bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modernism, Nominalism, and the Hidden God in Samuel Beckett, Wallace Stevens, and David Jones
Authors: Tonning Erik 
Published: March 2023

Abstract
The idea that human language is an inherently inadequate instrument for grasping reality is widespread in modernist literature. While the ‘radical nominalism’ of this position has been recognised, this article argues that a genealogical understanding of its theological roots in medieval nominalism can highlight how modernist writers like Samuel Beckett and Wallace Stevens still wrestle with a voluntarist God of absolute and arbitrary power. By contrast, for a writer like David Jones, the historical choice of nominalism amounts to a theological mistake, and the modern artist needs to rediscover a God who consecrates and redeems the human capacity for sign-making.
Optical polarization and spectral properties of the hydrogen-poor superluminous supernovae SN 2021bnw and SN 2021fpl
Authors: Poidevin F , Omand C M B , Könyves-Tóth Réka , Pérez-Fournon I , Clavero R , Geier S , Jimenez Angel C , Marques-Chaves R , Shirley R 
Published: March 2023

ABSTRACTNew optical photometric, spectroscopic, and imaging polarimetry data are combined with publicly available data to study some of the physical properties of the two hydrogen-poor superluminous supernovae (SLSNe) SN 2021bnw and SN 2021fpl. For each SLSN, the best-fitting parameters obtained from the magnetar model with Modular Open-Source Fitter for Transients do not depart from the range of parameter obtained on other SLSNe discussed in the literature. A spectral analysis with SYN++ shows that SN 2021bnw is a W type, fast evolver, while SN 2021fpl is a 15bn type, slow evolver. The analysis of the polarimetry data obtained on SN 2021fpl at four epochs (+1.8, +20.6, +34.1, and +43.0 d, rest frame) shows &gt;3σ polarization detections in the range of 0.8–1 per cent. A comparison of the spectroscopy data suggests that SN 2021fpl underwent a spectral transition a bit earlier than SN 2015bn, during which, similarly, it could have underwent a polarization transition. The analysis of the polarimetry data obtained on SN 2021bnw does not show any departure from symmetry of the photosphere at an empirical diffusion time-scale of ≈2 (+81.1 d rest frame). This result is consistent with those on the sample of W-type SLSN observed at empirical diffusion time-scale ≤ 1 with that technique, even though it is not clear the effect of limited spectral windows varying from one object to the other. Measurements at higher empirical diffusion time-scale may be needed to see any departure from symmetry as it is discussed in the literature for SN 2017egm.
Estimating stellar parameters from LAMOST low-resolution spectra
Authors: Li Xiangru , Lin Boyu 
Published: March 2023

ABSTRACTThe Large Sky Area Multi-Object Fiber Spectroscopic Telescope (LAMOST) has acquired tens of millions of low-resolution spectra of stars. This paper investigates the parameter estimation problem for these spectra. To this end, we propose the deep learning model StarGRU network (StarGRUNet). This network is applied to estimate the stellar atmospheric physical parameters and 13 elemental abundances from LAMOST low-resolution spectra. On the spectra with signal-to-noise ratios greater than or equal to 5, the estimation precisions are 94 K and 0.16 dex on $T_\texttt {eff}$ and log  g respectively, 0.07 to 0.10 dex on [C/H], [Mg/H], [Al/H], [Si/H], [Ca/H], [Ni/H] and [Fe/H], 0.10 to 0.16 dex on [O/H], [S/H], [K/H], [Ti/H] and [Mn/H], and 0.18 and 0.22 dex on [N/H] and [Cr/H]. The model shows advantages over other available models and high consistency with high-resolution surveys. We released the estimated catalogue computed from about 8.21 million low-resolution spectra in LAMOST DR8, code, trained model, and experimental data for astronomical science exploration and data processing algorithm research.
Sterol regulatory element-binding protein 2 maintains glioblastoma stem cells by keeping the balance between cholesterol biosynthesis and uptake
Authors: Gu Danling , Zhou Fengqi , You Hao , Gao Jiancheng , Kang Tao , Dixit Deobrat , Wu Qiulian , Yang Kailin , Ci Shusheng , Shan Danyang , Fan Xiao , Yuan Wei , Zhang Qian , Lu Chenfei , Li Daqi , Zhao Ningwei , Shi Zhumei , Gao Wei , Lin Fan , Man Jianghong , Wang Qianghu , Qian Xu , Mack Stephen C , Tao Weiwei , Agnihotri Sameer , Zhang Nu , You Yongping , Rich Jeremy N , Zhang Junxia , Wang Xiuxing 
Published: March 2023

