bluuebunny/crossref_metadata_2025_split huggingface dataset:
Plasticity of the Arabidopsis leaf lipidome and proteome in response to pathogen infection and heat stress
Authors: Scholz Patricia , Doner Nathan M , Gutbrod Katharina , Herrfurth Cornelia , Niemeyer Philipp W , Lim Magdiel S S , Blersch Katharina F , Schmitt Kerstin , Valerius Oliver , Shanklin John , Feussner Ivo , Dörmann Peter , Braus Gerhard H , Mullen Robert T , Ischebeck Till 
Published: May 2024

Abstract
Plants must cope with a variety of stressors during their life cycle, and the adaptive responses to these environmental cues involve all cellular organelles. Among them, comparatively little is known about the contribution of cytosolic lipid droplets (LDs) and their core set of neutral lipids and associated surface proteins to the rewiring of cellular processes in response to stress. Here, we analyzed the changes that occur in the lipidome and proteome of Arabidopsis (Arabidopsis thaliana) leaves after pathogen infection with Botrytis cinerea or Pseudomonas syringae, or after heat stress. Analyses were carried out in wild-type plants and the oil-rich double mutant trigalactosyldiacylglycerol1-1 sugar dependent 1-4 (tgd1-1 sdp1-4) that allowed for an allied study of the LD proteome in stressed leaves. Using liquid chromatography-tandem mass spectrometry-based methods, we showed that a hyperaccumulation of the primary LD core lipid TAG is a general response to stress and that acyl chain and sterol composition are remodeled during cellular adaptation. Likewise, comparative analysis of the LD protein composition in stress-treated leaves highlighted the plasticity of the LD proteome as part of the general stress response. We further identified at least two additional LD-associated proteins, whose localization to LDs in leaves was confirmed by confocal microscopy of fluorescent protein fusions. Taken together, these results highlight LDs as dynamic contributors to the cellular adaptation processes that underlie how plants respond to environmental stress.
Tracking and optimizing toxic chemical exposure pathways through food trade: A case study in SCCPs contaminated seafood in China
Authors: Song Shijie , Huang Tao , Xu Yuting , Ling Zaili , Gou Ling , Mao Xiaoxuan , Zhao Yuan , Chen Kaijie , Liu Yao , Wei Zijian , Wang Jiaxin , Gao Hong , Ma Jianmin 
Published: May 2024

Abstract
Food safety is related to human health and sustainable development. International food trade poses food safety risks through the collateral transport of toxic chemicals that are detrimental to human health. Domestic interprovincial trade has similar effects within countries but has not been comprehensively investigated previously. Here, we assessed the effects of interprovincial trade on food safety and human dietary exposure to short-chain chlorinated paraffins (SCCPs), a group of emerging persistent toxic chemicals, in seafood across China by synthesizing data from field observation and various models. Our findings indicate that there is a higher level of SCCPs exposure risk in coastal provinces compared to inland provinces. Approximately, 70.3% of human exposure to SCCPs through seafood consumption in China was embodied in the interprovincial seafood trade in 2021. Specifically, the domestic trade led to a remarkable increase in SCCPs exposure in the coastal provinces in South China, attributable to low SCCPs pollution in these provinces and imported seafood from those provinces with high SCCPs pollution. In contrast, human exposure to SCCPs decreased in those coastal provinces in East China due to importing seafood from those provinces with low SCCPs concentrations. The interprovincial seafood trade routes were optimized by linear programming to minimize human exposure to SCCPs considering both shipping cost and health risk constraints. The optimized trade routes reduced the national per capita SCCPs exposure through seafood consumption by over 12%. This study highlights the importance of interprovincial food trade in the risk assessment of toxic chemicals.
Integrative analysis of transcriptome, DNA methylome, and chromatin accessibility reveals candidate therapeutic targets in hypertrophic cardiomyopathy
Authors: Gao Junpeng , Liu Mengya , Lu Minjie , Zheng Yuxuan , Wang Yan , Yang Jingwei , Xue Xiaohui , Liu Yun , Tang Fuchou , Wang Shuiyun , Song Lei , Wen Lu , Wang Jizheng 
Published: May 2024

