bluuebunny/crossref_metadata_2025_split huggingface dataset:
Byrd Ice Core Debris Constrains the Sediment Provenance Signature of Central West Antarctica
Authors: Marschalek J. W. , Blard P.‐H. , Sarigulyan E. , Ehrmann W. , Hemming S. R. , Thomson S. N. , Hillenbrand C.‐D. , Licht K. , Tison J.‐L. , Ardoin L. , Fripiat F. , Allen C. S. , Marrocchi Y. , Siegert M. J. , van de Flierdt T. 
Published: March 2024

AbstractProvenance records from sediments deposited offshore of the West Antarctic Ice Sheet (WAIS) can help identify past major ice retreat, thus constraining ice‐sheet models projecting future sea‐level rise. Interpretations from such records are, however, hampered by the ice obscuring Antarctica's geology. Here, we explore central West Antarctica's subglacial geology using basal debris from within the Byrd ice core, drilled to the bed in 1968. Sand grain microtextures and a high kaolinite content (∼38–42%) reveal the debris consists predominantly of eroded sedimentary detritus, likely deposited initially in a warm, pre‐Oligocene, subaerial environment. Detrital hornblende 40Ar/39Ar ages suggest proximal late Cenozoic subglacial volcanism. The debris has a distinct provenance signature, with: common Permian‐Early Jurassic mineral grains; absent early Ross Orogeny grains; a high kaolinite content; and high 143Nd/144Nd and low 87Sr/86Sr ratios. Detecting this “fingerprint” in Antarctic sedimentary records could imply major WAIS retreat, revealing the WAIS's sensitivity to future warming.
CS2 Cycling in Seawater: Dark Production and UV Light Driven Consumption
Authors: Lennartz S. T. , Simon H. , Booge D. , Zhou L. , Marandino C. 
Published: March 2024

AbstractCarbon disulfide (CS2) has recently gained attention as an important precursor for the atmospheric trace gas carbonyl sulfide (OCS), which delivers sulfur to the stratospheric sulfur layer and impacts the radiative budget of the Earth. CS2 is naturally produced in the ocean and emitted to the atmosphere. However, the magnitude of its marine emissions is only poorly constrained due to lacking understanding of its production and consumption processes. Here, we present incubation experiments with and without UV light treatment and provide evidence for a previously not considered UV‐light‐driven degradation process of CS2 in seawater, following first‐order kinetics. In addition to its already known photochemical production process, CS2 production is found in the dark, depending on the amount of dissolved organic sulfur present in seawater. We provide novel production and consumption rates of CS2 in seawater that pave the way toward mechanistically quantifying marine emissions of this important trace gas.
Particulate Nitrate Photolysis as a Possible Driver of Rising Tropospheric Ozone
Authors: Shah Viral , Keller Christoph A. , Knowland K. Emma , Christiansen Amy , Hu Lu , Wang Haolin , Lu Xiao , Alexander Becky , Jacob Daniel J. 
Published: March 2024

AbstractTropospheric ozone is an air pollutant and a greenhouse gas whose anthropogenic production is limited principally by the supply of nitrogen oxides (NOx) from combustion. Tropospheric ozone in the northern hemisphere has been rising despite the flattening of NOx emissions in recent decades. Here we propose that this sustained increase could result from the photolysis of nitrate particles (pNO3−) to regenerate NOx. Including pNO3− photolysis in the GEOS‐Chem atmospheric chemistry model improves the consistency with ozone observations. Our simulations show that pNO3− concentrations have increased since the 1960s because of rising ammonia and falling SO2 emissions, augmenting the increase in ozone in the northern extratropics by about 50% to better match the observed ozone trend. pNO3− will likely continue to increase through 2050, which would drive a continued increase in ozone even as NOx emissions decrease. More work is needed to better understand the mechanism and rates of pNO3− photolysis.
Surface Heat Fluxes Drive a Two‐Phase Response in Southern Ocean Mode Water Stratification
Authors: Pimm Ciara , Williams Richard G. , Jones Dani , Meijers Andrew J. S. 
Published: March 2024

