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Complex models of infectious diseases are used to understand the transmission dynamics of the disease, project the course of an epidemic, predict the effect of interventions and/or provide information for power calculations of community level intervention studies. However, there have been relatively few opportunities to rigorously evaluate the predictions of such models till now. Indeed, while there is a large literature on calibration (fitting model parameters) and validation (comparing model outputs to data) of complex models based on empirical data, the lack of uniformity in accepted criteria for such procedures for models of infectious diseases has led to simple procedures being prevalent for such steps. However, recently, several community level randomized trials of combination HIV intervention have been planned and/or initiated, and in each case, significant epidemic modeling efforts were conducted during trial planning which were integral to the design of these trials. The existence of these models and the (anticipated) availability of results from the related trials, provide a unique opportunity to evaluate the models and their usefulness in trial design. In this project, we outline a framework for evaluating the predictions of complex epidemiological models and describe experiments that can be used to test their predictions.
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http://dx.doi.org/10.1016/j.epidem.2021.100514 | DOI Listing |
Comput Biol Med
September 2025
INSIGNEO Institute for in silico medicine, University of Sheffield, UK; School of Mechanical, Aerospace and Civil Engineering, University of Sheffield, UK. Electronic address:
Modelling cardiovascular disease is at the forefront of efforts to use computational tools to assist in the analysis and forecasting of an individual's state of health. To build trust in such tools, it is crucial to understand how different approaches perform when applied to a nominally identical scenario, both singularly and across a population. To examine such differences, we have studied the flow in aneurysms located on the internal carotid artery and middle cerebral artery using the commercial solver Ansys CFX and the open-source code HemeLB.
View Article and Find Full Text PDFStem Cell Res
September 2025
Department of General Pediatrics, Neonatology, and Pediatric Cardiology, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine-University, Düsseldorf 40225, Germany. Electronic address:
Pathogenic variants in the gene COQ4 cause primary coenzyme Q deficiency, which is associated with symptoms ranging from early epileptic encephalopathy up to adult-onset ataxia-spasticity spectrum disease. We genetically modified commercially available wild-type iPS cells by using a CRISPR/Cas9 approach to create heterozygous and homozygous isogenic cell lines carrying the disease-causing COQ4 variants c.458C > T, p.
View Article and Find Full Text PDFEur J Radiol
September 2025
Department of Radiology, Affiliated Hospital of Hebei University, Baoding 071000, China. Electronic address:
Purpose: The present study aimed to develop a noninvasive predictive framework that integrates clinical data, conventional radiomics, habitat imaging, and deep learning for the preoperative stratification of MGMT gene promoter methylation in glioma.
Materials And Methods: This retrospective study included 410 patients from the University of California, San Francisco, USA, and 102 patients from our hospital. Seven models were constructed using preoperative contrast-enhanced T1-weighted MRI with gadobenate dimeglumine as the contrast agent.
Arch Med Res
September 2025
Department and Graduate Institute of Microbiology and Immunology, National Defense Medical Center, Taipei, Taiwan. Electronic address:
Background: Atherosclerosis, a leading cause of cardiovascular disease (CVD) mortality worldwide, is characterized by dysregulated lipid metabolism and unresolved inflammation. Macrophage-derived foam cell formation and apoptosis contribute to plaque formation and vulnerability. Elevated serum galectin-3 (Gal-3) levels are associated with increased CVD risk, and Gal-3 in plaques is strongly associated with macrophages.
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