bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Role of Coastal Yedoma Deposits and Continental Shelf Sediments in the Arctic Ocean Silicon Cycle
Authors: Ray Nicholas E. , Martens Jannik , Ajmar Marco , Tesi Tommaso , Yakushev Evgeniy , Gangnus Ivan , Strauss Jens , Schirrmeister Lutz , Semiletov Igor , Wild Birgit 
Published: January 2024

AbstractThe availability of silicon (Si) in the ocean plays an important role in regulating biogeochemical and ecological processes. The Si budget of the Arctic Ocean appears balanced, with inputs equivalent to outputs, though it is unclear how a changing climate might aggravate this balance. In this study, we focus on Si cycling in Arctic coastal areas and continental shelf sediments to better constrain the Arctic Ocean Si budget. We provide the first estimate of amorphous Si (ASi) loading from erosion of coastal Yedoma deposits (30–90 Gmol yr−1), demonstrating comparable rates to particulate Si loading from rivers (10–90 Gmol yr−1). We found a positive relationship between surface sediment ASi and organic matter content on continental shelves. Combining these values with published Arctic shelf sediment properties and burial rates we estimate 70 Gmol Si yr−1 is buried on Arctic continental shelves, equivalent to 4.5% of all Si inputs to the Arctic Ocean. Sediment dissolved Si fluxes increased with distance from river mouths along cruise transects of shelf regions influenced by major rivers in the Laptev and East Siberian seas. On an annual basis, we estimate that Arctic shelf sediments recycle approximately up to twice as much DSi (680 Gmol Si) as is loaded from rivers (340–500 Gmol Si).
Apportionment and Inventory Optimization of Agriculture and Energy Sector Methane Emissions Using Multi‐Month Trace Gas Measurements in Northern Colorado
Authors: Mead Griffin J. , Herman Daniel I. , Giorgetta Fabrizio R. , Malarich Nathan A. , Baumann Esther , Washburn Brian R. , Newbury Nathan R. , Coddington Ian , Cossel Kevin C. 
Published: January 2024

AbstractQuantifying sector‐resolved methane fluxes in complex emissions environments is challenging yet necessary to improve emissions inventories and guide policy. Here, we separate energy and agriculture sector emissions using a dynamic linear model analysis of methane, ethane, and ammonia data measured at a Northern Colorado site from November 2021 to January 2022. By combining these sector‐apportioned observations with spatially resolved inventories and Bayesian inverse methods, energy and agriculture methane fluxes are optimized across the study's ∼850 km2 sensitivity area. Energy sector fluxes are synthesized with previous literature to evaluate trends in energy sector methane emissions. Optimized agriculture fluxes in the study area were 3.5× larger than inventory estimates; we demonstrate this discrepancy is consistent with differences in the modeled versus real‐world spatial distribution of agricultural sources. These results highlight how sector‐apportioned methane observations can yield multi‐sector inventory optimizations in complex environments.
A Novel Backtracing Model to Study the Emission of Energetic Neutral Atoms at Titan
Authors: Tippens Tyler , Roussos Elias , Simon Sven , Liuzzo Lucas 
Published: January 2024