AbstractSubantarctic mode waters have low stratification and are formed through subduction from thick winter mixed layers in the Southern Ocean. To investigate how surface forcing affects the stratification in mode water formation regions in the Southern Ocean, a set of adjoint sensitivity experiments are conducted. The objective function is the annual‐average stratification over the mode water formation region, which is evaluated from potential temperature and salinity adjoint sensitivity experiments. The analysis of impacts, from the product of sensitivities and forcing variability, identifies the separate effects of the wind stress, heat flux, and freshwater flux, revealing that the dominant control on stratification is from surface heat fluxes, as well as a smaller effect from zonal wind stress. The adjoint sensitivities of stratification to surface heat flux reveal a surprising change in sign over 2 years lead time: surface cooling leads to the expected initial local decrease in stratification, but there is a delayed response leading to an increase in stratification. This delayed response in stratification involves effective atmospheric damping of the surface thermal contribution, so that eventually the oppositely‐signed advective haline contribution dominates. This two‐phase response of stratification is found to hold over mode water formation regions in the South Indian and Southeast Pacific sectors of the Southern Ocean, where there are strong advective flows linked to the Antarctic Circumpolar Current.
Surface Rupturing Earthquakes of the Greater Caucasus Frontal Thrusts, Azerbaijan
Authors: Pierce Ian , Guliyev Ibrahim , Yetirmishli Gurban , Muradov Rauf , Kazimova Sabina , Javanshir Rashid , De Pascale Gregory P. , Johnson Ben , Marshall Neill , Walker Richard , Wordsworth Paul 
Published: March 2024

AbstractHere we present the results of the first paleoseismic study of the Kura fold‐thrust belt in Azerbaijan based on field mapping, fault trenching, and Quaternary dating. Convergence at rates of ∼10 mm/yr between the Arabian and Eurasian Plates is largely accommodated by the Kura fold‐thrust belt which stretches between central Azerbaijan and Georgia along the southern front of the Greater Caucasus (45–48°E). Although destructive historic earthquakes are known here, little is known about the active faults responsible for these earthquakes. A paleoseismic trench was excavated across a 2‐m‐high fault scarp near Agsu revealing evidence of two surface rupturing earthquakes. Radiocarbon dating of the faulted sediments limits the earthquake timing to AD 1713–1895 and AD 1872–2003. Allowing for uncertainties in dating, the two events likely correspond to historical destructive M ∼ 7 earthquakes near Shamakhi, Azerbaijan in AD 1668 and 1902. A second trench 60 km west of Agsu was excavated near Goychay also revealing evidence of at least one event that occurred 334–118 BC. Holocene shortening and dip‐slip rates for the Kura fold‐thrust belt are ∼8.0 and 8.5 mm/yr, respectively, based on an uplifted strath terrace west of Agsu. The only known historical devastating (M > ∼7) earthquakes in the Kura region, west of Shamakhi, occurred in 1139 and possibly 1668. The lack of reported historical ruptures from the past 4–8 centuries in the Kura, in contrast with the numerous recorded destructive earthquakes in Shamakhi, suggests that the Kura fold‐thrust belt may have accumulated sufficient strain to produce a M > 7.7 earthquake.
Evidence for a Constant Slip Rate Over the Last ∼40 ka Along the Mt. Morrone Fault System in Central Apennines
Authors: Puliti I. , Benedetti L. , Pizzi A. , Fleury J. , Francescone M. , Guillou V. , Team Aster 
Published: March 2024

AbstractLocated in the easternmost portion of the Central Apennines, the Mt. Morrone normal fault system is one of the highest seismic hazards in Italy. Previous geological and geomorphological observations revealed the presence of a ∼22 km‐long NW‐SE right‐lateral en echelon fault system made of two parallel faults affecting Quaternary deposits. Our analysis focused on the westernmost fault, which bounds the Sulmona Basin. Cumulative offsets were identified and quantified using high‐resolution Digital Elevation Models derived from LiDAR, Satellite Pleiades images, and drone acquisition at the three sites. Morphological markers displaced from a few to tens of meters were dated using 36Cl exposure dating. The results would be suggesting a fault slip rate of 0.2–0.4 mm/a. The deformed markers that dated at 36–44 ka consist of alluvial terraces emplaced by the main streams flowing down from Mt. Morrone to the Sulmona Basin, subsequently incised, and preserved when the fluvial base level dropped because of the former Sulmona lake fluctuations. The yielded ages for these markers fit well with the last major aggradational event associated with the 35–40 ka Heinrich event described and dated to other fluvial basins in the Apennines. Furthermore, the estimated rate agrees with the values obtained in previous studies over shorter and longer periods (105−6 years) and within similar uncertainties. This might then suggest that the period recovered by this study encompasses the entire seismic cycle.
Childbirth rates in women with myeloproliferative neoplasms
Authors: Landtblom Anna Ravn , Andersson Therese M-L , Johansson Anna L. V. , Lundberg Frida E. , Samuelsson Jan , Björkholm Magnus , Hultcrantz Malin 
Published: March 2024

