As the size of phylogenetic trees and comparative data continue to grow and more complex models are developed to investigate the processes that gave rise to them, macroevolutionary analyses are becoming increasingly limited by computational requirements. Here, we introduce a novel algorithm, based on the "flow" of the differential equations that describe likelihoods along tree edges in backward time, to reduce redundancy in calculations and efficiently compute the likelihood of various macroevolutionary models. Our algorithm applies to several diversification models, including birth-death models and models that account for state- or time-dependent rates, as well as many commonly used models of discrete-trait evolution, and provides an alternative way to describe macroevolutionary model likelihoods. As a demonstration of our algorithm's utility, we implemented it for a popular class of state-dependent diversification models-BiSSE, MuSSE, and their extensions to hidden-states. Our implementation is available through the R package $\texttt{castor}$. We show that, for these models, our algorithm is one or more orders of magnitude faster than existing implementations when applied to large phylogenies. Our algorithm thus enables the fitting of state-dependent diversification models to modern massive phylogenies with millions of tips and may lead to potentially similar computational improvements for many other macroevolutionary models.
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http://dx.doi.org/10.1093/sysbio/syz055 | DOI Listing |
Nurs Health Sci
March 2025
Nursing Services Manager, Memorial Health Group Ataşehir, Istanbul, Türkiye.
The aim of this study is to determine the mediating role of moral sensitivity in the effect of nurses' professional values on missed nursing care. A descriptive and correlational study was conducted with 640 nurses working in the inpatient units of a public and a private hospital with the MISSCARE Survey-Turkish, the Moral Sensitivity Questionnaire, and the Revised Nursing Professional Values Scale. Data analyses were performed using the Statistical Package for Social Sciences 26.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Department of Molecular Biology, Cellular Biology, and Biochemistry, Brown University, Providence, RI, 02912, USA.
Pulmonary hypertension (PH) increases the mortality of preterm infants with bronchopulmonary dysplasia (BPD). There are no curative therapies for this disease. Lung endothelial carnitine palmitoyltransferase 1a (Cpt1a), the rate-limiting enzyme of the carnitine shuttle system, is reduced in a rodent model of BPD.
View Article and Find Full Text PDFImmun Inflamm Dis
January 2025
Department of Clinical Laboratory, the Second Affiliated Hospital of Anhui Medical University, Hefei, China.
Backgrounds And Aims: CD8+T cells are crucially associated with the fight against hepatitis B virus (HBV) infection. CD161 has been shown to express remarkably on HCV-specific CD8+T cells. However, the accurate function of CD161+CD8+T cells in HBV immunity or pathogenesis remains undetermined.
View Article and Find Full Text PDFAnn N Y Acad Sci
January 2025
NewClimate Institute, Cologne, Germany.
Globally, more than 100 countries have adopted net-zero targets. Most studies agree on how this increases the chance of keeping end-of-century global warming below 2°C. However, they typically make assumptions about net-zero targets that do not capture uncertainties related to gas coverage, sector coverage, sinks, and removals.
View Article and Find Full Text PDFSTAR Protoc
January 2025
Department of Experimental Vascular Medicine, Amsterdam UMC, location AMC, Meibergdreef 9, Amsterdam, the Netherlands; Amsterdam Cardiovascular Sciences, Atherosclerosis & Ischemic Syndromes, Amsterdam, the Netherlands; Laboratory of Angiogenesis and Vascular Metabolism, VIB-KU Leuven Center for Cancer Biology, VIB, 3000 Leuven, Belgium; Laboratory of Angiogenesis and Vascular Metabolism, Department of Oncology, KU Leuven and Leuven Cancer Institute (LKI), 3000 Leuven, Belgium. Electronic address:
The endothelium is the gatekeeper of vessel health, and its dysfunction is pivotal in driving atherogenesis. Here, we present a protocol to replicate endothelial-macrophage crosstalk during atherogenesis, called the "atherogenesis-on-chip" model, based on the Emulate dual-channel perfusion system. We describe a model for studying endothelial-macrophage interactions during atherogenesis in human aortic endothelial cells and human macrophages using qPCR and secretome analysis, fluorescence microscopy, and flow cytometry.
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