bluuebunny/crossref_metadata_2025_split huggingface dataset:
Joint involvement in sarcoidosis: systematic review and meta-analysis of prevalence, clinical pattern and outcome
Authors: Yeung Terence , Grebowicz Adrian , Nevskaya Tatiana , Zahid Sulman , Pope Janet E 
Published: January 2024

Abstract

Objectives
To characterize joint involvement (JI) in sarcoidosis, a systematic search of MEDLINE, EMBASE and Cochrane Library was conducted from inception to July 2022 for publications reporting its prevalence, pattern, treatment and outcome.

Methods
The pooled prevalence estimates (PPE) with 95% CI were calculated using binomial distribution and random effects. Meta-regression method was used to examine factors affecting heterogeneity between studies.

Results
Forty-nine articles were identified comprising a total of 8574 sarcoidosis patients, where 12% presented with JI (95% CI 10, 14; I2 = 0%). The PPE for sarcoid arthritis (SA) was 19% (95% CI 14, 24; I2 = 95%), and 32% (95% CI 13, 51; I2 = 99%) for arthralgia. Heterogeneity was due to higher JI prevalence reported in Western Asia and the Middle East, in rheumatology clinics and via surveys. Sample size of SA varied from 12 to 117 cases. Ankles were most frequently affected (PPE 80%) followed by knees and wrists. Monoarthritis was uncommon (PPE 1%; 95% CI 0, 2; I2 = 55%). Acute SA prevailed (PPE 79%; 95% CI 72, 88; I2 = 69%) with an equal proportion of oligo and polyarthritis and was frequently accompanied by erythema nodosum (PPE 62%; 95% CI 52, 71; I2 = 16%). Chronic SA was predominantly polyarticular with a higher frequency of the upper extremity joints affected. Most common non-articular manifestations with SA included fever (52%), erythema nodosum (41%), hilar adenopathy (86%) and interstitial lung disease (23%) of which one-third required corticosteroids and/or immunosuppressants.

Conclusion
SA occurred early in the disease with a PPE of 19% and most frequent pattern of acute oligo- or polyarthritis predominantly affecting the lower extremity large joints.
Tracing carbon and nitrogen reserve remobilization during spring leaf flush and growth following defoliation
Authors: Hart Ashley T , Landhäusser Simon M , Wiley Erin 
Published: January 2024

Abstract
Woody plants rely on the remobilization of carbon (C) and nitrogen (N) reserves to support growth and survival when resource demand exceeds supply at seasonally predictable times like spring leaf flush and following unpredictable disturbances like defoliation. However, we have a poor understanding of how reserves are regulated and whether distance between source and sink tissues affects remobilization. This leads to uncertainty about which reserves—and how much—are available to support plant functions like leaf growth. To better understand the source of remobilized reserves and constraints on their allocation, we created aspen saplings with organ-specific labeled reserves by using stable isotopes (13C,15N) and grafting unlabeled or labeled stems to labeled or unlabeled root stocks. We first determined which organs had imported root or stem-derived C and N reserves after spring leaf flush. We then further tested spatial and temporal variation in reserve remobilization and import by comparing (i) upper and lower canopy leaves, (ii) early and late leaves, and (iii) early flush and re-flush leaves after defoliation. During spring flush, remobilized root C and N reserves were preferentially allocated to sinks closer to the reserve source (i.e., lower vs upper canopy leaves). However, the reduced import of 13C in late versus early leaves indicates reliance on C reserves declined over time. Following defoliation, re-flush leaves imported the same proportion of root N as spring flush leaves, but they imported a lower proportion of root C. This lower import of reserve C suggests that, after defoliation, leaf re-flush rely more heavily on current photosynthate, which may explain the reduced leaf mass recovery of re-flush canopies (31% of initial leaf mass). The reduced reliance on reserves occurred even though roots retained significant starch concentrations (~5% dry wt), suggesting that aspen prioritizes the maintenance of root reserves at the expense of fast canopy recovery.
Maize Kernel-Associated Metagenomes Reveal Potential Microbe–Microbe Interactions that Underlie Fusarium Ear Rot Disease
Authors: Adams Alison , Landry Dana , Sykes Virginia , Rickman Tara , Cham Alhagie K. , Timling Annemarie , Kelly Heather , McBeath Jenifer H. , Olukolu Bode A. 
Published: January 2024