AbstractMyeloproliferative neoplasms (MPN) are associated with inferior pregnancy outcome, however, little is known about fertility and childbearing potential in women with MPN. In this study we aimed to describe reproductive patterns, as well as to quantify risk of miscarriage and stillbirth. Women aged 15–44 years with an MPN diagnosis 1973–2018, were identified in Swedish health care registers, and age-matched 1:4 to population controls. We identified 1141 women with MPN and 4564 controls. Women with MPN had a lower rate of childbirth (hazard ratio [HR] with 95% confidence interval was 0.78 (0.68–0.90)). Subgroup analysis showed that the rate was not significantly reduced in essential thrombocythemia, HR 1.02 (0.86–1.22) while the HR was 0.50 (0.33–0.76) in PV and 0.45 (0.28–0.74) in PMF. The risk of miscarriage was not significantly increased before MPN diagnosis, the HR during follow-up after diagnosis was 1.25 (0.89-1.76). Women with MPN were more likely to have had a previous stillbirth. Women with MPN had fewer children at diagnosis, and fewer children in total. In conclusion, the childbirth rate was lower among women with MPN than controls, but not among women with essential thrombocythemia.
Effect of serum concentrations of IL-6 and TNF-α on brain structure in anorexia nervosa: a combined cross-sectional and longitudinal study
Authors: Bernardoni Fabio , Tam Friederike , Poitz David M. , Hellerhoff Inger , Arold Dominic , Geisler Daniel , Lemme Frances , Keeler Johanna , Weidner Kerstin , Pariante Carmine , Roessner Veit , King Joseph A. , Ehrlich Stefan 
Published: March 2024

AbstractPrevious studies of brain structure in anorexia nervosa (AN) have reported reduced gray matter in underweight patients, which largely normalizes upon weight gain. One underlying biological mechanism may be glial cell alterations related to low-grade inflammation. Here, we investigated relationships between brain structure as measured by magnetic resonance imaging and serum concentrations of two pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor alpha) cross-sectionally in 82 underweight adolescent and young adult female patients (mean age 16.8 years; 59 of whom were observed longitudinally after short-term weight restoration; mean duration 2.8 months), 20 individuals long-term weight-recovered from AN (mean age 22.7 years) and 105 healthy control (HC) participants (mean age 17.2 years). We measured cortical thickness, subcortical volumes and local gyrification index, a measure of cortical folding. In contrast to most previous studies of cytokine concentrations in AN, we found no cross-sectional group differences (interleukin-6: p = 0.193, tumor necrosis factor alpha: p = 0.057) or longitudinal changes following weight restoration (interleukin-6: p = 0.201, tumor necrosis factor alpha: p = 0.772). As expected, widespread gray matter reductions (cortical thickness, subcortical volumes, cortical folding) were observed in underweight patients with AN compared to HC. However, we found no evidence of associations between cytokine concentrations and structural brain measures in any participant group. Furthermore, longitudinal changes in cytokine concentrations were unrelated to changes in gray matter. In conclusion, we did not identify any association between (sub-)inflammatory processes and structural brain changes in AN. Future studies are needed to elucidate which other factors besides nutritional status may contribute to brain morphological alterations.
Tet methylcytosine dioxygenase 2 (TET2) deficiency elicits EGFR-TKI (tyrosine kinase inhibitors) resistance in non-small cell lung cancer
Authors: Zhang Jian , Zhao Kejia , Zhou Wenjing , Kang Ran , Wei Shiyou , Shu Yueli , Yu Cheng , Ku Yin , Mao Yonghong , Luo Hao , Yang Juqin , Mei Jiandong , Pu Qiang , Deng Senyi , Zha Zhengyu , Yuan Gang , Shen Shensi , Chen Yaohui , Liu Lunxu 
Published: March 2024