Abstract
Hypertrophic cardiomyopathy (HCM) is the most common inherited heart disease and is characterized by primary left ventricular hypertrophy usually caused by mutations in sarcomere genes. The mechanism underlying cardiac remodeling in HCM remains incompletely understood. An investigation of HCM through integrative analysis at multi-omics levels will be helpful for treating HCM. DNA methylation and chromatin accessibility, as well as gene expression, were assessed by nucleosome occupancy and methylome sequencing (NOMe-seq) and RNA-seq, respectively, using the cardiac tissues of HCM patients. Compared with those of the controls, the transcriptome, DNA methylome, and chromatin accessibility of the HCM myocardium showed multifaceted differences. At the transcriptome level, HCM hearts returned to the fetal gene program through decreased sarcomeric and metabolic gene expression and increased extracellular matrix gene expression. In the DNA methylome, hypermethylated and hypomethylated differentially methylated regions were identified in HCM. At the chromatin accessibility level, HCM hearts showed changes in different genome elements. Several transcription factors, including SP1 and EGR1, exhibited a fetal-like pattern of binding motifs in nucleosome-depleted regions in HCM. In particular, the inhibition of SP1 or EGR1 in an HCM mouse model harboring sarcomere mutations markedly alleviated the HCM phenotype of the mutant mice and reversed fetal gene reprogramming. Overall, this study not only provides a high-precision multi-omics map of HCM heart tissue but also sheds light on the therapeutic strategy by intervening in the fetal gene reprogramming in HCM.
Protest and Legislative Behavior in Perilous Times
Authors: Minnite Lorraine C 
Published: May 2024

Abstract
A long-standing tradition in the study of social movements documents the multitude of ways protest “matters” for policy and politics. LaGina Gause's book, The Advantage of Disadvantage makes a contribution to this literature. Gause develops a formal theory of the influence of protest on legislative behavior and representation and tests it with data from a range of empirical sources. She finds that protest is most effective for disadvantaged groups. What is admirable here is the attempt to integrate the study of social movements with the study of legislative behavior. But limitations that result from an exclusive reliance on quantitative analysis ultimately weaken the strength of her claims. That said, given the proliferation of protest movements around the world, we need to better understand how movement politics influence legislative politics. This is especially true for the mature democracies of the West where Far Right, nationalist, racist, and fascist movements seek to move from fringe to center by manipulating the institutions of electoral politics to undermine democracy itself. The review article concludes with thoughts on an expanded inquiry into the dynamics of contention of today's rightwing political movements.
Consumption Quality and Employment Across the Wealth Distribution
Authors: Ferraro Domenico , Valaitis Vytautas 
Published: May 2024

Abstract
In the U.S., market hours worked are approximately flat across the wealth distribution. Accounting for this phenomenon is a standing challenge for standard heterogeneous-agent macro models. In these models, wealthier households consume more and work fewer hours. We propose a theory that generates the cross-sectional wealth-hours relation as in the data. We quantify this theory in a heterogeneous-agent incomplete-markets model with three key features: a quality choice in consumption, non-homothetic preferences, and a multi-sector production structure. We show that the model produces consumption expenditure patterns consistent with the data and realistic “quality Engel curves”.
B cell depletion after treatment with rituximab predicts relapse of IgG4-related disease
Authors: Lanzillotta Marco , Ramirez Giuseppe Alvise , Milani Raffaella , Dagna Lorenzo , Della-Torre Emanuel 
Published: May 2024

Abstract

Objectives
B cell depletion therapy with rituximab is effective in most patients with IgG4-related disease (IgG4-RD) but requires repeated cycles to prevent disease flares. We here aimed to assess B cells after rituximab to predict relapse of IgG4-RD and guide retreatment.

Methods
Patients with active IgG4-RD included in this retrospective study fulfilled the ACR/EULAR Classification Criteria. Total CD19+ B cells, plasmablasts, naïve and memory B cells were measured on peripheral blood by flow-cytometry at baseline and 6 months after rituximab. All patients were treated with two 1 g infusions of rituximab 15 days apart and monitored for 48 months. Disease response was assessed using the IgG4-RD Responder Index.

Results
Thirty-three patients were included. Six months after rituximab, disease response was observed in all patients. Complete depletion of CD19+ B cells, plasmablasts, naïve and memory B cell depletion was achieved in 30%, 55%, 39% and 42% of cases, respectively. Twenty-three relapses (70%) were observed at a median time of 24 months after rituximab. Relapse rate was significantly higher in patients who failed to achieve complete depletion of CD19+ cells (60% vs 17%, P = 0.02), naïve B cells (54% vs 15%, P = 0.01), or memory B cells (50% vs 16%, P = 0.03) 6 months after rituximab. The median relapse free survival time was shorter in patients who failed to achieve complete depletion of CD19+ cells (19 vs 38 months, P = 0.02), naïve B cells (16 vs 38 months, P = 0.01), or memory B cells (19 vs 38 months, P = 0.03) 6 months after rituximab.