Abstract

Background
Glioblastomas (GBMs) display striking dysregulation of metabolism to promote tumor growth. Glioblastoma stem cells (GSCs) adapt to regions of heterogeneous nutrient availability, yet display dependency on de novo cholesterol biosynthesis. The transcription factor Sterol Regulatory Element-Binding Protein 2 (SREBP2) regulates cholesterol biosynthesis enzymes and uptake receptors. Here, we investigate adaptive behavior of GSCs under different cholesterol supplies.

Methods
In silico analysis of patient tumors demonstrated enrichment of cholesterol synthesis associated with decreased angiogenesis. Comparative gene expression of cholesterol biosynthesis enzymes in paired GBM specimens and GSCs were performed. In vitro and in vivo loss-of-function genetic and pharmacologic assays were conducted to evaluate the effect of SREBP2 on GBM cholesterol biosynthesis, proliferation, and self-renewal. Chromatin immunoprecipitation quantitative real-time PCR was leveraged to map the regulation of SREBP2 to cholesterol biosynthesis enzymes and uptake receptors in GSCs.

Results
Cholesterol biosynthetic enzymes were expressed at higher levels in GBM tumor cores than in invasive margins. SREBP2 promoted cholesterol biosynthesis in GSCs, especially under starvation, as well as proliferation, self-renewal, and tumor growth. SREBP2 governed the balance between cholesterol biosynthesis and uptake in different nutrient conditions.

Conclusions
SREBP2 displays context-specific regulation of cholesterol biology based on its availability in the microenvironment with induction of cholesterol biosynthesis in the tumor core and uptake in the margin, informing a novel treatment strategy for GBM.
Loss Aversion and Current, Former, and Never-Smoking Status
Authors: Thrailkill Eric A , DeSarno Michael , Higgins Stephen T 
Published: March 2023

Abstract

Introduction
Loss aversion (LA) is a bias in decision-making wherein potential losses have a greater influence on choices than equivalent gains. Such a bias may protect individuals from harm. Consistent with this idea, lower LA has been measured in individuals who endorse current cigarette smoking as well as other substance use compared to controls matched on important sociodemographic variables (age, gender, and educational attainment). The goal of the present study was to systematically replicate and extend this association between LA and smoking status by comparing those meeting criteria for current-, former-, and never-smoking status.

Aims and Methods
In total, 984 individuals (N = 984) that endorsed current cigarette smoking (past 30-day use; n = 361), former-smoking (no past 30-day use, &gt;100 cigarettes lifetime; n = 317), and never-smoking (no past 30-day use, &lt;100 cigarettes lifetime; n = 306) were recruited using standard crowdsourcing methods and completed measures of LA (50–50 gambles) and delay discounting (DD) (monetary choice questionnaire), an important decision-making bias with an established relationship to cigarette-smoking status.

Results
Lower LA was observed in those endorsing current smoking compared to former smoking (t[952] = −9.57, Bonferroni corrected p &lt; .0001), and never-smoking (t[952] = −3.99, Bonferroni corrected p = .0002). LA was also greater in former- compared to the never-smoking (t[952] = −5.26, Bonferroni corrected p &lt; .0001). This pattern did not change when accounting for DD and sociodemographics. DD results replicated prior findings.

Conclusions
The results support LA as a decision-making bias related to the risk of cigarette smoking and other substance use. Further research is needed to understand the causal contributions of LA and DD and their potential intersections.

Implications
Low LA is a risk factor for cigarette smoking. This study reports higher LA among individuals that endorsed never-smoking and former-smoking status in comparison to those endorsing current cigarette smoking. LA may influence or be influenced by a change in smoking status.
Impact of COVID-19 on Spanish mortality rates in 2020 by age and sex
Authors: Navarro Eliseo , Requena Pilar 
Published: March 2023

Abstract

Background
Previous studies have used different biometric indicators to measure the effect of Covid-19 on population mortality such as the number of deaths or the decrease of life expectancy showing a dependence of mortality on age and sex. According to them, the impact of the pandemic was greater on women than in men and that the older the population, the greater the number of deaths caused by Covid-19.