As an alternative to host resistance, transgenic expression of entomocidal and antimicrobial proteins from Bacillus thuringiensis ( Bt) in maize can mitigate Fusarium ear rot (FER). This study evaluated FER in Bt and conventional maize and the role of microbes in the kernel-associated metagenome using quantitative reduced representation sequencing. Our results revealed significant differences in FER severity across environments and varieties and between inoculation treatments. The lower FER scores of conventional maize Spectrum 6416 relative to other varieties highlighted resistant alleles in maize germplasm, whereas strong correlations indicated FER-induced yield loss. Mitigation of FER by transgenes was validated by about threefold enrichment of Fusarium verticillioides ( Fv) postinoculation compared with nonsignificant Fv enrichment in conventional maize. Although the major causal pathogen of FER, Fv, was the most abundant species in the metagenomes ( r = 0.41 to 0.49), a similar degree of correlation was observed between FER and several Fusarium spp. ( r = 0.2 to 0.56). The potential FER-suppressing properties of Talaromyces stipitatus and Ustilago maydis were indicated by negative correlations with FER ( r = –0.22 to –0.42), Fv, and some Fusarium spp. The more FER-resistant varieties consistently enriched for potential FER-suppressing Burkholderia cenocepacia (negatively correlated with Fv). This suggests host genetic background-dependent recruitment of beneficial microbes that suppress pathogens and that microbe–microbe interactions play a role in FER severity. Quantitative and species/strain-level metagenomic profiles hold promise for identifying robust disease-suppressing microbes and microbes that act in synergy with pathogens and for developing holobiont-aware breeding strategies that account for host–microbiome coevolution and host genotype, microbiome/metagenome, and environment interactions. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .
Comparative Multi-Omics Analysis of Broomcorn Millet in Response to Anthracocystis destruens Infection
Authors: Wu Enguo , Li Xuepei , Ma Qian , Wang Honglu , Han Xiaowei , Feng Baili 
Published: January 2024

Anthracocystis destruens is the causal agent of broomcorn millet ( Panicum miliaceum) smut disease, which results in serious yield losses in broomcorn millet production. However, the molecular basis underlying broomcorn millet defense against A. destruens is less understood. In this study, we investigated how broomcorn millet responds to infection by A. destruens by employing a comprehensive multi-omics approach. We examined the responses of broomcorn millet across transcriptome, metabolome, and microbiome levels. Infected leaves exhibited an upregulation of genes related to photosynthesis, accompanied by a higher accumulation of photosynthesis-related compounds and alterations in hormonal levels. However, broomcorn millet genes involved in immune response were downregulated post A. destruens infection, suggesting that A. destruens may suppress broomcorn millet immunity. In addition, we show that the immune suppression and altered host metabolism induced by A. destruens have no significant effect on the microbial community structure of broomcorn millet leaf, thus providing a new perspective for understanding the tripartite interaction between plant, pathogen, and microbiota.
Application of a U-Net Neural Network to the Puccinia sorghi–Maize Pathosystem
Authors: Holan Katerina L. , White Charles H. , Whitham Steven A. 
Published: January 2024

Computer vision approaches to analyze plant disease data can be both faster and more reliable than traditional, manual methods. However, the requirement of manually annotating training data for the majority of machine learning applications can present a challenge for pipeline development. Here, we describe a machine learning approach to quantify Puccinia sorghi incidence on maize leaves utilizing U-Net convolutional neural network models. We analyzed several U-Net models with increasing amounts of training image data, either randomly chosen from a large data pool or randomly chosen from a subset of disease time course data. As the training dataset size increases, the models perform better, but the rate of performance decreases. Additionally, the use of a diverse training dataset can improve model performance and reduce the amount of annotated training data required for satisfactory performance. Models with as few as 48 whole-leaf training images are able to replicate the ground truth results within our testing dataset. The final model utilizing our entire training dataset performs similarly to our ground truth data, with an intersection over union value of 0.5002 and an F1 score of 0.6669. This work illustrates the capacity of U-Nets to accurately answer real-world plant pathology questions related to quantification and estimation of plant disease symptoms. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .
Longitudinal Association of Mid-Life Ten Year Cardiovascular Disease Risk Score with Brain Biomarkers of Alzheimer’s Disease, Neurodegeneration and White Matter Hyper Intensities in Cognitively Unimpaired Older Adults: Heart SCORE Brain Study
Authors: Saeed Anum , Chang Yue Fang , Swanson Justin , Vu Michael , Mapstone Mark , Villemagne Victor L , Snitz Beth E. , Royse Sarah K , Lopresti Brian , Aizenstein Howard J. , Wu Minjie , Kip Kevin , Reis Steven E. , Lopez Oscar , Cohen Ann 
Published: January 2024