AbstractTo study the emission of energetic neutral atoms (ENAs) at Titan, we have developed a novel model that takes into account a spacecraft detector's limited field of view and traces energetic magnetospheric particles backward in time. ENAs are generated by charge exchange between Titan's atmospheric neutrals and energetic magnetospheric ions. By tracing these ions through the draped electromagnetic fields in Titan's environment, we generate synthetic ENA images and compare them to Cassini observations from the TA flyby. Our model can reproduce the intensity and morphology of the observed images only when field line draping is included. Using a realistic detector geometry is necessary to determine the influence of this draping on the ENA images: the non‐uniform fields eliminate a localized feature of increased ENA flux, which is a different effect than in models utilizing an infinitely extended detector. We demonstrate that ENA observations from TA contain signatures of the time‐varying Saturnian magnetospheric environment at Titan: the modeled ENA emission morphology and the effect of field line draping are different for the background field vectors measured during the inbound and outbound legs of TA. The visibility and qualitative effect of the draping on observed ENA images vary strongly between different detector locations and pointings. Depending on the viewing geometry, field line draping may add segments of elevated flux to the synthetic ENA images, remove such segments, or have no qualitative effect at all. Our study emphasizes the challenges and the potential for remote sensing of Titan's interaction region using ENA imaging.
PRKCSH contributes to TNFSF resistance by extending IGF1R half-life and activation in lung cancer
Authors: Shin Gu-Choul , Lee Hyeong Min , Kim Nayeon , Seo Sang-Uk , Kim Kwang Pyo , Kim Kyun-Hwan 
Published: January 2024

AbstractTumor necrosis factor superfamily (TNFSF) resistance contributes to the development and progression of tumors and resistance to various cancer therapies. Tumor-intrinsic alterations involved in the adaptation to the TNFSF response remain largely unknown. Here, we demonstrate that protein kinase C substrate 80K-H (PRKCSH) abundance in lung cancers boosts oncogenic IGF1R activation, leading to TNFSF resistance. PRKCSH abundance is correlated with IGF1R upregulation in lung cancer tissues. Specifically, PRKCSH interacts with IGF1R and extends its half-life. The PRKCSH-IGF1R axis in tumor cells impairs caspase-8 activation, increases Mcl-1 expression, and inhibits caspase-9, leading to an imbalance between cell death and survival. PRKCSH deficiency augmented the antitumor effects of natural killer (NK) cells, representative TNFSF effector cells, in a tumor xenograft IL-2Rg-deficient NOD/SCID (NIG) mouse model. Our data suggest that PRKCSH plays a critical role in TNFSF resistance and may be a potential target to improve the efficacy of NK cell-based cancer therapy.
Effects of fine particulate matter on bone marrow-conserved hematopoietic and mesenchymal stem cells: a systematic review
Authors: Bhattarai Govinda , Shrestha Saroj Kumar , Sim Hyun-Jaung , Lee Jeong-Chae , Kook Sung-Ho 
Published: January 2024

AbstractThe harmful effects of fine particulate matter ≤2.5 µm in size (PM2.5) on human health have received considerable attention. However, while the impact of PM2.5 on the respiratory and cardiovascular systems has been well studied, less is known about the effects on stem cells in the bone marrow (BM). With an emphasis on the invasive characteristics of PM2.5, this review examines the current knowledge of the health effects of PM2.5 exposure on BM-residing stem cells. Recent studies have shown that PM2.5 enters the circulation and then travels to distant organs, including the BM, to induce oxidative stress, systemic inflammation and epigenetic changes, resulting in the reduction of BM-residing stem cell survival and function. Understanding the broader health effects of air pollution thus requires an understanding of the invasive characteristics of PM2.5 and its direct influence on stem cells in the BM. As noted in this review, further studies are needed to elucidate the underlying processes by which PM2.5 disturbs the BM microenvironment and inhibits stem cell functionality. Strategies to prevent or ameliorate the negative effects of PM2.5 exposure on BM-residing stem cells and to maintain the regenerative capacity of those cells must also be investigated. By focusing on the complex relationship between PM2.5 and BM-resident stem cells, this review highlights the importance of specific measures directed at safeguarding human health in the face of rising air pollution.
Maintaining Drosha expression with Cdk5 inhibitors as a potential therapeutic strategy for early intervention after TBI
Authors: Huang Lu , Xia Li , Nie Tiejian , Cui Bozhou , Lu Jianjun , Lu Fangfang , Fan Feiyan , Ren Dongni , Lu Yuan , Gao Guodong , Yang Qian 
Published: January 2024