Methods
We apply graduation techniques and non-parametric methods to estimate mortality rates allowing us to obtain an age-by-age picture of changes in mortality rates from 2018–2019 to 2020.

Results
Graduation techniques have detected a significant U-shaped reduction in infant mortality rates although with an anomalous peak in girls aged 10–12. Likewise, we have observed a notable increase in mortality rates of the female population between 28 and 40 years of age. The increase of mortality rates after the age of 70 years was similar for both men and women with a slight decline after the age of 80.

Conclusions
The use of graduation techniques and the focus on age-by-age changes in mortality rates showed a complex behaviour in some tranches of the mortality curve that might otherwise have gone unnoticed.
Socioenvironmental Adversity and Adolescent Psychotic Experiences: Exploring Potential Mechanisms in a UK Longitudinal Cohort
Authors: Newbury Joanne B , Arseneault Louise , Moffitt Terrie E , Odgers Candice L , Howe Laura D , Bakolis Ioannis , Reuben Aaron , Danese Andrea , Sugden Karen , Williams Benjamin , Rasmussen Line J H , Trotta Antonella , Ambler Antony P , Fisher Helen L 
Published: March 2023

Abstract

Background and Hypothesis
Children exposed to socioenvironmental adversities (eg, urbanicity, pollution, neighborhood deprivation, crime, and family disadvantage) are more likely to subsequently develop subclinical psychotic experiences during adolescence (eg, hearing voices, paranoia). However, the pathways through which this occurs have not been previously investigated. We hypothesized that cognitive ability and inflammation would partly explain this association.

Study Design
Data were utilized from the Environmental-Risk Longitudinal Twin Study, a cohort of 2232 children born in 1994–1995 in England and Wales and followed to age 18. Socioenvironmental adversities were measured from birth to age 10 and classified into physical risk (defined by high urbanicity and air pollution) and socioeconomic risk (defined by high neighborhood deprivation, neighborhood disorder, and family disadvantage). Cognitive abilities (overall, crystallized, fluid, and working memory) were assessed at age 12; and inflammatory markers (C-reactive protein, interleukin-6, soluble urokinase plasminogen activator receptor) were measured at age 18 from blood samples. Participants were interviewed at age 18 regarding psychotic experiences.

Study Results
Higher physical risk and socioeconomic risk were associated with increased odds of psychotic experiences in adolescence. The largest mediation pathways were from socioeconomic risk via overall cognitive ability and crystallized ability, which accounted for ~11% and ~19% of the association with psychotic experiences, respectively. No statistically significant pathways were found via inflammatory markers in exploratory (partially cross-sectional) analyses.

Conclusions
Cognitive ability, especially crystallized ability, may partly explain the association between childhood socioenvironmental adversity and adolescent psychotic experiences. Interventions to support cognitive development among children living in disadvantaged settings could buffer them against developing subclinical psychotic phenomena.
Hypothyroidism‐associated immunosuppression involves induction of galectin‐1‐producing regulatory T cells
Authors: Valli Eduardo , Dalotto‐Moreno Tomás , Sterle Helena A. , Méndez‐Huergo Santiago P. , Paulazo María A. , García Silvia I. , Pirola Carlos J. , Klecha Alicia J. , Rabinovich Gabriel A. , Cremaschi Graciela A. 
Published: March 2023

AbstractHypothyroidism exerts deleterious effects on immunity, but the precise role of the hypothalamic–pituitary–thyroid (HPT) axis in immunoregulatory and tolerogenic programs is barely understood. Here, we investigated the mechanisms underlying hypothyroid‐related immunosuppression by examining the regulatory role of components of the HPT axis. We first analyzed lymphocyte activity in mice overexpressing the TRH gene (Tg‐Trh). T cells from Tg‐Trh showed increased proliferation than wild‐type (WT) euthyroid mice in response to polyclonal activation. The release of Th1 pro‐inflammatory cytokines was also increased in Tg‐Trh and TSH levels correlated with T‐cell proliferation. To gain further mechanistic insights into hypothyroidism‐related immunosuppression, we evaluated T‐cell subpopulations in lymphoid tissues of hypothyroid and control mice. No differences were observed in CD3/CD19 or CD4/CD8 ratios between these strains. However, the frequency of regulatory T cells (Tregs) was significantly increased in hypothyroid mice, and not in Tg‐Trh mice. Accordingly, in vitro Tregs differentiation was more pronounced in naïve T cells isolated from hypothyroid mice. Since Tregs overexpress galectin‐1 (Gal‐1) and mice lacking this lectin (Lgals1−/−) show reduced Treg function, we investigated the involvement of this immunoregulatory lectin in the control of Tregs in settings of hypothyroidism. Increased T lymphocyte reactivity and reduced frequency of Tregs were found in hypothyroid Lgals1−/− mice when compared to hypothyroid WT animals. This effect was rescued by the addition of recombinant Gal‐1. Finally, increased expression of Gal‐1 was found in Tregs purified from hypothyroid WT mice compared with their euthyroid counterpart. Thus, a substantial increase in the frequency and activity of Gal‐1‐expressing Tregs underlies immunosuppression associated with hypothyroid conditions, with critical implications in immunopathology, metabolic disorders, and cancer.
A single‐cell gene expression atlas of human follicular aspirates: Identification of leukocyte subpopulations and their paracrine factors
Authors: Choi Yohan , Jeon Hayce , Brännström Mats , Akin James W. , Curry Thomas E. , Jo Misung 
Published: March 2023

