Self-reported motivations for engaging or declining to engage in cyber-dependent offending and the role of autistic traits

Cyber-dependent offending, i.e. criminal behaviour reliant on computing and the online domain, has been reportedly associated with particular characteristics and motivations such as being young, male, autistic and motivated by challenge. These associations are anecdotal however and empirical evidence is limited. The present study investigated reasons for engaging or declining to commit cyber-dependent offending in cyber-skilled non-offenders (n = 175) and offenders(n = 7) via an online survey measuring cyber-dependent criminality. The potential role of autism and autistic traits was also considered. Qualitative interviews about motivations for offending were carried out with the offenders. The cyber-dependent offenders reported seven main reasons for engaging in cyber-dependent offending: (1) lack of understanding; (2) entertainment; (3) peer influence; (4) experience and career; (5) anonymity and risk perception; (6) life events; and (7)morals. Twenty-nine (approximately 17 %) of the non-offenders had been asked to engage in cyber-dependent offending but had declined. Their reasons and motivations for declining to commit cyber-dependent offences were compared with the cyber-dependent offenders reasons and motivations for engaging in cybercrime. Seven main reasons for declining to offend were identified: (1) moral principles; (2) perception of risk; (3) fear of consequences; (4) not wanting to; (5) wanting to adhere to the law; (6) behaviour being too complicated; and (7) price being too low. Implications for practise are discussed

Angiotensin II increases superoxide production in human arteries

Background: Increased vascular superoxide (O2 -) production contributes to endothelial dysfunction and vascular hypertrophy. We investigated whether, and by what mechanisms, angiotensin II (AII) might increase O2 - production in blood vessels. Methods: Internal mammary arteries (IMA) and saphenous veins (SV) were collected from patients undergoing coronary revascularisation surgery. Five mm rings were incubated in the absence (control) or presence 1 μmol/L of AII, or 1 μmol/L of norepinephrine (NE, positive control) for 4 hours. All-incubated rings were co-incubated with an NADH oxidase inhibitor, diphenyleneiodonium (DPI, 100 μmol/L) or a specific All type 1 (AT1) receptor antagonist, losartan (1 μmol/L). O2 - production was measured by lucigenin chemiluminescence. Identification of NADH oxidase within IMA and SV was undertaken using specific antibodies to its active subunits (p22 and p91 phox). Results: All increased O2 - production in IMA (control=978±117 pmol/min/mg, AII 1690±213 pmol/min/mg; n=27, p<0.0001) but not in SV (n=8). NE had no effect on O2 - production in either IMA (control 731±323 pmol/min/mg, NE 636±241; n=10, p=0.76), or SV (n=8). Losartan blocked the AII-mediated increase of O2 - production (losartan 947±245 pmol/min/mg, losartan + AII 1037±231 pmol/min/mg; n=11, p=0.15). DPI inhibited the AII mediated increase in O2 - production (DPI 1124±338 pmol/min/mg, AII + DPI 1055±146 pmol/min/mg; n=8, p=0.9). P22 and p91 phox proteins were localised principally within vascular smooth muscle cells. Conclusion: All increases O2 - production in human arteries by an AT1 receptor-specific, NADH oxidase-dependent mechanism. This suggests a novel therapeutic role for AT1 receptor antagonists in reducing oxidative stress in patients with cardiovascular disease

Mapping and sequencing rat dishevelled-1: a candidate gene for cerebral ischaemic insult in a rat model of stroke

A quantitative trait locus on chromosome 5 in the rat is linked to sensitivity to brain ischemia in the stroke-prone spontaneously hypertensive rat (SHRSP). The genes encoding atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) that map to this location have been excluded as candidate genes. We examined dishevelled-1 (DVL-1) as a further candidate gene. DVL-1 had not yet been identified in the rat, but Anp, Bnp, and DVL-1 map to the homologous regions of the rat chromosome 5 quantitative trait locus in both mice and man. Furthermore, DVL-1 is involved in the Notch signalling system, which plays a role in the disorder cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, the symptoms of which include ischaemic stroke. We show with radiation hybrid mapping that rat DVL-1 indeed maps to chromosome 5, where it is positioned immediately next to microsatellite marker D5Rat49. We sequenced the complete coding sequence and a large part of the intronic genomic sequence for the SHRSP strain and its reference Wistar-Kyoto strain. The DVL-1 sequence in the two strains was identical. Our results essentially exclude the DVL-1 gene as the cause for sensitivity to cerebral ischaemic insult in this rat model of strok