bluuebunny/crossref_metadata_2025_split huggingface dataset:
Greater Emotional and Psychological Well-being Are Associated With Reduced Employee Self-report Illness-Related Absenteeism
Authors: Fannin Austin , Hooley Cole , Nelson Erik J. 
Published: January 2024

Objective
The purpose of this study is to determine the relationship that emotional, psychological, and social well-being has with self-reported illness-related absenteeism.

Methods
This study examines the relationship between three dimensions of well-being (emotional, psychological, and social) and self-report illness-related absenteeism among 133 workers spanning multiple industries across 16 different companies. This secondary, cross-sectional data were analyzed using multiple linear regression.

Results
As hypothesized, emotional well-being and psychological well-being were found to be negatively associated with absenteeism, with emotional well-being being the stronger predictor. Contrary to our hypothesis, we found that social well-being was not associated with absenteeism among workers.

Conclusions
Employee emotional well-being and psychological well-being are associated with self-reported illness-related absenteeism. Future work should explore causal relationships between these constructs.
Prognostic impact of resection margin status on survival after neoadjuvant treatment for pancreatic cancer: systematic review and meta-analysis
Authors: Leonhardt Carl-Stephan , Hank Thomas , Pils Dietmar , Gustorff Charlotte , Sahora Klaus , Schindl Martin , Verbeke Caroline S. , Strobel Oliver , Klaiber Ulla 
Published: January 2024

Background:
A greater than 1 mm tumour-free resection margin (R0 >1 mm) is a prognostic factor in upfront-resected pancreatic ductal adenocarcinoma. After neoadjuvant treatment (NAT); however, the prognostic impact of resection margin (R) status remains controversial.

Methods:
Randomised and non-randomised studies assessing the association of R status and survival in resected pancreatic ductal adenocarcinoma after NAT were sought by systematic searches of MEDLINE, Web of Science and CENTRAL. Hazard ratios (HR) and their corresponding 95% CI were collected to generate log HR using the inverse-variance method. Random-effects meta-analyses were performed and the results presented as weighted HR. Sensitivity and meta-regression analyses were conducted to account for different surgical procedures and varying length of follow-up, respectively.

Results:
Twenty-two studies with a total of 4929 patients were included. Based on univariable data, R0 greater than 1 mm was significantly associated with prolonged overall survival (OS) (HR 1.76, 95% CI 1.57–1.97; P<0.00001) and disease-free survival (DFS) (HR 1.66, 95% CI 1.39–1.97; P<0.00001). Using adjusted data, R0 greater than 1 mm was significantly associated with prolonged OS (HR 1.65, 95% CI 1.39–1.97; P<0.00001) and DFS (HR 1.76, 95% CI 1.30–2.39; P=0.0003). Results for R1 direct were comparable in the entire cohort; however, no prognostic impact was detected in sensitivity analysis including only partial pancreatoduodenectomies.

Conclusion:
After NAT, a tumour-free margin greater than 1 mm is independently associated with improved OS as well as DFS in patients undergoing surgical resection for pancreatic cancer.
An exploration of how practitioners make meaning in a Chinese medicine consultation and treatment
Authors: Moir Felicity Clare 
Published: January 2024

Abstract:
In Chinese medicine, practitioners assess patients’ complaints, analyze their underlying problems, identify causes and come to a diagnosis, which then directs treatment. What is not obvious and not recorded in a consultation is the clinical reasoning process that practitioners use. The research filmed three practitioners in the UK while they conducted a consultation and treatment on new patients. The practitioners and researchers viewed the films and used them as aide-memoirs, the reasoning process throughout was discussed. In order to determine the pattern, practitioners used the four examinations to gather information from the patient in an iterative process; their aesthetic reasoning was highly developed. Through triangulation they checked the information they received against a detailed understanding of the qi-dynamic. They used highly analytical strategies of forward (inductive) and backward (deductive) reasoning against the prototypes of the signs and symptoms that indicate a specific Zheng. This was achieved through an abductive process that linked description with explanation and causal factors with pathological mechanisms. The feedback loop with the patient continued through the consultation and into the treatment. A process of translation and interpretation was needed to turn the patient’s story into the practitioner’s story of qi-dynamics that then directed the treatment.Awareness of our clinical reasoning process will mitigate against biases, improve our diagnoses and treatment choices and support the training of students.
Novel functions of Tribbles-homolog 1 in liver, adipocytes and atherosclerosis
Authors: Hernandez-Resendiz Ileana , Burkhardt Ralph 
Published: January 2024

Purpose of review
Human genetics studies have sparked great interest in the pseudokinase Tribbles homolog 1, as variant at the TRIB1 gene locus were robustly linked to several cardiometabolic traits, including plasma lipids and coronary artery disease. In this review, we summarize recent findings from mouse models that investigated the function of hepatic and adipocyte Trib1 in lipid metabolism and its role in atherosclerosis.