AbstractIntroductionAtherosclerotic cardiovascular disease (ASCVD) risk factors in mid-life have been associated with cognitive decline and late-life dementia. However, the role of these risk factors in preclinical Alzheimer’s disease (AD) pathophysiology remains elusive. We investigated whether mid-life 10-year pooled cohort equations (PCE) based ASCVD risk is associated with late-life amyloid, tau, neurodegeneration [AT(N)] measures and white matter hyperintensities (WMHI).MethodsParticipants enrolled in the Heart Strategies Concentrating on Risk Evaluation (Heart SCORE) study between 2003-2005 (mid-life) and underwent brain MRI and PET scans in 2018-2022 (age >65 years, late-life) to detect and quantify amyloid (A, PiB-PET) and tau (T, Flortaucipir (FTP) PET) deposition, cortical thickness (N) and white matter hyperintensities (WMHIs). Mid-life PCE ASCVD risk was categorized as; borderline (5%-7.4%), intermediate (7.5%-<15%), or high (≥15%). Association of midlife ASCVD risk HR (5% CI) was assessed using logistic and linear regressions with A, T, or N and chi square beta coefficients for WMHI in latelife.ResultsOver a ∼16y follow up, in 135 participants (mean age 73y), A and T showed no significant association with mid-life ASCVD risk. Neurodegeneration had a graded association with mid-life ASCVD risk categories (ORASCVDhighvslowrisk%6.98 [2.44-19.95]; p<0.05) driven by self-identified Black race and age. In a subset n=60, ASCVD risk score was also associated with WMHIs ((β=0.42 ± 0.22; p=0.05)in a model adjusted for inflammation and education.ConclusionsIn this asymptomatic, diverse cohort, 10y ASCVD risk was predictive of late-life neurodegeneration and white matter hyperintensities but not amyloid or tau. These data suggest that ASCVD risk factors in midlife may lead to a state of vulnerability (through increased neurodegeneration and white matter hyperintensities) which may progress to cognitive decline and dementia. Further mechanistic studies are warranted to test this hypothesis.Abstract Figure
A self-report tool for identification of individuals with coronary atherosclerosis – The Swedish CArdioPulmonary BioImage Study
Authors: Bergström Göran , Hagberg Eva , Björnson Elias , Adiels Martin , Bonander Carl , Strömberg Ulf , Andersson Jonas , Brunström Mattias , Carlhäll Carl-Johan , Engström Gunnar , Erlinge David , Goncalves Isabel , Gummesson Anders , Hagström Emil , Hjelmgren Ola , James Stefan , Janzon Magnus , Jonasson Lena , Lind Lars , Magnusson Martin , Oskarsson Viktor , Sundström Johan , Svensson Per , Söderberg Stefan , Themudo Raquel , Östgren Carl Johan , Jernberg Tomas 
Published: January 2024

