Scientists often respond to failures to replicate by citing differences between the experimental components of an original study and those of its attempted replication. In this paper, we investigate these purported . We assess a body of failures to replicate in neuroscience studies on spinal cord injury. We argue that a defensible mismatch explanation is one where (1) a mismatch of components is a for a mismatch of outcomes, and (2) the components are in the follow-up study, given the scope of the original study. With this account, we argue that not all differences between studies are meaningful, even if they are difference makers. As our examples show, focusing only on these differences results in disregarding the representativeness of the original experiment's components and the scope of its outcomes, undercutting other epistemic aims, such as translation, in the process.
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http://dx.doi.org/10.1007/s10539-022-09873-y | DOI Listing |
Neurology
February 2025
Department of Neurology, University of Michigan, Ann Arbor.
Background And Objectives: An adverse social exposome negatively affects many diseases, but its association with amyotrophic lateral sclerosis (ALS) survival is unknown. This study examined the association between the social exposome measure Area Deprivation Index (ADI) and ALS survival.
Methods: This is a retrospective analysis of patients with ALS at the University of Michigan Pranger ALS Clinic diagnosed after January 1, 2012.
Open Forum Infect Dis
January 2025
CHU d'Orléans, Orléans, France.
Background: To better understand factors associated with virologic response, we retrospectively characterized the HIV proviruses of 7 people with HIV who received long-acting cabotegravir/rilpivirine (CAB/RPV-LA) and were selected according to the following criteria: virologic control achieved despite a history of viral replication on 1 or both corresponding antiretroviral classes (n = 6) and virologic failure (VF) after CAB/RPV-LA initiation (n = 1).
Methods: Last available blood samples before the initiation of CAB/RPV-LA were analyzed retrospectively. Near full-length HIV DNA genome haplotypes were inferred from Nanopore sequencing by the in vivo Genome Diversity Analyzer to search for archived drug resistance mutations (DRMs) and evaluate the frequency and intactness of proviruses harboring DRMs.
eNeuro
January 2025
Department of Biology, University of Ottawa, Ottawa, ON K1N 6N5, Canada.
Axons in the mammalian brain show significant diversity in myelination motifs, displaying spatial heterogeneity in sheathing along individual axons and across brain regions. However, its impact on neural signaling and susceptibility to injury remains poorly understood. To address this, we leveraged cable theory and developed model axons replicating the myelin sheath distributions observed experimentally in different regions of the mouse central nervous system.
View Article and Find Full Text PDFThyroid
January 2025
Division of Endocrinology, Diabetes and Metabolism, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
Epidemiological data suggest the population distribution of thyrotropin (TSH) values is shifted toward lower values in self-identified Black non-Hispanic individuals compared with self-identified White non-Hispanic individuals. It is unknown whether genetic differences between individuals with genetic similarities to African reference populations (GSA) and those with similarities to European reference populations (GSE) contribute to these observed differences. We aimed to compare genome-wide associations with TSH and putative causal TSH-associated variants between GSA and GSE groups.
View Article and Find Full Text PDFLiver Int
February 2025
Division of Bioinformatics and Statistics, The FDA's National Center for Toxicological Research, Jefferson, Arkansas, USA.
Background And Aims: Acute liver failure (ALF) is a serious condition, typically in individuals without prior liver disease. Drug-induced ALF (DIALF) constitutes a major portion of ALF cases. Our research aimed to identify potential genetic predispositions to DIALF.
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