AbstractLeukocytes are in situ regulators critical for ovarian function. However, little is known about leukocyte subpopulations and their interaction with follicular cells in ovulatory follicles, especially in humans. Single‐cell RNA sequencing (scRNA‐seq) was performed using follicular aspirates obtained from four IVF patients and identified 13 cell groups: one granulosa cell group, one thecal cell group, 10 subsets of leukocytes, and one group of RBC/platelet. RNA velocity analyses on five granulosa cell populations predicted developmental dynamics denoting two projections of differentiation states. The cell type‐specific transcriptomic profiling analyses revealed the presence of a diverse array of leukocyte‐derived factors that can directly impact granulosa cell function by activating their receptors (e.g., cytokines and secretory ligands) and are involved in tissue remodeling (e.g., MMPs, ADAMs, ADAMTSs, and TIMPs) and angiogenesis (e.g., VEGFs, PGF, FGF, IGF, and THBS1) in ovulatory follicles. Consistent with the findings from the scRNA‐seq data, the leukocyte‐specific expression of CD68, IL1B, and MMP9 was verified in follicle tissues collected before and at defined hours after hCG administration from regularly cycling women. Collectively, this study demonstrates that this data can be used as an invaluable resource for identifying important leukocyte‐derived factors that promote follicular cell function, thereby facilitating ovulation and luteinization in women.
ZNF32 prevents the activation of cancer‐associated fibroblasts through negative regulation of TGFB1 transcription in breast cancer
Authors: Li Qin , Yuan Hang , Zhao Gang , Zhang Jie , Li Siqi , Gong Di , Feng Tianyu , Kou Qiming , Wang Qijing , Wang Guanru , Li Shan , Li Kai , Lin Ping 
Published: March 2023

AbstractBreast cancer is the most frequently diagnosed malignancy and the leading cause of cancer‐related deaths in women worldwide. Cancer‐associated fibroblasts (CAFs) are one of the fundamental cellular components of the tumor microenvironment and play a critical role in the initiation, progression, and therapy resistance of breast cancer. However, the detailed molecular mechanisms of CAFs activation from normal fibroblasts (NFs) are still not well understood. In the present study, we reported that ZNF32 expression in breast cancer cells was negatively correlated with CAF‐related markers (FSP1, α‐SMA, and FAP) in stromal fibroblasts, and loss of ZNF32 promoted the activation of CAFs, as evidenced by the enhanced proliferation and contractility of CAFs. ZNF32 deficiency‐mediated fibroblast activation promoted the growth and metastasis of breast cancer cells in vitro and in vivo. Mechanistically, we demonstrated that ZNF32 inhibited TGFB1 transcription by directly binding to the −1968/−1962 region of the TGFB1 promoter, leading to the prevention of fibroblast activation. Altogether, our findings reveal an important mechanism by which ZNF32 suppression increases the transcription of the TGFB1 gene in breast cancer cells, and subsequently, elevated levels of secretory TGF‐β stimulate NFs transformation into CAFs, which in turn facilitates the malignant progression of breast cancer. Our data implicated ZNF32 as a potential therapeutic strategy against breast cancer.
FGF1 ameliorates obesity‐associated hepatic steatosis by reversing IGFBP2 hypermethylation
Authors: Wang Jie , Zhang Feng , Yang Weiwei , Gao Dandan , Yang Linglong , Yu Chenhua , Chen Chengshui , Li Xiaokun , Zhang Jin‐San 
Published: March 2023

