We will present the latest developments in CutLang, the runtime interpreter of a recently-developed analysis description language (ADL) for collider data analysis. ADL is a domain-specific, declarative language that describes the contents of an analysis in a standard and unambiguous way, independent of any computing framework. In ADL, analyses are written in human-readable plain text files, separating object, variable and event selection definitions in blocks, with a syntax that includes mathematical and logical operations, comparison and optimisation operators, reducers, four-vector algebra and commonly used functions. Adopting ADLs would bring numerous benefits to the LHC experimental and phenomenological communities, ranging from analysis preservation beyond the lifetimes of experiments or analysis software to facilitating the abstraction, design, visualization, validation, combination, reproduction, interpretation and overall communication of the analysis contents. Since their initial release, ADL and CutLang have been used for implementing and running numerous LHC analyses. In this process, the original syntax from CutLang v1 has been modified for better ADL compatibility, and the interpreter has been adapted to work with that syntax, resulting in the current release v2. Furthermore, CutLang has been enhanced to handle object combinatorics, to include tables and weights, to save events at any analysis stage, to benefit from multi-core/multi-CPU hardware among other improvements. In this contribution, these and other enhancements are discussed in details. In addition, real life examples from LHC analyses are presented together with a user manual.
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http://dx.doi.org/10.3389/fdata.2021.659986 | DOI Listing |
JCI Insight
January 2025
Medical Oncology Department, Research Institute for Medical Innovation, Radboud University Medical Center, Nijmegen, Netherlands.
Background: Previously, we demonstrated that changes in circulating tumor DNA (ctDNA) are promising biomarkers for early response prediction (ERP) to immune checkpoint inhibitors (ICI) in metastatic urothelial cancer (mUC). In this study, we investigated the value of whole blood immunotranscriptomics for ERP-ICI and integrated both biomarkers into a multimodal model to boost accuracy.
Methods: Blood samples of 93 patients were collected at baseline and after 2-6 weeks of ICI for ctDNA (N=88) and immunotranscriptome (N=79) analyses.
J Clin Invest
January 2025
Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Metabolic reprogramming shapes tumor microenvironment (TME) and may lead to immunotherapy resistance in pancreatic ductal adenocarcinoma (PDAC). Elucidating the impact of pancreatic cancer cell metabolism in the TME is essential to therapeutic interventions. "Immune cold" PDAC is characterized by elevated lactate levels resulting from tumor cell metabolism, abundance of pro-tumor macrophages, and reduced cytotoxic T cell in the TME.
View Article and Find Full Text PDFJCI Insight
January 2025
Dianne Hoppes Nunnally Laboratory Research Division, Joslin Diabetes Center, Boston, United States of America.
Background: We aimed to characterize factors associated with the under-studied complication of cognitive decline in aging people with long-duration type 1 diabetes (T1D).
Methods: Joslin "Medalists" (n = 222; T1D ≥ 50 years) underwent cognitive testing. Medalists (n = 52) and age-matched non-diabetic controls (n = 20) underwent neuro- and retinal imaging.
Br J Dermatol
January 2025
Centre of Evidence Based Dermatology, School of Medicine, Faculty of Medicine & Health Sciences, University of Nottingham, UK.
Background: Randomised controlled trials (RCTs) evaluating new systemic treatments for atopic dermatitis (AD) have increased dramatically over the last decade. These trials often incorporate topical therapies either as permitted concomitant or rescue treatments. Differential use of these topicals post-randomisation introduces potential bias as they may nullify or exaggerate treatment responses.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Department of Medicine, University of California San Francisco, San Francisco, United States of America.
Hypoxia is a major cause of pulmonary hypertension (PH) worldwide, and it is likely that interstitial pulmonary macrophages contribute to this vascular pathology. We observed in hypoxia-exposed mice an increase in resident interstitial macrophages, which expanded through proliferation and expressed the monocyte recruitment ligand CCL2. We also observed an increase in CCR2+ macrophages through recruitment, which express the protein thrombospondin-1 that functionally activates TGF-beta to cause vascular disease.
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