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Z-residual diagnostic tool for assessing covariate functional form in shared frailty models.
J Appl Stat
May 2024
Department of Community Health and Epidemiology, Faculty of Medicine, Dalhousie University, Halifax, CA, Canada.
Survival analysis often involves modeling hazard functions while considering frailty to account for unobserved cluster-level factors in clustered survival data. Shared frailty models have gained popularity for this purpose, but assessing covariate functional form in these models presents unique challenges. Martingale and deviance residuals are commonly used for visually assessing covariate functional form against continuous covariates.
View Article and Find Full Text PDFKidney REPLACEment therapies in patients with acute kidney injury and RHABDOmyolysis (ReplaceRhabdo): a pilot trial.
BMC Nephrol
January 2025
Medical Department III, Division of Nephrology, University Hospital Leipzig, Leipzig, Germany.
Background: Rhabdomyolysis is frequently associated with acute kidney injury (AKI). Due to the nephrotoxic properties of myoglobin, its rapid removal is relevant. If kidney replacement therapy (KRT) is necessary for AKI, a procedure with effective myoglobin elimination should be preferred.
View Article and Find Full Text PDFSingle-cell and bulk RNA sequencing-based screening and identification of extracellular trap network-related genes in neutrophils in acute myocardial infarction.
Medicine (Baltimore)
November 2024
Yantai Yuhuangding Hospital, Shandong, China.
Background: The neutrophil-mediated generation of neutrophil extracellular traps (NETs) results in an augmented inflammatory response and cellular tissue injury during acute myocardial infarction (AMI). Through the analysis of public database information, we discovered and confirmed putative critical genes involved in NETs-mediated AMI.
Methods: The AMI dataset GSE66360 and the single-cell dataset GSE163465 were downloaded from the Gene Expression Omnibus database.
Tumor Vaccine Exploiting Membranes with Influenza Virus-Induced Immunogenic Cell Death to Decorate Polylactic Coglycolic Acid Nanoparticles.
ACS Nano
January 2025
Laboratory of Molecular Immunology, Institute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Kunming 650031, China.
Immunogenic cell death (ICD) of tumor cells, which is characterized by releasing immunostimulatory "find me" and "eat me" signals, expressing proinflammatory cytokines and providing personalized and broad-spectrum tumor antigens draws increasing attention in developing a tumor vaccine. In this study, we aimed to investigate whether the influenza virus (IAV) is efficient enough to induce ICD in tumor cells and an extra modification of IAV components such as hemeagglutinin (HA) will be helpful for the ICD-induced cells to elicit robust antitumor effects; in addition, to evaluate whether the membrane-engineering polylactic coglycolic acid nanoparticles (PLGA NPs) simulating ICD immune stimulation mechanisms hold the potential to be a promising vaccine candidate, a mouse melanoma cell line (B16-F10 cell) was infected with IAV rescued by the reverse genetic system, and the prepared cells and membrane-modified PLGA NPs were used separately to immunize the melanoma-bearing mice. IAV-infected tumor cells exhibit dying status, releasing high mobility group box-1 (HMGB1) and adenosine triphosphate (ATP), and exposing calreticulin (CRT), IAV hemeagglutinin (HA), and tumor antigens like tyrosinase-related protein 2 (TRP2).
View Article and Find Full Text PDFPrognostic, biological, and structural implications of FLT3-JMD point mutations in acute myeloid leukemia: an analysis of Alliance studies.
Leukemia
January 2025
The Clara D. Bloomfield Center for Leukemia Outcomes Research, The Ohio State University Comprehensive Cancer Center, Columbus, OH, USA.
The FLT3 gene frequently undergoes mutations in acute myeloid leukemia (AML), with internal tandem duplications (ITD) and tyrosine kinase domain (TKD) point mutations (PMs) being most common. Recently, PMs and deletions in the FLT3 juxtamembrane domain (JMD) have been identified, but their biological and clinical significance remains poorly understood. We analyzed 1660 patients with de novo AML and found FLT3-JMD mutations, mostly PMs, in 2% of the patients.
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