AbstractObesity is a major contributing factor for metabolic‐associated fatty liver disease (MAFLD). Fibroblast growth factor (FGF) 1 is the first paracrine FGF family member identified to exhibit promising metabolic regulatory properties capable of conferring glucose‐lowering and insulin‐sensitizing effect. This study explores the role and molecular underpinnings of FGF1 in obesity‐associated hepatic steatosis. In a mouse high‐fat diet (HFD)‐induced MAFLD model, chronic treatment with recombinant FGF1(rFGF1) was found to effectively reduce the severity of insulin resistance, hyperlipidemia, and inflammation. FGF1 treatment decreased lipid accumulation in the mouse liver and palmitic acid‐treated AML12 cells. These effects were associated with decreased mature form SREBF1 expression and its target genes FASN and SCD1. Interestingly, we uncovered that rFGF1 significantly induced IGFBP2 expression at both mRNA and protein levels in HFD‐fed mouse livers and cultured hepatocytes treated with palmitic acid. Adeno‐associated virus‐mediated IGFBP2 suppression significantly diminished the therapeutic benefit of rFGF1 on MAFLD‐associated phenotypes, indicating that IGFBP2 plays a crucial role in the FGF1‐mediated reduction of hepatic steatosis. Further analysis revealed that rFGF1 treatment reduces the recruitment of DNA methyltransferase 3 alpha to the IGFBP2 genomic locus, leading to decreased IGFBP2 gene methylation and increased mRNA and protein expression. Collectively, our findings reveal FGF1 modulation of lipid metabolism via epigenetic regulation of IGFBP2 expression, and unravel the therapeutic potential of the FGF1‐IGFBP2 axis in metabolic diseases associated with obesity.
SAMHD1restricts the deoxyguanosine triphosphate pool contributing to telomere stability in telomerase‐positive cells
Authors: D'Aronco Giulia , Ferraro Paola , Sassano Valentina , Dagostino Claudia , Biancotto Melissa , Palumbo Elisa , Presot Ettore , Russo Antonella , Bianchi Vera , Rampazzo Chiara 
Published: March 2023

AbstractSAMHD1 (Sterile alpha motif and histidine/aspartic acid domain‐containing protein 1) is a dNTP triphosphohydrolase crucial in the maintenance of balanced cellular dNTP pools, which support genome integrity. In SAMHD1 deficient fibroblasts isolated from Aicardi‐Goutières Syndrome (AGS) patients, all four DNA precursors are increased and markedly imbalanced with the largest effect on dGTP, a key player in the modulation of telomerase processivity. Here, we present data showing that SAMHD1, by restricting the dGTP pool, contributes to telomere maintenance in hTERT‐immortalized human fibroblasts from AGS patients as well as in telomerase positive cancer cell lines. Only in cells expressing telomerase, the lack of SAMHD1 causes excessive lengthening of telomeres and telomere fragility, whereas primary fibroblasts lacking both SAMHD1 and telomerase enter normally into senescence. Telomere lengthening observed in SAMHD1 deficient but telomerase proficient cells is a gradual process, in accordance with the intrinsic property of telomerase of adding only a few tens of nucleotides for each cycle. Therefore, only a prolonged exposure to high dGTP content causes telomere over‐elongation. hTERT‐immortalized AGS fibroblasts display also high fragility of chromosome ends, a marker of telomere replication stress. These results not only demonstrate the functional importance of dGTP cellular level but also reveal the critical role played by SAMHD1 in restraining telomerase processivity and safeguarding telomere stability.
Increased Influenza Severity in Children in the Wake of SARS-CoV-2
Authors: Hoy Gregory , Maier Hannah E. , Kuan Guillermina , Sánchez Nery , López Roger , Meyers Alyssa , Plazaola Miguel , Ojeda Sergio , Balmaseda Angel , Gordon Aubree 
Published: March 2023

AbstractThe SARS-CoV-2 pandemic and subsequent interruption of influenza circulation has lowered population immunity to influenza, especially among children with few pre-pandemic exposures. We compared the incidence and severity of influenza A/H3N2 and influenza B/Victoria between 2022 and two pre-pandemic seasons and found an increased frequency of severe influenza in 2022.