AbstractDespite epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKI) have shown remarkable efficacy in patients with EGFR-mutant non-small cell lung cancer (NSCLC), acquired resistance inevitably develops, limiting clinical efficacy. We found that TET2 was poly-ubiquitinated by E3 ligase CUL7FBXW11 and degraded in EGFR-TKI resistant NSCLC cells. Genetic perturbation of TET2 rendered parental cells more tolerant to TKI treatment. TET2 was stabilized by MEK1 phosphorylation at Ser 1107, while MEK1 inactivation promoted its proteasome degradation by enhancing the recruitment of CUL7FBXW11. Loss of TET2 resulted in the upregulation of TNF/NF-κB signaling that confers the EGFR-TKI resistance. Genetic or pharmacological inhibition of NF-κB attenuate the TKI resistance both in vitro and in vivo. Our findings exemplified how a cell growth controlling kinase MEK1 leveraged the epigenetic homeostasis by regulating TET2, and demonstrated an alternative path of non-mutational acquired EGFR-TKI resistance modulated by TET2 deficiency. Therefore, combined strategy exploiting EGFR-TKI and inhibitors of TET2/NF-κB axis holds therapeutic potential for treating NSCLC patients who suffered from this resistance.
Machine learning and the prediction of suicide in psychiatric populations: a systematic review
Authors: Pigoni Alessandro , Delvecchio Giuseppe , Turtulici Nunzio , Madonna Domenico , Pietrini Pietro , Cecchetti Luca , Brambilla Paolo 
Published: March 2024

AbstractMachine learning (ML) has emerged as a promising tool to enhance suicidal prediction. However, as many large-sample studies mixed psychiatric and non-psychiatric populations, a formal psychiatric diagnosis emerged as a strong predictor of suicidal risk, overshadowing more subtle risk factors specific to distinct populations. To overcome this limitation, we conducted a systematic review of ML studies evaluating suicidal behaviors exclusively in psychiatric clinical populations. A systematic literature search was performed from inception through November 17, 2022 on PubMed, EMBASE, and Scopus following the PRISMA guidelines. Original research using ML techniques to assess the risk of suicide or predict suicide attempts in the psychiatric population were included. An assessment for bias risk was performed using the transparent reporting of a multivariable prediction model for individual prognosis or diagnosis (TRIPOD) guidelines. About 1032 studies were retrieved, and 81 satisfied the inclusion criteria and were included for qualitative synthesis. Clinical and demographic features were the most frequently employed and random forest, support vector machine, and convolutional neural network performed better in terms of accuracy than other algorithms when directly compared. Despite heterogeneity in procedures, most studies reported an accuracy of 70% or greater based on features such as previous attempts, severity of the disorder, and pharmacological treatments. Although the evidence reported is promising, ML algorithms for suicidal prediction still present limitations, including the lack of neurobiological and imaging data and the lack of external validation samples. Overcoming these issues may lead to the development of models to adopt in clinical practice. Further research is warranted to boost a field that holds the potential to critically impact suicide mortality.
Cannabinoids induce cell death in leukaemic cells through Parthanatos and PARP-related metabolic disruptions
Authors: Medrano M. , Contreras M. , Caballero-Velázquez T. , Martínez L. , Bejarano-García J. A. , Calderón-Ruiz R. , García-Calderón C. B. , Rosado I. V. , Pérez-Simón J. A. 
Published: March 2024

Abstract
Background
Several studies have described a potential anti-tumour effect of cannabinoids (CNB). CNB receptor 2 (CB2) is mostly present in hematopoietic stem cells (HSC). The present study evaluates the anti-leukaemic effect of CNB.

Methods
Cell lines and primary cells from acute myeloid leukaemia (AML) patients were used and the effect of the CNB derivative WIN-55 was evaluated in vitro, ex vivo and in vivo.

Results
We demonstrate a potent antileukemic effect of WIN-55 which is abolished with CB antagonists. WIN-treated mice, xenografted with AML cells, had better survival as compared to vehicle or cytarabine. DNA damage-related genes were affected upon exposure to WIN. Co-incubation with the PARP inhibitor Olaparib prevented WIN-induced cell death, suggesting PARP-mediated apoptosis which was further confirmed with the translocation of AIF to the nucleus observed in WIN-treated cells. Nicotinamide prevented WIN-related apoptosis, indicating NAD+ depletion. Finally, WIN altered glycolytic enzymes levels as well as the activity of G6PDH. These effects are reversed through PARP1 inhibition.