AbstractTraumatic brain injury (TBI) is a major cause of death and disability in adults. The pathological process of TBI involves a multifactorial cascade in which kinases have been proven contribute to interactions between relevant factors and amplification of signaling cascades. Cyclin-dependent kinase 5 (Cdk5) is a promising kinase that has been implicated in various brain disorders, including TBI. However, the mechanism by which Cdk5 induces neuronal damage remains unclear. Here, we show for the first time that Drosha, a key enzyme in microRNA biogenesis, is a pivotal substrate of abnormally activated Cdk5. Cdk5-mediated phosphorylation decreases Drosha expression and exacerbates nerve injury in TBI. We proved that maintaining Drosha expression via the administration of repurposed Cdk5 inhibitors that were previously studied in clinical trials is a promising approach for the early treatment of TBI. Together, our work identifies Drosha as a novel target for neuroprotective strategies after TBI and suggests Cdk5-mediated regulation of Drosha expression as a potential therapeutic strategy for early TBI intervention.
Mapping gray and white matter volume abnormalities in early-onset psychosis: an ENIGMA multicenter voxel-based morphometry study
Authors: Si Shuqing , Bi Anbreen , Yu Zhaoying , See Cheryl , Kelly Sinead , Ambrogi Sonia , Arango Celso , Baeza Inmaculada , Banaj Nerisa , Berk Michael , Castro-Fornieles Josefina , Crespo-Facorro Benedicto , Crouse Jacob J. , Díaz-Caneja Covadonga M. , Fett Anne-Kathrin , Fortea Adriana , Frangou Sophia , Goldstein Benjamin I. , Hickie Ian B. , Janssen Joost , Kennedy Kody G. , Krabbendam Lydia , Kyriakopoulos Marinos , MacIntosh Bradley J. , Morgado Pedro , Nerland Stener , Pascual-Diaz Saül , Picó-Pérez Maria , Piras Fabrizio , Rund Bjørn Rishovd , de la Serna Elena , Spalletta Gianfranco , Sugranyes Gisela , Suo Chao , Tordesillas-Gutiérrez Diana , Vecchio Daniela , Radua Joaquim , McGuire Philip , Thomopoulos Sophia I. , Jahanshad Neda , Thompson Paul M. , Barth Claudia , Agartz Ingrid , James Anthony , Kempton Matthew J. 
Published: January 2024

Abstract
Introduction
Regional gray matter (GM) alterations have been reported in early-onset psychosis (EOP, onset before age 18), but previous studies have yielded conflicting results, likely due to small sample sizes and the different brain regions examined. In this study, we conducted a whole brain voxel-based morphometry (VBM) analysis in a large sample of individuals with EOP, using the newly developed ENIGMA-VBM tool.

Methods
15 independent cohorts from the ENIGMA-EOP working group participated in the study. The overall sample comprised T1-weighted MRI data from 482 individuals with EOP and 469 healthy controls. Each site performed the VBM analysis locally using the standardized ENIGMA-VBM tool. Statistical parametric T-maps were generated from each cohort and meta-analyzed to reveal voxel-wise differences between EOP and healthy controls as well as the individual-based association between GM volume and age of onset, chlorpromazine (CPZ) equivalent dose, and other clinical variables.

Results
Compared with healthy controls, individuals with EOP showed widespread lower GM volume encompassing most of the cortex, with the most marked effect in the left median cingulate (Hedges’ g = 0.55, p = 0.001 corrected), as well as small clusters of lower white matter (WM), whereas no regional GM or WM volumes were higher in EOP. Lower GM volume in the cerebellum, thalamus and left inferior parietal gyrus was associated with older age of onset. Deficits in GM in the left inferior frontal gyrus, right insula, right precentral gyrus and right superior frontal gyrus were also associated with higher CPZ equivalent doses.