Recent findings
Studies in atherosclerosis prone low-density lipoprotein (LDL)-receptor knockout mice suggested that systemic Trib1-deficiency promotes atherosclerotic lesion formation through the modulation of plasma lipids and inflammation. Further, investigations in mice with hepatocyte specific deletion of Trib1 identified a novel role in the catabolism of apoB-containing lipoproteins via regulation of the LDL-receptor. Moreover, recent studies on Trib1 in adipocytes uncovered critical functions in adipose tissue biology, including the regulation of plasma lipid and adiponectin levels and the response to β3-adrenergic receptor activation.

Summary
Functional studies in mice have expanded our understanding of how Trib1 contributes to various aspects of cardiometabolic diseases. They support the notion that Trib1 exerts tissue-specific effects, which can result in opposing effects on cardiometabolic traits. Additional studies are required to fully elucidate the molecular mechanisms underlying the cellular and systemic effects of Trib1.
Urine CXCL10 as a biomarker in kidney transplantation
Authors: Hirt-Minkowski Patricia , Schaub Stefan 
Published: January 2024

Purpose of review
Urine CXCL10 is a promising biomarker for posttransplant renal allograft monitoring but is currently not widely used for clinical management.

Recent findings
Large retrospective studies and data from a prospective randomized trial as well as a prospective cohort study demonstrate that low urine CXCL10 levels are associated with a low risk of rejection and can exclude BK polyomavirus replication with high certainty. Urine CXCL10 can either be used as part of a multiparameter based risk assessment tool, or as an individual biomarker taking relevant confounders into account. A novel Luminex-based CXCL10 assay has been validated in a multicenter study, and proved to be robust, reproducible, and accurate.

Summary
Urine CXCL10 is a well characterized inflammation biomarker, which can be used to guide performance of surveillance biopsies. Wide implementation into clinical practice depends on the availability of inexpensive, thoroughly validated assays with approval from regulatory authorities.
Restraint Validation of Biomolecular Structures Determined by NMR in the Protein Data Bank
Authors: Baskaran Kumaran , Ploskon Eliza , Tejero Roberto , Yokochi Masashi , Harrus Deborah , Liang Yuhe , Peisach Ezra , Persikova Irina , Ramelot Theresa A. , Sekharan Monica , Tolchard James , Westbrook John D. , Bardiaux Benjamin , Schwieters Charles D. , Patwardhan Ardan , Velankar Sameer , Burley Stephen K. , Kurisu Genji , Hoch Jeffrey C. , Montelione Gaetano T. , Vuister Geerten W. , Young Jasmine Y. 
Published: January 2024

SummaryBiomolecular structure analysis from experimental NMR studies generally relies on restraints derived from a combination of experimental and knowledge-based data. A challenge for the structural biology community has been a lack of standards for representing these restraints, preventing the establishment of uniform methods of model-vs-data structure validation against restraints and limiting interoperability between restraint-based structure modeling programs. The NMR exchange (NEF) and NMR-STAR formats provide a standardized approach for representing commonly used NMR restraints. Using these restraint formats, a standardized validation system for assessing structural models of biopolymers against restraints has been developed and implemented in the wwPDB OneDep data deposition-validation-biocuration system. The resulting wwPDB Restraint Violation Report provides a model vs. data assessment of biomolecule structures determined using distance and dihedral restraints, with extensions to other restraint types currently being implemented. These tools are useful for assessing NMR models, as well as for assessing biomolecular structure predictions based on distance restraints.Graphical AbstractHighlightsPDB Structure Validation Report expanded to include Restraint AnalysisNMR Exchange Format (NEF) and NMR-STAR for distance restraint representationStandard distance and dihedral restraint formats for model vs. restraint assessmentStandardized restraint formats provide interoperability between modeling programs
BSAlign: a library for nucleotide sequence alignment
Authors: Shao Haojing , Ruan Jue 
Published: January 2024