Conclusion
The degree of B cell depletion 6 months after rituximab may predict disease flare and may instruct on the pacing of B cell depletion therapy in IgG4-RD.
Prospective assessment of glucocorticoid toxicity in rheumatology practice: a focus on the glucocorticoid toxicity index
Authors: Bahap-Kara Melda , Sariyildiz Emine , Zengin Hatice Yagmur , Karadag Omer , Bayraktar-Ekincioglu Aygin 
Published: May 2024

Abstract

Objective
The glucocorticoid toxicity index (GTI) is developed to measure glucocorticoid (GC)-related morbidity over time. This study aimed to assess GC-toxicity in patients at a rheumatology outpatient clinic by using the GTI and to identify the factors that interfere with the GTI.

Methods
This prospective study included patients with inflammatory arthritis (IA), connective tissue disease and vasculitis who were newly prescribed GC-treatment (GC-naive) or have been still on GC-treatment for ≤2 years (GC-experienced). Patient demographics and disease characteristics, aggregate improvement score (GTI-AIS), cumulative worsening score (GTI-CWS) and cumulative GC-doses were recorded at baseline, 3rd month and 6th month. Generalized estimating equations (GEE) were used to evaluate the GTI scores and associated factors including cumulative GC-doses.

Results
The study included 156 (48.7% GC-naive) patients with a mean age of 49.1 ± 17.1 years. More than half of the patients in both groups had a diagnosis of vasculitis. A higher cumulative GC-dose was found to be associated with higher GTI-scores in both groups (P &lt; 0.001). In the GC-naive group, patients with vasculitis showed higher GTI-scores than IA patients (P &lt; 0.001); there was also a significant increase in the GTI-CWS at the 6th month compared with the 3rd month. In the GC-experienced group, GTI-AIS and GTI-CWS were significantly different at 3rd and 6th month (P &lt; 0.05).

Conclusion
It was shown that GTI scores were associated with cumulative GC-doses and vasculitis patients in the GC-naive patients had higher GTI scores than inflammatory arthritis. The GTI allows individualized assessment and management of adverse effects experienced by patients as a result of GC treatment.
Combination of scavenger receptor-A with anti-cyclic citrullinated peptide antibody for the diagnosis of rheumatoid arthritis
Authors: Wei Chaonan , Wang Ping , Zhang Jian , Jiang Xiang , Xie Yang , Li Yingni , Zhang Wei , Du Yan , Zheng Xi , Fang Xiangyu , Liu Shuyan , Cao Lulu , Yao Ranran , Jin Xu , Zhu Danxue , Wu Huaxiang , Wang Yongfu , Li Zhanguo , Hu Fanlei 
Published: May 2024

Abstract

Objectives
The routine biomarkers for RA, including anti-CCP, RF, IgM, ESR and CRP, have limited sensitivity and specificity. Scavenger receptor-A (SR-A) is a novel RA biomarker identified recently by our group, especially for seronegative RA. Here, we performed a large-scale, multicentre study to further assess the diagnostic value of SR-A in combination with other biomarkers for RA.

Methods
The performance of SR-A in combination with other biomarkers for RA diagnosis was first revealed by a pilot study, and was further elucidated by a large-scale, multicentre study. A total of 1129 individuals from three cohorts were recruited in the study, including RA patients, healthy controls and patients with other common rheumatic diseases. Diagnostic properties were evaluated by the covariate-adjusted receiver operating characteristic curve, sensitivity, specificity and clinical association.

Results
Large-scale multicentre analysis showed that SR-A and anti-CCP dual combination was the optimal method for RA diagnosis, increasing the sensitivity of anti-CCP by 13% (87% vs 74%) while maintaining a specificity of 90%. In early RA patients, SR-A and anti-CCP dual combination also showed promising diagnostic value, increasing the sensitivity of anti-CCP by 7% (79% vs 72%) while maintaining a specificity of 94%. Moreover, SR-A and anti-CCP dual combination was correlated with ESR, IgM and autoantibodies of RA patients, further revealing its clinical significance.