Conclusions
WIN-55 exerts an antileukemic effect through Parthanatos, leading to translocation of AIF to the nucleus and depletion of NAD+, which are reversed through PARP1 inhibition. It also induces metabolic disruptions. These effects are not observed in normal HSC.
Deficiency of skeletal muscle Agrin contributes to the pathogenesis of age-related sarcopenia in mice
Authors: Chen Jie , Chen Hong , Dong Xia , Hui Tiankun , Yan Min , Ren Dongyan , Zou Suqi , Wang Shunqi , Fei Erkang , Zhang Wenhua , Lai Xinsheng 
Published: March 2024

AbstractSarcopenia, a progressive and prevalent neuromuscular disorder, is characterized by age-related muscle wasting and weakening. Despite its widespread occurrence, the molecular underpinnings of this disease remain poorly understood. Herein, we report that levels of Agrin, an extracellular matrix (ECM) protein critical for neuromuscular formation, were decreased with age in the skeletal muscles of mice. The conditional loss of Agrin in myogenic progenitors and satellite cells (SCs) (Pax7 Cre:: Agrin flox/flox) causes premature muscle aging, manifesting a distinct sarcopenic phenotype in mice. Conversely, the elevation of a miniaturized form of Agrin in skeletal muscle through adenovirus-mediated gene transfer induces enhanced muscle capacity in aged mice. Mechanistic investigations suggest that Agrin-mediated improvement in muscle function occurs through the stimulation of Yap signaling and the concurrent upregulation of dystroglycan expression. Collectively, our findings underscore the pivotal role of Agrin in the aging process of skeletal muscles and propose Agrin as a potential therapeutic target for addressing sarcopenia.
Identification of the growth cone as a probe and driver of neuronal migration in the injured brain
Authors: Nakajima Chikako , Sawada Masato , Umeda Erika , Takagi Yuma , Nakashima Norihiko , Kuboyama Kazuya , Kaneko Naoko , Yamamoto Satoaki , Nakamura Haruno , Shimada Naoki , Nakamura Koichiro , Matsuno Kumiko , Uesugi Shoji , Vepřek Nynke A. , Küllmer Florian , Nasufović Veselin , Uchiyama Hironobu , Nakada Masaru , Otsuka Yuji , Ito Yasuyuki , Herranz-Pérez Vicente , García-Verdugo José Manuel , Ohno Nobuhiko , Arndt Hans-Dieter , Trauner Dirk , Tabata Yasuhiko , Igarashi Michihiro , Sawamoto Kazunobu 
Published: March 2024

AbstractAxonal growth cones mediate axonal guidance and growth regulation. We show that migrating neurons in mice possess a growth cone at the tip of their leading process, similar to that of axons, in terms of the cytoskeletal dynamics and functional responsivity through protein tyrosine phosphatase receptor type sigma (PTPσ). Migrating-neuron growth cones respond to chondroitin sulfate (CS) through PTPσ and collapse, which leads to inhibition of neuronal migration. In the presence of CS, the growth cones can revert to their extended morphology when their leading filopodia interact with heparan sulfate (HS), thus re-enabling neuronal migration. Implantation of an HS-containing biomaterial in the CS-rich injured cortex promotes the extension of the growth cone and improve the migration and regeneration of neurons, thereby enabling functional recovery. Thus, the growth cone of migrating neurons is responsive to extracellular environments and acts as a primary regulator of neuronal migration.
FUS unveiled in mitochondrial DNA repair and targeted ligase-1 expression rescues repair-defects in FUS-linked motor neuron disease
Authors: Kodavati Manohar , Wang Haibo , Guo Wenting , Mitra Joy , Hegde Pavana M. , Provasek Vincent , Rao Vikas H. Maloji , Vedula Indira , Zhang Aijun , Mitra Sankar , Tomkinson Alan E. , Hamilton Dale J. , Van Den Bosch Ludo , Hegde Muralidhar L. 
Published: March 2024

AbstractThis study establishes the physiological role of Fused in Sarcoma (FUS) in mitochondrial DNA (mtDNA) repair and highlights its implications to the pathogenesis of FUS-associated neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS). Endogenous FUS interacts with and recruits mtDNA Ligase IIIα (mtLig3) to DNA damage sites within mitochondria, a relationship essential for maintaining mtDNA repair and integrity in healthy cells. Using ALS patient-derived FUS mutant cell lines, a transgenic mouse model, and human autopsy samples, we discovered that compromised FUS functionality hinders mtLig3’s repair role, resulting in increased mtDNA damage and mutations. These alterations cause various manifestations of mitochondrial dysfunction, particularly under stress conditions relevant to disease pathology. Importantly, rectifying FUS mutations in patient-derived induced pluripotent cells (iPSCs) preserves mtDNA integrity. Similarly, targeted introduction of human DNA Ligase 1 restores repair mechanisms and mitochondrial activity in FUS mutant cells, suggesting a potential therapeutic approach. Our findings unveil FUS’s critical role in mitochondrial health and mtDNA repair, offering valuable insights into the mechanisms underlying mitochondrial dysfunction in FUS-associated motor neuron disease.