AbstractBackgroundCoronary atherosclerosis detected by imaging is a marker of elevated cardiovascular risk. However, imaging involves large resources and exposure to radiation. The aim was, therefore, to test whether non-imaging data, specifically data that can be self-reported, could be used to identify individuals with moderate to severe coronary atherosclerosis.MethodsWe used data from the population based Swedish CArdioPulmonary BioImage Study (SCAPIS) in individuals with coronary computed tomography angiography (CCTA, n=25,182) and coronary artery calcification score (CACS, n=28,701), aged 50-64 years without previous ischemic heart disease. We developed a risk prediction tool utilizing variables that could be assessed from home (a so-called self-report tool). For comparison, we also developed a tool utilizing variables from laboratory tests, physical examinations and self-report (a so-called clinical tool) and evaluated both models using receiver operating characteristic curve analysis, external validation, and bench-marked against factors in the Pooled Cohort Equation (PCE).ResultsThe self-report tool (n=14 variables) and the clinical tool (n=23 variables) showed high-to-excellent discriminative ability to identify SIS ≥4 (AUC 0.79 and 0.80, respectively) and significantly better than PCE (AUC 0.76, p<0.001). The tools showed a larger net benefit in clinical decision making at relevant threshold probabilities. The self-report tool identified 65% of all individuals with SIS ≥4 in the top 30% of the highest-risk individuals. Tools developed for CACS ≥100 performed similarly.ConclusionsWe have developed a self-report tool which effectively identifies individuals with moderate to severe coronary atherosclerosis. The self-report tool may serve as pre-screening tool towards a cost-effective CT-based screening program for high-risk individuals.Clinical PerspectiveWhat Is New?We have developed a self-report tool which with a good-to-excellent discriminative ability identifies individuals with moderate to severe coronary atherosclerosis.The self-report tool can be executed from home and has a similar performance to a clinical tool requiring a clinical visit involving blood tests and physical examination.What Are the Clinical Implications?The self-report tool could serve as an initial step towards a cost-effective screening program to identify high-risk individuals or used to identify individuals who would benefit from further risk refinement by cardiac imaging.
Crosstalk between the RNA-binding proteins Regnase-1 and -3 shapes mast cell survival and cytokine expression
Authors: Bataclan Marian , Leoni Cristina , Moro Simone G. , Pecoraro Matteo , Wong Elaine H. , Heissmeyer Vigo , Monticelli Silvia 
Published: January 2024

AbstractPost-transcriptional regulation of immune-related transcripts by RNA-binding proteins (RBPs) impacts immune cell responses, including mast cell functionality. Despite their importance in immune regulation, the functional role of most RBPs remains to be understood. By manipulating the expression of specific RBPs in mast cells, coupled with mass spectrometry and transcriptomic analyses, we found that the Regnase family of proteins acts as a potent regulator of mast cell physiology. Specifically, Regnase-1 is required to maintain basic cell proliferation and survival, while both Regnase-1 and −3 cooperatively regulate the expression of inflammatory transcripts upon mast cell activation, withTnfbeing a primary target of both proteins. In mast cells, Regnase-3 directly interacts with Regnase-1 and is necessary to restrain Regnase-1 expression through the destabilization of its transcript. Overall, our study identifies protein interactors of endogenously expressed Regnase factors, characterizes the regulatory interplay between Regnase family members in mast cells, and establishes their role in the control of mast cell homeostasis and inflammatory responses.
Mitochondrial Transplantation promotes protective effector and memory CD4+T cell response duringMycobacterium tuberculosisinfection and diminishes exhaustion and senescence in elderly CD4+T cells
Authors: Headley Colwyn A. , Gautam Shalini , Olmo-Fontanez Angelica , Garcia-Vilanova Andreu , Dwivedi Varun , Schami Alyssa , Weintraub Susan , Tsao Philip S. , Torrelles Jordi B. , Turner Joanne 
Published: January 2024

AbstractTuberculosis (TB), caused by the bacteriumMycobacterium tuberculosis(M.tb), remains a significant health concern worldwide, especially in populations with weakened or compromised immune systems, such as the elderly. Proper adaptive immune function, particularly a CD4+T cell response, is central to host immunity againstM.tb. Chronic infections, such asM.tb, as well as aging promote T cell exhaustion and senescence, which can impair immune control and promote progression to TB disease. Mitochondrial dysfunction contributes to T cell dysfunction, both in aging and chronic infections and diseases. Mitochondrial perturbations can disrupt cellular metabolism, enhance oxidative stress, and impair T-cell signaling and effector functions. This study examined the impact of mitochondrial transplantation (mito-transfer) on CD4+T cell differentiation and function using aged mouse models and human CD4+T cells from elderly individuals. Our study revealed that mito-transfer in naïve CD4+T cells promoted the generation of protective effector and memory CD4+T cells duringM.tbinfection in mice. Further, mito-transfer enhanced the function of elderly human T cells by increasing their mitochondrial mass and modulating cytokine production, which in turn reduced exhaustion and senescence cell markers. Our results suggest that mito-transfer could be a novel strategy to reestablish aged CD4+T cell function, potentially improving immune responses in the elderly and chronic TB patients, with a broader implication for other diseases where mitochondrial dysfunction is linked to T cell exhaustion and senescence.
Computation-aided Design of Rod-Shaped Janus Base Nanopieces for Improved Tissue Penetration and Therapeutics Delivery
Authors: Lee Jinhyung , Zhang Wuxia , Nguyen Danh , Zhou Libo , Amengual Justin , Zhai Jin , Cote Trystin , Landolina Maxwell , Ahmadi Elham , Sands Ian , Mishra Neha , Yu Hongchuan , Nieh Mu-Ping , Wang Kepeng , Li Ying , Chen Yupeng 
Published: January 2024

