Applying the techniques of neutralization to the study of cybercrime

Cybercrime scholars have used a wide range of criminological theories to understand crime and deviance within digital contexts. Among the most frequently cited theoretical frameworks used in this space has been the techniques of neutralization, first proposed by Gresham Sykes and David Matza. This body of work has demonstrated the myriad ways that individual cyber-delinquents have applied the techniques of neutralization as a justification for their deviance. A thorough review of this research reveals decidedly mixed support for neutralization theory. This chapter provides an in-depth review of these studies and seeks to account for this mixed result. This is done by chronicling the methodological underpinnings of this work, and in doing so highlights the challenges facing this literature with respect to the conceptualization and measurement of Sykes and Matza’s theory in the cyber realm. This is accomplished in two parts. First, we review the body of literature that analyzes the techniques of neutralization as a single combined construct (i.e., items are combined to produce a single measure of neutralization), and flag some of the advantages, but also pitfalls of this approach. Second, we review the treatment of individual techniques of neutralization as distinct constructs within the literature (i.e., a technique is measured and analyzed separate to others) and detail some of the common methodological hurdles encountered by researchers. The chapter concludes by elaborating on persistent gaps or challenges posed in making such assessments and proposes a path forward for future cybercrime research incorporating this framework.Russell Brewer, Sarah Fox, Caitlan Mille

Genetic compensation triggered by actin mutation prevents the muscle damage caused by loss of actin protein

<div><p>The lack of a mutant phenotype in homozygous mutant individuals’ due to compensatory gene expression triggered upstream of protein function has been identified as genetic compensation. Whilst this intriguing process has been recognized in zebrafish, the presence of homozygous loss of function mutations in healthy human individuals suggests that compensation may not be restricted to this model. Loss of skeletal α-actin results in nemaline myopathy and we have previously shown that the pathological symptoms of the disease and reduction in muscle performance are recapitulated in a zebrafish antisense morpholino knockdown model. Here we reveal that a genetic <i>actc1b</i> mutant exhibits mild muscle defects and is unaffected by injection of the <i>actc1b</i> targeting morpholino. We further show that the milder phenotype results from a compensatory transcriptional upregulation of an actin paralogue providing a novel approach to be explored for the treatment of actin myopathy. Our findings provide further evidence that genetic compensation may influence the penetrance of disease-causing mutations.</p></div