Crime and punishment are usually connected. An agent intentionally causes harm, other people find out, and they punish the agent in response. We investigated whether people care about the integrity of this causal chain. Across seven experiments, participants (total N = 1,709) rated the acceptability of punishing agents for one crime when the agents had committed a different crime. Overall, participants generally approved of such wayward punishment. They endorsed it more strongly than punishing totally innocent agents, though they often approved of punishing agents for their correct crimes more strongly. Participants sometimes supported wayward punishment when wrongdoers were punished for a different kind of crime than the one committed, and they supported several different kinds of wayward punishments. Together the findings show that people often tolerate breaks in the causal chain between crime and punishment.
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http://dx.doi.org/10.3758/s13421-024-01528-5 | DOI Listing |
Am J Hum Genet
January 2025
Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.
Each human genome has approximately 5 million DNA variants. Even for complete loss-of-function variants causing inherited, monogenic diseases, current understanding based on gene-specific molecular function does not adequately predict variability observed between people with identical mutations or fluctuating disease trajectories. We present a parallel paradigm for loss-of-function variants based on broader consequences to the cell when aberrant polypeptide chains of amino acids are translated from mutant RNA to generate mutated proteins.
View Article and Find Full Text PDFMol Cell
January 2025
Department of Biochemistry, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. Electronic address:
While most of the regulation of translation initiation occurs in the cytosol predominantly through phosphorylation, Ly et al. have discovered the first instance of regulation via protein concentration due to disruption of the nuclear membrane at mitosis. Only eIF1 appears to be involved in this regulation, and its release at mitosis enhances translational accuracy of start codon recognition.
View Article and Find Full Text PDFNeurol Neuroimmunol Neuroinflamm
March 2025
Department of Neurology with Institute of Translational Neurology, University Hospital 4 Münster, Germany.
Background And Objectives: Levels of activated complement proteins in the CSF are increased in people with multiple sclerosis (MS) and are associated with clinical disease severity. In this study, we determined whether complement activation profiles track with quantitative MRI metrics and liquid biomarkers indicative of disease activity and progression.
Methods: Complement components and activation products (Factor H and I, C1q, C3, C4, C5, Ba, Bb, C3a, C4a, C5a, and sC5b-9) and liquid biomarkers (neurofilament light chain, glial fibrillary acidic protein [GFAP], CXCL-13, CXCL-9, and IL-12b) were quantified in the CSF of 112 patients with clinically isolated syndromes and 127 patients with MS; longitudinal MRIs according to a standardized protocol of the Swiss MS cohort were assessed.
PLoS One
January 2025
Department of Clinical Support Services, Division of Laboratory and Pathology Medicine, Uganda Cancer Institute, Kampala, Uganda.
The detection of Estrogen Receptor (ER), Progesterone Receptor (PR), and Human epidermal growth factor receptor 2 (HER-2) is important for the stratification of breast cancer and the selection of therapeutic modalities. This study aimed to determine the quantitative expression of ER, PR and HER-2 using Immunohistochemistry and their correlation with quantitative baseline Ct values measured using Quantitative Polymerase Chain Reaction (PCR). This study also assessed the use of fresh breast tissue biopsies preserved in RNAlater solution in the quantitative detection of these receptors using PCR technique.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Orthopedics, Shanghai Pudong New Area People's Hospital, Shanghai, China.
Aim: To explore the role of the hub gene Transforming Growth Factor Beta Induced (TGFBI) in Intervertebral disc degeneration (IDD) pathogenesis and its regulatory relationship with Membrane Associated Ring-CH-Type Finger 8 (MARCHF8).
Background: IDD is a prevalent musculoskeletal disorder leading to spinal pathology. Despite its ubiquity and impact, effective therapeutic strategies remain to be explored.
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