AbstractIncreasing the accuracy of the nucleotide sequence alignment is an essential issue in genomics research. Although classic dynamic-programming algorithms (e.g., Smith-Waterman and Needleman–Wunsch) guarantee to produce the optimal result, their time complexity hinders the application of large-scale sequence alignment. Many optimization efforts that aim to accelerate the alignment process generally come from three perspectives: re-designing data structures (e.g., diagonal or striped Single Instruction Multiple Data (SIMD) implementations), increasing the number of parallelisms in SIMD operations (e.g., difference recurrence relation), or reducing searching space (e.g., banded dynamic programming). However, no methods combine all these three aspects to build an ultra-fast algorithm. We have developed a Banded Striped Aligner(library) named BSAlign that delivers accurate alignment results at an ultra-fast speed by knitting a series of novel methods together to take advantage of all of the aforementioned three perspectives with highlights such as active F-loop in striped vectorization and striped move in banded dynamic programming. We applied our new acceleration design on both regular and edit-distance pairwise alignment. BSAlign achieved 2-fold speed-up than other SIMD based implementations for regular pairwise alignment, and 1.5 to 4-fold speedup in edit distance based implementations for long reads. BSAlign is implemented in C programing language and is available athttps://github.com/ruanjue/bsalign.
Diabetes Advances Cardiomyocyte Senescence through miR-103a-3p/Rnd3/STAT3 Signaling
Authors: Wu Linxu , Zhu Xinglin , Luo Cai , Chen Yan , Liu Yin , Zhao Yangyang , Pan Shanshan , Shi Kaijia , Xing Jingci , Lin Xuebin , Qiu Jianmin , Zhang Shuya , Chai Jinxuan , Shen Zhihua , Jie Wei , Guo Junli 
Published: January 2024

AbstractBACKGROUNDRnd3, a small Rho-GTPase, is involved in various cardiovascular diseases, but its role in diabetes-induced cardiomyocyte senescence is unclear. This study aims to investigate the role of Rnd3 in cardiomyocyte senescence in diabetes cardiomyopathy (DCM).METHODSRnd3expression was assessed in human tissue using qPCR, and its correlation with clinical parameters was analyzed.Rnd3and Senescence-associated secretory phenotype (SASP)-related marker expression was determined in heart tissue from juvenile/mature mice and streptozotocin-induced diabetic Sprague–Dawley rats. H9C2 and AC16 cardiomyocytes were exposed to high glucose ([HG] =35 mmol/L D-glucose), and Rnd3 and SASP-related marker expression was examined.Rnd3expression in H9C2 cells was disrupted using CRISPR/Cas9 technology, and cellular senescence of HG-treated H9C2 cells was evaluated. MicroRNA sequencing was conducted on AC16 cells to identify differentially expressed microRNAs regulated by HG. Among these microRNAs, miR-103a-3p was selected for further investigation in a clinical diabetes cohort and to examine its binding toRnd33′UTR and its effect on cell senescence. Finally, the role of interaction of Rnd3 and STAT3 in cardiomyocyte senescence was investigated.RESULTSRnd3mRNA levels were reduced in peripheral blood mononuclear cells in diabetic patients, which was negatively correlated to patients age but positively correlated to cardiac function. Older mice exhibited compromised cardiac function, increased SA-β-gal-positive cells, and SASP marker levels versus younger mice. HG stimulation inhibited Rnd3 expression but enhanced cellular senescence.Rnd3knockout resulted in greater cellular senescence on HG-insulted cardiomyocytes. miR-103a-3p was identified as a key HG-regulated microRNA that binds toRnd33′UTR. AAV9 carrying miR-103a-3p sponges andRnd3-overexpressing plasmids mitigated cellular senescence in diabetic rats. Interestingly, miR-103a-3p levels positively correlated with blood glucose concentrations. HG stimulation amplified phosphorylated STAT3(Tyr705) in H9C2 cells, which was intensified byRnd3knockout. Rnd3 binds with STAT3 in cytoplasm and promote proteasome-induced ubiquitination of STAT3. S3I-201 mitigated HG-activated STAT3 and cardiomyocyte senescence.CONCLUSIONDiabetes causes cardiomyocyte senescence through miR-103a-3p/Rnd3/STAT3 signaling, suggesting a potential treatment strategy for DCM.
Validation ofInternational Classification of Diseases, 10thEdition, Clinical Modification (ICD-10-CM)Code I68.0 for Cerebral Amyloid Angiopathy
Authors: Bruce Samuel S. , Murthy Santosh , Kamel Hooman 
Published: January 2024