Conclusion
SR-A and anti-CCP dual combination could potentially improve early diagnosis of RA, thus improving the prognosis and reducing mortality.
Polyarticular juvenile idiopathic arthritis has a distinct co-inhibitor receptor profile
Authors: Sag Erdal , Balik Zeynep , Demir Selcan , Akca Kaya Ummusen , Sener Seher , Kasap Cuceoglu Muserref , Atalay Erdal , Bocutcu Sena , Vural Tayfun , Tasdemir Nur Kubra , Aydin Busra , Bilginer Yelda , Deleuran Bent , Ozen Seza 
Published: May 2024

Abstract

Objectives
JIA is the most common rheumatic disease of childhood; the pathogenesis is associated with T-cell activation. T-cell activation can be counterbalanced by signals generated by inhibitory receptors (IRs) such as CTLA-4, PD-1, LAG-3 and TIM-3. Here, we identify the role of IRs in the pathogenesis of different JIA subtypes.

Methods
In total, we included 67 oligoarticular JIA, 12 IgM-RF negative polyarticular JIA, 17 enthesitis-related arthritis, 11 systemic JIA patients and 10 healthy controls. We collected plasma (and SF) samples from the patients either at the onset or during a flare of their disease. We measured the soluble levels of co-IRs (IL-2Rα, 4-1BB, CD86, TGF-β1, CTLA-4, PD-L1, PD-1, TIM-3, LAG- 3, Galectin-9) by cytometric bead array kits and their cellular expression (PD-1, CTLA-4, TIM-3, LAG-3) by flow cytometry. We compared the plasma levels and cellular expressions of different co-IRs within different JIA subgroups.

Results
The polyarticular JIA group was different from the three other examined JIA subgroups, having higher levels of plasma sCTLA-4 (P &lt; 0.001), sPD-1 (P &lt; 0.05) and s4-1BB (P &lt; 0.05) when compared with the other JIA subgroups and healthy controls. We analysed the cellular surface expression of different co-IRs on the peripheral blood mononuclear cells of different JIA subtypes. Similar to plasma levels, both the percentage (P &lt; 0.05) and the mean fluorescence intensity (P &lt; 0.01) of CTLA4 expression were higher in the polyarticular JIA subgroup.

Conclusion
This is the first report studying the expression profile of different co-IRs in different subtypes of JIA. Polyarticular JIA patients had a different co-IR profile, having more CTLA-4, PD-1 and 4-1BB in their plasma than the other subtypes of JIA.
Pharmacological Treatment of Cognitive Impairment Associated With Schizophrenia: State of the Art and Future Perspectives
Authors: Vita Antonio , Nibbio Gabriele , Barlati Stefano 
Published: May 2024

Abstract
Cognitive Impairment Associated with Schizophrenia (CIAS) represents one of the core dimensions of Schizophrenia Spectrum Disorders (SSD), with an important negative impact on real-world functional outcomes of people living with SSD. Treatment of CIAS represents a therapeutic goal of considerable importance, and while cognition-oriented evidence-based psychosocial interventions are available, effective pharmacological treatment could represent a game-changer in the lives of people with SSD. The present critical review reports and discusses the evidence regarding the effects of several pharmacological agents that are available in clinical practice or are under study, commenting on both current and future perspectives of CIAS treatment. In particular, the effects on CIAS of antipsychotic medications, anticholinergic medications, benzodiazepines, which are currently commonly used in the treatment of SSD, and of iclepertin, d-serine, luvadaxistat, xanomeline-trospium, ulotaront, anti-inflammatory molecules, and oxytocin, which are undergoing regulatory trials or can be considered as experimental agents, will be reported and discussed. Currently, available pharmacological agents do not appear to provide substantial benefits on CIAS, but accurate management of antipsychotic medications and avoiding treatments that can further exacerbate CIAS represent important strategies. Some molecules that are currently being investigated in Phase 2 and Phase 3 trials have provided very promising preliminary results, but more information is currently required to assess their effectiveness in real-world contexts and to provide clear recommendations regarding their use in clinical practice. The results of ongoing and future studies will reveal whether any of these molecules represents the awaited pharmacological game-changer in the treatment of CIAS.
Integrative taxonomy of new neomphaloidean gastropods from deep-sea hot vents of the southwestern Pacific
Authors: Chen Chong , Poitrimol Camille , Matabos Marjolaine 
Published: May 2024