Conclusion
EOP is associated with widespread reductions in cortical GM volume, while WM is affected to a smaller extent. GM volume alterations are associated with age of onset and CPZ equivalent dose but these effects are small compared to case-control differences. Mapping anatomical abnormalities in EOP may lead to a better understanding of the role of psychosis in brain development during childhood and adolescence.
Targeting suicidal ideation in major depressive disorder with MRI-navigated Stanford accelerated intelligent neuromodulation therapy
Authors: Li Baojuan , Zhao Na , Tang Nailong , Friston Karl J. , Zhai Wensheng , Wu Di , Liu Junchang , Chen Yihuan , Min Yan , Qiao Yuting , Liu Wenming , Shu Wanqing , Liu Min , Zhou Ping , Guo Li , Qi Shun , Cui Long-Biao , Wang Huaning 
Published: January 2024

AbstractHigh suicide risk represents a serious problem in patients with major depressive disorder (MDD), yet treatment options that could safely and rapidly ameliorate suicidal ideation remain elusive. Here, we tested the feasibility and preliminary efficacy of the Stanford Accelerated Intelligent Neuromodulation Therapy (SAINT) in reducing suicidal ideation in patients with MDD. Thirty-two MDD patients with moderate to severe suicidal ideation participated in the current study. Suicidal ideation and depression symptoms were assessed before and after 5 days of open-label SAINT. The neural pathways supporting rapid-acting antidepressant and suicide prevention effects were identified with dynamic causal modelling based on resting-state functional magnetic resonance imaging. We found that 5 days of SAINT effectively alleviated suicidal ideation in patients with MDD with a high response rate of 65.63%. Moreover, the response rates achieved 78.13% and 90.63% with 2 weeks and 4 weeks after SAINT, respectively. In addition, we found that the suicide prevention effects of SAINT were associated with the effective connectivity involving the insula and hippocampus, while the antidepressant effects were related to connections of the subgenual anterior cingulate cortex (sgACC). These results show that SAINT is a rapid-acting and effective way to reduce suicidal ideation. Our findings further suggest that distinct neural mechanisms may contribute to the rapid-acting effects on the relief of suicidal ideation and depression, respectively.
The LRR receptor-like kinase ALR1 is a plant aluminum ion sensor
Authors: Ding Zhong Jie , Xu Chen , Yan Jing Ying , Wang Yu Xuan , Cui Meng Qi , Yuan Jun Jie , Wang Ya Nan , Li Gui Xin , Wu Jian Xiang , Wu Yun Rong , Xu Ji Ming , Li Chun Xiao , Shi Yuan Zhi , Mao Chuan Zao , Guo Jiang Tao , Zhou Jian Min , Benhamed Moussa , Harberd Nicholas P. , Zheng Shao Jian 
Published: January 2024

AbstractPlant survival requires an ability to adapt to differing concentrations of nutrient and toxic soil ions, yet ion sensors and associated signaling pathways are mostly unknown. Aluminum (Al) ions are highly phytotoxic, and cause severe crop yield loss and forest decline on acidic soils which represent ∼30% of land areas worldwide. Here we found an Arabidopsis mutant hypersensitive to Al. The gene encoding a leucine-rich-repeat receptor-like kinase, was named Al Resistance1 (ALR1). Al ions binding to ALR1 cytoplasmic domain recruits BAK1 co-receptor kinase and promotes ALR1-dependent phosphorylation of the NADPH oxidase RbohD, thereby enhancing reactive oxygen species (ROS) generation. ROS in turn oxidatively modify the RAE1 F-box protein to inhibit RAE1-dependent proteolysis of the central regulator STOP1, thus activating organic acid anion secretion to detoxify Al. These findings establish ALR1 as an Al ion receptor that confers resistance through an integrated Al-triggered signaling pathway, providing novel insights into ion-sensing mechanisms in living organisms, and enabling future molecular breeding of acid-soil-tolerant crops and trees, with huge potential for enhancing both global food security and forest restoration.
Nuclear receptor coactivator 6 is a critical regulator of NLRP3 inflammasome activation and gouty arthritis
Authors: Lee Kang-Gu , Hong Bong-Ki , Lee Saseong , Lee Naeun , Kim Seung-Whan , Kim Donghyun , Kim Wan-Uk 
Published: January 2024