AbstractIntroductionCerebral amyloid angiopathy (CAA) is a common cause of intracerebral hemorrhage and cognitive impairment in the elderly. Though definitive diagnosis requires post-mortem pathological analysis, clinical and radiographic criteria allow for noninvasive, in vivo diagnosis. We sought to validate the new ICD-10-CM diagnostic code for CAA with respect to the recently updated Boston criteria, version 2.0.MethodsWe conducted a retrospective study of inpatient and outpatient encounters at a single hospital center, Weill Cornell Medicine (WCM), from 10/1/2015 to 12/31/2018. We randomly selected 25 encounters with the ICD-10-CM code I68.0 and 25 encounters with a primary diagnosis of intracerebral hemorrhage or ischemic stroke, without code I68.0. A single board-certified neurologist, blinded to ICD codes, reviewed detailed medical records and images from brain MRI and CT scans from all 50 selected encounters and identified subjects with possible or probable CAA by Boston criteria 2.0. Sensitivity and specificity of ICD-10-CM code I68.0 was calculated.ResultsOf the 50 selected encounters, 21 (42%) met criteria for possible or probable CAA: 18 (36%) met criteria for probable CAA, 2 (4%) met criteria for probable CAA with supporting pathology, and 1 (2%) met criteria for possible CAA. The ICD-10-CM code I68.0 was found to have a sensitivity of 81% (95% CI, 58-95%) and specificity of 72% (95% CI, 53-87%) for identifying possible or probable CAA.ConclusionThe ICD-10-CM code I68.0 was found to have good sensitivity and moderate specificity for CAA as defined by current clinical and radiographic diagnostic criteria. Based on our results, this code may be useful for identifying patients with CAA in future research using administrative claims data.
Conservation of symbiotic signalling across 450 million years of plant evolution
Authors: Vernié Tatiana , Rich Mélanie , Pellen Tifenn , Teyssier Eve , Garrigues Vincent , Chauderon Lucie , Medioni Lauréna , van Beveren Fabian , Libourel Cyril , Keller Jean , Girou Camille , Lefort Corinne , Le Ru Aurélie , Reinhardt Didier , Kodama Kyoichi , Shimazaki Syota , Morel Patrice , Kyozuka Junko , Mbengue Malick , Vandenbussche Michiel , Delaux Pierre-Marc 
Published: January 2024

SummaryHighlightThe common symbiotic pathway is activated during arbuscular mycorrhizal symbiosis inMarchantia paleaceaThe three core members of the common symbiotic pathway are essential for symbiosis inMarchantia paleaceaThe molecular function of the CCaMK/CYCLOPS module is conserved across land plantsSymbiotic signalling has been conserved in plants for 450 million yearsThe colonization of land by plants 450 million years ago revolutionized life on Earth1. The fossil record2and genetic evidence in extant species3suggest that this transition was facilitated by interactions with symbiotic arbuscular mycorrhizal (AM) fungi4. This ancestral symbiosis relied on the biosynthesis of chemicals by the host plant, both as signals5and as nutrients3. In angiosperms, a signalling pathway involving the receptor-like kinase SYMRK/DMI26,7, the Calcium and Calmodulin-dependent protein kinase CCaMK/DMI38and the transcription factor CYCLOPS/IPD39,10has been described as the common symbiosis pathway (CSP), essential for the establishment of the AM symbiosis and the root-nodule symbiosis11. Phylogenetic and comparative phylogenomic analyses indicated an ancient origin of the CSP, present in all extant land plants forming intracellular symbioses12–15. Trans-complementation assays of the angiosperm mutants with orthologs from diverse species further indicated the conservation of the molecular function of the CSP across the embryophytes9,12,14–16. However, this correlative evidence did not allow testing the ancestral biological function of the CSP. In this study we demonstrate that SYMRK, CCaMK and CYCLOPS are essential for the colonization by AM fungi in bryophytes, indicating that plants have maintained a dedicated signalling pathway to support symbiotic interactions for 450 million years.
Discrete and conserved inflammatory signatures drive thrombosis in different organs afterSalmonellainfection
Authors: Perez-Toledo Marisol , Beristain-Covarrubias Nonantzin , Pillaye Jamie , Persaud Ruby R , Marcial-Juarez Edith , Jossi Sian E. , Hitchcock Jessica R. , Alshayea Areej , Channell William M. , Lamerton Rachel E , Kavanagh Dean P , Carestia Agostina , Horsnell William G , Henderson Ian R. , Mackman Nigel , Clark Andrew R , Jenne Craig N , Rayes Julie , Watson Steve P. , Cunningham Adam F. 
Published: January 2024

