport by FLVCR1 and FLVCR2, enhance our comprehension of disease-associated mutations that interfere with these vital processes and shed light on the conformational dynamics of these major facilitator superfamily proteins during the transport cycle.
Kainate receptor channel opening and gating mechanism
Authors: Gangwar Shanti Pal , Yelshanskaya Maria V. , Nadezhdin Kirill D. , Yen Laura Y. , Newton Thomas P. , Aktolun Muhammed , Kurnikova Maria G. , Sobolevsky Alexander I. 
Published: May 2024

AbstractKainate receptors, a subclass of ionotropic glutamate receptors, are tetrameric ligand-gated ion channels that mediate excitatory neurotransmission1–4. Kainate receptors modulate neuronal circuits and synaptic plasticity during the development and function of the central nervous system and are implicated in various neurological and psychiatric diseases, including epilepsy, depression, schizophrenia, anxiety and autism5–11. Although structures of kainate receptor domains and subunit assemblies are available12–18, the mechanism of kainate receptor gating remains poorly understood. Here we present cryo-electron microscopy structures of the kainate receptor GluK2 in the presence of the agonist glutamate and the positive allosteric modulators lectin concanavalin A and BPAM344. Concanavalin A and BPAM344 inhibit kainate receptor desensitization and prolong activation by acting as a spacer between the amino-terminal and ligand-binding domains and a stabilizer of the ligand-binding domain dimer interface, respectively. Channel opening involves the kinking of all four pore-forming M3 helices. Our structures reveal the molecular basis of kainate receptor gating, which could guide the development of drugs for treatment of neurological disorders.
Merging adoption of natural climate solutions in agriculture with climatic and non-climatic risks within an (intra)gendered framework
Authors: Antwi Kwabena 
Published: May 2024

AbstractThe extant research on climate variability shares significant theoretical contributions to vulnerability and risks. However, the literature mostly focuses on technical solutions to climate extremes which undermines efforts to identify and solve the dynamics within gender groups in using agricultural-based natural climate solutions (NCS) to address climatic and non-climatic risks. With this in mind, this study implements both quantitative and qualitative approaches including household surveys, key informant interviews, and focus group discussions to investigate the adoption of NCS within gender groups to address climatic and non-climatic risks in three selected communities (Katanga, Dakio, and Zonno) in the Bolgatanga East District of Upper East Region of Ghana. The Relative Importance Index (RII) was used to rank the key climatic and non-climatic risks confronting smallholder farmers in the district. Male and female smallholder farmers affirmed that there has been variation in the climate compared to their childhood. The results indicated climate change-induced erosion (RII = 0.268) as the highest climatic risk among male smallholder farmers. Increased bushfire (RII = 0.263) was the highest climatic risk affecting female smallholder farmers. The findings show that the high cost of farm inputs (RII = 0.505) is the highest non-climatic risk among the male smallholder farmers whereas inadequate credit facilities (RII = 0.295) affected most of the female smallholder farmers. In adapting to the climatic risks, both male and female smallholder farmers with no formal education plant early maturing crop varieties and cover crops on their farmland. Others engage in traditional non-farm activities such as weaving by using renewable materials with reduced ecological footprints to address non-climatic risks. The male and female smallholder farmers with post-secondary education typically resort to temporal migration during the dry season to work on non-farm jobs. Acknowledging the intra-gendered adoption of NCS among marginalized farming households; not only protects against maladaptation but also improves local-level resilience and climate risk management in Ghana.
KAT8 compound inhibition inhibits the initial steps of PINK1-dependant mitophagy
Authors: de Talhouët Capucine , Esteras Noemi , Soutar Marc P. M. , O’Callaghan Benjamin , Plun-Favreau Helene 
Published: May 2024

AbstractIt has recently been shown that KAT8, a genome-wide association study candidate risk gene for Parkinson’s Disease, is involved in PINK1/Parkin-dependant mitophagy. The KAT8 gene encodes a lysine acetyltransferase and represents the catalytically active subunit of the non-specific lethal epigenetic remodelling complex. In the current study, we show that contrary to KAT5 inhibition, dual inhibition of KAT5 and KAT8 via the MG149 compound inhibits the initial steps of the PINK1-dependant mitophagy process. More specifically, our study shows that following mitochondrial depolarisation induced by mitochondrial toxins, MG149 treatment inhibits PINK1-dependant mitophagy initiation by impairing PINK1 activation, and subsequent phosphorylation of Parkin and ubiquitin. While this inhibitory effect of MG149 on PINK1-activation is potent, MG149 treatment in the absence of mitochondrial toxins is sufficient to depolarise the mitochondrial membrane, recruit PINK1 and promote partial downstream recruitment of the autophagy receptor p62, leading to an increase in mitochondrial delivery to the lysosomes. Altogether, our study provides additional support for KAT8 as a regulator of mitophagy and autophagy processes.