Theorists of human evolution are interested in understanding major shifts in human behavioural capacities (e.g. the creation of a novel technological industry, such as the Acheulean). This task faces empirical challenges arising both from the complexity of these events and the time-depths involved. However, we also confront issues of a more philosophical nature, such as how to best think about causation and explanation. This article considers such fundamental questions from the perspective of a prominent theory of causation in the philosophy of science literature, namely, the . A signature feature of this framework is its recognition of a family of distinct types of causes. We set out several of these causal notions and show how they can contribute to explaining transitions in human behavioural complexity. We do so, first, in a preliminary way, and then in a more detailed way, taking the origins of behavioural modernity as our extended case study. We conclude by suggesting some ways in which the approach developed here might be elaborated and extended.
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http://dx.doi.org/10.1017/ehs.2024.27 | DOI Listing |
Addict Sci Clin Pract
January 2025
Center for Technology and Behavioral Health, Geisel School of Medicine, Dartmouth College, Lebanon, NH, 03766, USA.
Background: Opioid-related fatal overdoses are occurring at historically high levels and increasing each year. Accessible social and financial support are imperative to the initiation and success of treatment for Opioid Use Disorder (OUD). Medications for Opioid Use Disorder (MOUD) offer effective treatment but there are many more people with untreated OUD than receiving evidence-based medication.
View Article and Find Full Text PDFBMC Psychol
January 2025
Doud Research Group, Khartoum, Sudan.
Introduction: Mental health is crucial for overcoming obstacles, completing tasks, and contributing to society. Mental, social, and cognitive healths are included. In demanding fields like medicine, academic pressure can cause exhaustion, poor performance, and behavioral changes.
View Article and Find Full Text PDFBiol Res
January 2025
School of Pharmacy, Hangzhou Medical College, Hangzhou, Zhejiang, China.
Background: Protein palmitoylation, a critical posttranslational modification, plays an indispensable role in various cellular processes, including the regulation of protein stability, mediation of membrane fusion, facilitation of intracellular protein trafficking, and participation in cellular signaling pathways. It is also implicated in the pathogenesis of diseases, such as cancer, neurological disorders, inflammation, metabolic disorders, infections, and neurodegenerative diseases. However, its regulatory effects on sperm physiology, particularly motility, remain unclear.
View Article and Find Full Text PDFJ Neuroinflammation
January 2025
Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, USA.
The thrombolytic protease tissue plasminogen activator (tPA) is expressed in the CNS, where it regulates diverse functions including neuronal plasticity, neuroinflammation, and blood-brain-barrier integrity. However, its role in different brain regions such as the substantia nigra (SN) is largely unexplored. In this study, we characterize tPA expression, activity, and localization in the SN using a combination of retrograde tracing and β-galactosidase tPA reporter mice.
View Article and Find Full Text PDFMol Brain
January 2025
Graduate Program in Neuroscience, University of Washington, Seattle, WA, 98195, USA.
Recent research has highlighted widespread dysregulation of alternative polyadenylation in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP). Here, we identify significant disruptions to 3` UTR polyadenylation in the ALS/FTLD-TDP mouse model rNLS8 that correlate with changes in gene expression and protein levels through the re-analysis of published RNA sequencing and proteomic data. A subset of these changes are shared with TDP-43 knock-down mice suggesting depletion of endogenous mouse TDP-43 is a contributor to polyadenylation dysfunction in rNLS8 mice.
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