AbstractInflammation-induced thrombosis is a common consequence of bacterial and viral infections, such as those caused bySalmonellaTyphimurium (STm) and SARS-CoV-2. The identification of multi-organ thrombosis and the chronological differences in its induction and resolution raises significant challenges for successfully targeting multi-organ infection-associated thrombosis. Here, we identified specific pathways and effector cells driving thrombosis in the spleen and liver following STm infection. Thrombosis in the spleen is independent of IFN-γ or the platelet C-type lectin-like receptor CLEC-2, while both molecules were previously identified as key drivers of thrombosis in the liver. Furthermore, we identified platelets, monocytes, and neutrophils as core constituents of thrombi in both organs. Depleting neutrophils or monocytic cells independently abrogated thrombus formation. Nevertheless, blocking TNFα, which is expressed by both myeloid cell types, diminished both thrombosis and inflammation which correlates with reduced endothelial expression of E-selectin and leukocyte infiltration. Moreover, tissue factor and P-selectin glycoprotein ligand 1 inhibition impair thrombosis in both spleen and liver, identifying multiple common checkpoints to target multi-organ thrombosis. Therefore, organ-specific, and broad mechanisms driving thrombosis potentially allow tailored treatments based on the clinical need and to define the most adequate strategy to target both thrombosis and inflammation associated with systemic infections.
LysM-RLK plays an ancestral symbiotic function in plants
Authors: Teyssier Eve , Grat Sabine , Landry David , Ouradou Mathilde , Rich Melanie K. , Fort Sebastien , Keller Jean , Lefebvre Benoit , Delaux Pierre-Marc , Mbengue Malick 
Published: January 2024

AbstractArbuscular mycorrhiza (AM) with soilborne Glomeromycota fungi was pivotal in the conquest of land by plants almost half a billion years ago. In flowering plants, it is hypothesised that AM is initiated by the perception of AM-fungi-derived chito- and lipochito-oligosaccharides (COs/LCOs) in the host via Lysin Motif Receptor-Like Kinases (LysM-RLKs). However, it remains uncertain whether plant perception of these molecules is a prerequisite for AM establishment and for its origin. Here, we made use of the reduced LysM-RLK complement present in the liverwortMarchantia paleaceato assess the conservation of the role played by this class of receptors during AM and in COs/LCOs perception. Our reverse genetic approach demonstrates the critical function of a single LysM-RLK, LYKa, in AM formation, thereby supporting an ancestral function for this receptor in symbiosis. Binding studies, cytosolic calcium variation recordings and genome-wide transcriptomics indicate that another LysM-RLK ofM. paleacea, LYR, is also required for triggering a response to COs/LCOs, despite being dispensable for AM formation. Collectively, our results demonstrate that the perception of symbionts by LysM-RLK is an ancestral feature in land plants, and suggest the existence of yet-uncharacterised AM-fungi signals.
Polymeric nanoparticles delivery of AMPK activator 991 prevents its toxicity and improves muscle homeostasis in Duchenne Muscular Dystrophy
Authors: Andreana Ilaria , Kneppers Anita , Larbi Sabrina Ben , Tifni Federica , Fessard Aurélie , Sidi-Boumedine Jaqueline , Kryza David , Stella Barbara , Arpicco Silvia , Bordes Claire , Chevalier Yves , Chazaud Bénédicte , Mounier Rémi , Lollo Giovanna , Juban Gaëtan 
Published: January 2024

AbstractMuscular dystrophies, such as Duchenne muscular dystrophy (DMD), are caused by permanent muscle injuries leading to chronic inflammation. In that context, macrophages harbor an altered inflammatory profile that contributes to fibrosis through the secretion of the profibrotic cytokine TGFβ1. We previously showed that AMP-activated protein kinase (AMPK) activation reduces TGFβ1 secretion by macrophages and improves muscle homeostasis and muscle force in a mouse model of DMD. This makes AMPK an attractive therapeutic target for treating chronic inflammation and fibrosis in DMD. However, potent direct AMPK activators like compound 991 show strong adverse effectsin vivo,preventing their direct use. Here, we encapsulated 991 into biodegradable polymeric poly(lactic-co-glycolic) acid (PLGA) nanoparticles forin vivodelivery, in an attempt to overcome toxicity issues. We show that 991-loaded PLGA nanoparticles retained drug activity on fibrotic macrophagesin vitro, by reducing their secretion of TGFβ1. In the D2-mdx pre-clinical DMD mouse model, intravenously injected PLGA nanoparticles reached gastrocnemius and diaphragm muscles, which are the most affected muscles in this model. Chronic intravenous injections of 991-loaded PLGA nanoparticles decreased inflammation in both muscles, which was associated with fibrosis reduction and increase in myofiber size and muscle mass in the gastrocnemius. No impact on blood cell counts and liver enzymes was observed. These results demonstrate that nanomedicine is an efficient strategy to deliver AMPK activatorsin vivoto target inflammation and improve the dystrophic muscle phenotype.