AbstractTranscriptional coactivators regulate the rate of gene expression in the nucleus. Nuclear receptor coactivator 6 (NCOA6), a coactivator, has been implicated in embryonic development, metabolism, and cancer pathogenesis, but its role in innate immunity and inflammatory diseases remains unclear. Here, we demonstrated that NCOA6 was expressed in monocytes and macrophages and that its level was increased under proinflammatory conditions. Unexpectedly, nuclear NCOA6 was found to translocate to the cytoplasm in activated monocytes and then become incorporated into the inflammasome with NLRP3 and ASC, forming cytoplasmic specks. Mechanistically, NCOA6 associated with the ATP hydrolysis motifs in the NACHT domain of NLRP3, promoting the oligomerization of NLRP3 and ASC and thereby instigating the production of IL-1β and active caspase-1. Of note, Ncoa6 deficiency markedly inhibited NLRP3 hyperactivation caused by the Nlrp3R258W gain-of-function mutation in macrophages. Genetic ablation of Ncoa6 substantially attenuated the severity of two NLRP3-dependent diseases, folic-induced acute tubular necrosis and crystal-induced arthritis, in mice. Consistent with these findings, NCOA6 was highly expressed in macrophages derived from gout patients, and NCOA6-positive macrophages were significantly enriched in gout macrophages according to the transcriptome profiling results. Conclusively, NCOA6 is a critical regulator of NLRP3 inflammasome activation and is therefore a promising target for NLRP3-dependent diseases, including gout.
Genome, HLA and polygenic risk score analyses for prevalent and persistent cervical human papillomavirus (HPV) infections
Authors: Adebamowo Sally N. , Adeyemo Adebowale , Adebayo Amos , Achara Peter , Alabi Bunmi , Bakare Rasheed A. , Famooto Ayotunde O. , Obende Kayode , Offiong Richard , Olaniyan Olayinka , Ologun Sanni , Rotimi Charles ,   ACCME Research Group as part of the H3Africa Consortium, Abdullahi Saurayya S. , Abdulsalam Maryam , Adebiyi Ruxton , Adekanmbi Victor , Adelekun Bukunmi , Adeyemo Segun , Akabueze Gerald , Akpobome Bernice , Akpomiemie Stella , Alabi Gabriel O. , Anichebe Chinyere , Anyanwu Claire , Ayogu Miriam C. , Bako Dorcas J. , Bamisaiye Patience , Blessing Nkechi U. , Chinye Osa A. , Dakum Patrick , Dareng Eileen , Dwana Grace , Erhunmwonsere Juliet I. , Eze Emelda O. , Fagbohun Tolani A. , Filade Temitope , Gbolahan Toluwalope , Anaedobe Gloria C. , Ibezim Stella , Iwaloye Racheal , James Jesse , Kehinde Dayo , Makinde Fiyinfoluwa , Mase Jessica , Mensah Charles , Nwoko Florence A. , Obende Kayode , Odonye George , Odubore Folake , Odunyemi Funmi , Odutola Michael , Oguama Uzoamaka , Oguoma Tochukwu , Oladimeji Temitayo , Olawande Toyosi , Olukomogbon Temitope , Oluwole Sefunmi , Omenuko Gladys , Onwuka Nkiruka , Owoade Yinka , Ugorji Thelma C. , Yohanna Syntyche , Yusuf Ibrahim , Adebamowo Clement A. 
Published: January 2024

