scholarly journals A qualitative and quantitative analysis of open citations to retracted articles: the Wakefield 1998 et al.'s case

2021 ◽  
Author(s):  
Ivan Heibi ◽  
Silvio Peroni

AbstractIn this article, we show the results of a quantitative and qualitative analysis of open citations on a popular and highly cited retracted paper: “Ileal-lymphoid-nodular hyperplasia, non-specific colitis and pervasive developmental disorder in children” by Wakefield et al., published in 1998. The main purpose of our study is to understand the behavior of the publications citing one retracted article and the characteristics of the citations the retracted article accumulated over time. Our analysis is based on a methodology which illustrates how we gathered the data, extracted the topics of the citing articles and visualized the results. The data and services used are all open and free to foster the reproducibility of the analysis. The outcomes concerned the analysis of the entities citing Wakefield et al.’s article and their related in-text citations. We observed a constant increasing number of citations in the last 20 years, accompanied with a constant increment in the percentage of those acknowledging its retraction. Citing articles have started either discussing or dealing with the retraction of Wakefield et al.’s article even before its full retraction happened in 2010. Articles in the social sciences domain citing the Wakefield et al.’s one were among those that have mostly discussed its retraction. In addition, when observing the in-text citations, we noticed that a large number of the citations received by Wakefield et al.’s article has focused on general discussions without recalling strictly medical details, especially after the full retraction. Medical studies did not hesitate in acknowledging the retraction of the Wakefield et al.’s article and often provided strong negative statements on it.

The Lancet ◽  
1998 ◽  
Vol 351 (9103) ◽  
pp. 637-641 ◽  
Author(s):  
AJ Wakefield ◽  
SH Murch ◽  
A Anthony ◽  
J Linnell ◽  
DM Casson ◽  
...  

2015 ◽  
Vol 26 (1) ◽  
pp. 18-24 ◽  
Author(s):  
Sandra Lucarelli ◽  
Ginevra Lastrucci ◽  
Giovanni Di Nardo ◽  
Ylenia D'Alfonso ◽  
Marina Aloi ◽  
...  

2018 ◽  
Vol 7 (2) ◽  
pp. 349-361 ◽  
Author(s):  
Sheena Ram ◽  
Mariann A. Howland ◽  
Curt A. Sandman ◽  
Elysia Poggi Davis ◽  
Laura M. Glynn

The etiology of autism spectrum disorder (ASD) is multifactorial, complex, and likely involves interactions among genetic, epigenetic, and environmental factors. With respect to environmental influences, a growing literature implicates intrauterine experiences in the origin of this pervasive developmental disorder. In this prospective longitudinal study, we examined the hypothesis that fetal exposure to maternal cortisol may confer ASD risk. In addition, because ASD is four times more prevalent in males than in females, and because sexually dimorphic responses to intrauterine experiences are commonly observed, we examined whether or not any associations differ by fetal sex. Maternal plasma cortisol was measured at 15, 19, 25, 31, and 37 weeks’ gestation in a sample of 84 pregnant women. ASD symptoms were assessed in their 5-year-old children with the Social Communication Questionnaire (SCQ). Fetal exposure to lower levels of maternal cortisol was associated with higher levels of ASD symptoms only among boys. The observed hypocortisolemic profile exhibited by these mothers may indicate a risk factor that precedes the stress of caregiving for a child with ASD and may not be solely a consequence of the stress of caregiving, as previously thought. These findings confirm the value of examining prenatal hormone exposures as predictors of ASD risk and support the premise that altered prenatal steroid exposures may play a role in the etiology of ASD.


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