Abstract
Neomphaloidean gastropods are endemic to chemosynthesis-based ecosystems ranging from hot vents to organic falls, and their diversity and evolutionary history remain poorly understood. In the southwestern Pacific, deep-sea hydrothermal vents on back-arc basins and volcanic arcs are found in three geographically secluded regions: a western region around Manus Basin, an eastern region around North Fiji and Lau Basins, and the intermediate Woodlark Basin where active venting was confirmed only recently, on the 2019 R/V L’Atalante CHUBACARC expedition. Although various lineages of neomphaloidean snails have been detected, typically restricted to one of the three regions, some of these have remained without names. Here, we use integrative taxonomy to describe three of these species: the neomphalid Symmetromphalus mithril sp. nov. from Woodlark Basin and the peltospirids Symmetriapelta becki sp. nov. from the eastern region and Symmetriapelta radiata sp. nov. from Woodlark Basin. A combination of shell sculpture and radular characters allow the morphological separation of these new species from their described congeners. A molecular phylogeny reconstructed from 570 bp of the mitochondrial cytochrome c oxidase subunit I gene confirmed the placement of the three new species in their respective genera and the superfamily Neomphaloidea. The finding of these new gastropods, particularly the ones from the Woodlark Basin, provides insights and implications on the historical role of Woodlark as a dispersing centre, in addition to highlighting the uniqueness of the Woodlark faunal community.
FOXS1 acts as an oncogene and induces EMT through FAK/PI3K/AKT pathway by upregulating HILPDA in prostate cancer
Authors: Ren Ruimin , Wang Huang , Xu Yuan , Wu Jinfeng , Ma Ding , Guan Wei 
Published: May 2024

AbstractProstate cancer (PCa) is a widespread global health concern characterized by elevated rates of occurrence, and there is a need for novel therapeutic targets to enhance patient outcomes. FOXS1 is closely linked to different cancers, but its function in PCa is still unknown. The expression of FOXS1, its prognostic role, clinical significance in PCa, and the potential mechanism by which FOXS1 affects PCa progression were investigated through bioinformatics analysis utilizing public data. The levels of FOXS1 and HILPDA were evaluated in clinical PCa samples using various methods, such as western blotting, immunohistochemistry, and qRT‐PCR. To examine the function and molecular mechanisms of FOXS1 in PCa, a combination of experimental techniques including CCK‐8 assay, flow cytometry, wound‐healing assay, Transwell assay, and Co‐IP assay were employed. The FOXS1 expression levels were significantly raised in PCa, correlating strongly with tumor aggressiveness and an unfavorable prognosis. Regulating FOXS1 expression, whether upregulating or downregulating it, correspondingly enhanced or inhibited the growth, migration, and invasion capabilities of PCa cells. Mechanistically, we detected a direct interaction between FOXS1 and HILPDA, resulting in the pathway activation of FAK/PI3K/AKT and facilitation EMT in PCa cells. FOXS1 collaborates with HILPDA to initiate EMT, thereby facilitating the PCa progression through the FAK/PI3K/AKT pathway activation.
Assessing Contraceptive Switching and Discontinuation Over 3 Years in the HER Salt Lake Study
Authors: Simmons Rebecca G. , Carter Gentry , Sanders Jessica N. , Turok David K. 
Published: May 2024

OBJECTIVE:
To assess contraceptive switching and discontinuation among participants enrolled in a contraceptive access project over 3 years and to identify variables associated with contraceptive change.

METHODS:
The HER Salt Lake study enrolled individuals between 2015 and 2017 from four clinics in Salt Lake County into a prospective, longitudinal cohort. All participants were able to switch or discontinue at no cost (between March 2016 and March 2020). We collected eight follow-up surveys over 3 years after enrollment. Each survey wave included questions about method use in the previous 4 weeks. We categorized participants in three ways, allowing for time-varying outcomes by wave: 1) those who reported using the same method as previous wave (continuers), 2) those who reported using a different method from previous wave (switchers), and 3) those who reported using no contraceptive method at that wave (discontinuers). We report the frequency of outcomes and conducted multinomial regression models assessing predictors of switching and discontinuation.

RESULTS:
Among 4,289 participants included in this analysis, 2,179 (50.8%) reported at least one instance of switching or discontinuation, and 2,110 (49.1%) reported continuing with their baseline method at the end of the study. Those reporting method change (switching or discontinuing) reported an average of 1.93 change events over the study follow-up period (range 1–8). Among those reporting any method change, 522 participants (23.9%) reporting at least one instance of both switching and discontinuation. Among those reporting any instance of discontinuation (n=966), 498 (51.6%) never reported uptake of a subsequent method. Among those who did report a subsequent method (n=468), 210 (44.8%) reported restarting a previously used method, and 258 (55.1%) reported starting a new method. Although we identified overlap among variables associated with switching and discontinuation, other predictors were discordant between switching and discontinuation.

CONCLUSION:
New contraceptive users commonly switch and discontinue methods. User behavior is associated with certain demographic characteristics and pregnancy planning.

CLINICAL TRIAL REGISTRATION:

ClinicalTrials.gov, NCT02734199.