AbstractDespite the development of various drug delivery technologies, there remains a significant need for vehicles that can improve targeting and biodistribution in “hard-to-penetrate” tissues. Some solid tumors, for example, are particularly challenging to penetrate due to their dense extracellular matrix (ECM). In this study, we have formulated a new family of rod-shaped delivery vehicles named Janus base nanopieces (Rod JBNps), which are more slender than conventional spherical nanoparticles, such as lipid nanoparticles (LNPs). These JBNp nanorods are formed by bundles of DNA-inspired Janus base nanotubes (JBNts) with intercalated delivery cargoes. To develop this novel family of delivery vehicles, we employed a computation-aided design (CAD) methodology that includes molecular dynamics and response surface methodology. This approach precisely and efficiently guides experimental designs. Using an ovarian cancer model, we demonstrated that JBNps markedly improve penetration into the dense ECM of solid tumors, leading to better treatment outcomes compared to FDA-approved spherical LNP delivery. This study not only successfully developed a rod-shaped delivery vehicle for improved tissue penetration but also established a CAD methodology to effectively guide material design.
Regulatory T cells control type 1-driven immunopathology restraining GM-CSF-producing helper T cells
Authors: Costa-Pereira Sara , Lanzinger Margit , Andreadou Myrto , Nunez Nicolas , Villar-Vesga Juan , Prisco Francesco , Häne Philipp , Roussel Elsa , Krishnarajah Sinduya , Lindemann Rachel Chanel , Westermann Frederike , Oberbichler Laura , Sethi Aakriti , Da Silva André Fonseca , Lutz Mirjam , Tugues Sonia , Mundt Sarah , Kipar Anja , Greter Melanie , De Feo Donatella , Becher Burkhard 
Published: January 2024

SUMMARYRegulatory T (Treg) cells are critical for maintaining peripheral tolerance and preventing autoimmunity. Tregcell depletion or dysfunction rapidly results in fatal multiorgan inflammation linked to unrestrained effector T cell expansion, but the cytokine network underlying immunopathology, and its direct cellular mediators, remain elusive. Here, we combined gene targeting, fate-mapping tools, and high-dimensional cytometry to identify the T helper (TH) cell-derived cytokines and responding cells that execute inflammatory tissue damage upon global loss of peripheral tolerance in mice. We found that THcell-derived GM-CSF, but not IL-17A, directed the ensuing immunopathology and thereby mortality through recruitment of tissue-invading phagocytes and granulocytes, and enhancement of their reactive oxygen species production and phagocytic proficiency. Our study highlights the critical role of Tregcells in controlling GM-CSF- producing THcells and type 1-responses to restrain phagocyte-mediated tissue destruction and provides a framework for the use of anti-GM-CSF therapies in patients with chronic inflammatory disorders.
Systemic Genome Correlation Loss as a Central Characteristic of Spaceflight
Authors: Sakharkar Anurag , Lukong Erique , Sanders Lauren M. , Costes Sylvain V. , Taghibiglou Changiz , Yang Jian 
Published: January 2024

AbstractSpace exploration has captured the imagination of humanity for generations. From the first steps on the moon to the recent Mars rover and Artemis lunar exploration missions, space travel has always been an ambitious goal for humanity. However, as we venture further into space and prepare for long-term missions to other planets, the physiological and health risks associated with prolonged space travel are becoming more prominent. Most current research on astronaut health focuses on identifying individual genes or pathways for specific symptoms astronauts face. The human system is complex and delicate, and the effects of microgravity, radiation, and isolation on astronaut health during long-duration spaceflight are still not fully understood. This study used a novel ranking and analysis methodology to combine space omics data from multiple datasets in the NASA OSDR repository. The data was used to generate a multi-omic, integrative bioinformatics analysis pipeline, which identified and characterized a genome-wide spaceflight gene expression correlation loss as a central biosignature for astronaut health on the International Space Station (ISS). Our findings indicate that genome-wide correlation loss corresponds to a breakdown in gene synchronization and cooperation, showcasing the systemic symptoms spaceflight induces and their genomic roots.