AbstractGenetic variants that underlie susceptibility to cervical high-risk human papillomavirus (hrHPV) infections are largely unknown. We conducted discovery genome-wide association studies (GWAS), replication, meta-analysis and colocalization, generated polygenic risk scores (PRS) and examined the association of classical HLA alleles and cervical hrHPV infections in a cohort of over 10,000 women. We identified genome-wide significant variants for prevalent hrHPV around LDB2 and for persistent hrHPV near TPTE2, SMAD2, and CDH12, which code for proteins that are significantly expressed in the human endocervix. Genetic variants associated with persistent hrHPV are in genes enriched for the antigen processing and presentation gene set. HLA-DRB1*13:02, HLA-DQB1*05:02 and HLA-DRB1*03:01 were associated with increased risk, and HLA-DRB1*15:03 was associated with decreased risk of persistent hrHPV. The analyses of peptide binding predictions showed that HLA-DRB1 alleles that were positively associated with persistent hrHPV showed weaker binding with peptides derived from hrHPV proteins and vice versa. The PRS for persistent hrHPV with the best model fit, had a P-value threshold (PT) of 0.001 and a p-value of 0.06 (-log10(0.06) = 1.22). The findings of this study expand our understanding of genetic risk factors for hrHPV infection and persistence and highlight the roles of MHC class II molecules in hrHPV infection.
A simulation-based analysis of the impact of rhetorical citations in science
Authors: Bao Honglin , Teplitskiy Misha 
Published: January 2024

AbstractAuthors of scientific papers are usually encouraged to cite works that meaningfully influenced their research (substantive citations) and avoid citing works that had no meaningful influence (rhetorical citations). Rhetorical citations are assumed to degrade incentives for good work and benefit prominent papers and researchers. Here, we explore if rhetorical citations have some plausibly positive effects for science and disproportionately benefit the less prominent papers and researchers. We developed a set of agent-based models where agents can cite substantively and rhetorically. Agents first choose papers to read based on their expected quality, become influenced by those that are sufficiently good, and substantively cite them. Next, agents fill any remaining slots in their reference lists with rhetorical citations that support their narrative, regardless of whether they were actually influential. We then turned agents’ ability to cite rhetorically on-and-off to measure its effects. Enabling rhetorical citing increased the correlation between paper quality and citations, increased citation churn, and reduced citation inequality. This occurred because rhetorical citing redistributed some citations from a stable set of elite-quality papers to a more dynamic set with high-to-moderate quality and high rhetorical value. Increasing the size of reference lists, often seen as an undesirable trend, amplified the effects. Overall, rhetorical citing may help deconcentrate attention and make it easier to displace established ideas.
Epstein-Barr virus-driven B cell lymphoma mediated by a direct LMP1-TRAF6 complex
Authors: Giehler Fabian , Ostertag Michael S. , Sommermann Thomas , Weidl Daniel , Sterz Kai R. , Kutz Helmut , Moosmann Andreas , Feller Stephan M. , Geerlof Arie , Biesinger Brigitte , Popowicz Grzegorz M. , Kirchmair Johannes , Kieser Arnd 
Published: January 2024

AbstractEpstein-Barr virus (EBV) latent membrane protein 1 (LMP1) drives viral B cell transformation and oncogenesis. LMP1’s transforming activity depends on its C-terminal activation region 2 (CTAR2), which induces NF-κB and JNK by engaging TNF receptor-associated factor 6 (TRAF6). The mechanism of TRAF6 recruitment to LMP1 and its role in LMP1 signalling remains elusive. Here we demonstrate that TRAF6 interacts directly with a viral TRAF6 binding motif within CTAR2. Functional and NMR studies supported by molecular modeling provide insight into the architecture of the LMP1-TRAF6 complex, which differs from that of CD40-TRAF6. The direct recruitment of TRAF6 to LMP1 is essential for NF-κB activation by CTAR2 and the survival of LMP1-driven lymphoma. Disruption of the LMP1-TRAF6 complex by inhibitory peptides interferes with the survival of EBV-transformed B cells. In this work, we identify LMP1-TRAF6 as a critical virus-host interface and validate this interaction as a potential therapeutic target in EBV-associated cancer.