Support services for victims and survivors of child sexual abuse

Some of the content in this report may be distressing to readers.Aims The four broad research aims were to: ● understand more about victims and survivors’ reasons for not accessing support services and any barriers to access; ● learn about victims and survivors’ perceptions and experiences of support services; ● understand what support services victims and survivors think are available to them and how to access them; and ● explore whether there are unmet needs for support services which impact on whether victims and survivors access support. Methods The sample was drawn from 634 adults who self-identified as victims and survivors of child sexual abuse as part of the ‘Abuse during childhood’ module in the Crime Survey for England and Wales (CSEW) year ending March 2019 (Office for National Statistics, 2020).3 A mixed-methods approach was used to explore the above research aims: ● A quantitative online survey4 of 181 victims and survivors from the CSEW recontact sample, including both those who had and had not accessed support. Descriptive and inferential analyses were conducted. ● Twenty-four qualitative in-depth interviews with three groups: (A) eight who had not accessed support services; (B) eight who self-identified as having had positive experiences of support services; and (C) eight who had negative experiences of support services. The interviews were analysed using thematic analysis. These were supplemented with six pen portraits (two from each of the above groups), and a network map to aid understanding of the service landscape. The research participants The ages of the survey respondents ranged from 19 to 74 years, with an average of 47 years. Around four in five identified as female (82%), the majority identified as being of a White ethnic background (92%), and one in three reported having a disability (33%). All regions of England and Wales were represented, with one in four living in London or South East England (26%). Nearly nine in ten identified as heterosexual (89%) Respondents reported experiencing between one and eight types of child sexual abuse. The two most common forms were being kissed or groped on any part of the body in a sexual way (73%) and penetration (64%). The age at first victimisation spanned from infancy to 17 years old, with an average of 9 years old. Child sexual abuse was more likely to have occurred in a familial setting (41%) than an institutional one (11%). Two in five (43%) respondents identified a friend, acquaintance or neighbour as the perpetrator. Around one in four (27%) identified an immediate – typically male – family member as the perpetrator. A stranger was identified by one in five (20%) respondents. Just over one in five respondents had never previously disclosed their experiences of child sexual abuse (21%), while four in five had made a disclosure (79%). Respondents were more than twice as likely to report making a disclosure later in life (75%) than at the time of the abuse (28%). A quarter disclosed at both points (24%)

Artificial light at night impacts night-time activity but not day-time behaviour in a diurnal coral reef fish

An important, yet overlooked form of anthropogenic pollution is sensory pollution, and one of the most pervasive forms of sensory pollution is artificial light at night (ALAN). Despite the growing use of ALAN across the globe, limited research has examined the impacts of ALAN on coral reef fish. This study aims to further our understanding of the behavioural impacts of light pollution on fish by exposing the humbug damselfish (Dascyllus aruanus) to ALAN (∼15–25 lux, white LED light) over a period of 14 days, in situ. We assessed nocturnal activity, and diurnal shelter use and emergence time following a simulated threat in natural (control) and ALAN conditions. D. aruanus colonies exposed to ALAN were active at night and were lacking cryptic colouration observed in control fish, however this altered nocturnal activity did not appear to impact the diurnal behaviours we measured. Our findings provide critical insight into the impact of ALAN exposure to nocturnal behaviour of a diurnal fish and highlight the potential for increased risk of nocturnal predation under ALAN. Further studies with a longer ALAN exposure time will help illuminate the extent of behavioural changes and implications caused by ALAN in shallow coral reef systems

A Novel Role for Plasminogen Activator Inhibitor Type-2 as a Hypochlorite-Resistant Serine Protease Inhibitor and Holdase Chaperone

Plasminogen activator inhibitor type-2 (PAI-2), a member of the serpin family, is dramatically upregulated during pregnancy and in response to inflammation. Although PAI-2 exists in glycosylated and non-glycosylated forms in vivo, the majority of in vitro studies of PAI-2 have exclusively involved the intracellular non-glycosylated form. This study shows that exposure to inflammation-associated hypochlorite induces the oligomerisation of PAI-2 via a mechanism involving dityrosine formation. Compared to plasminogen activator inhibitor type-1 (PAI-1), both forms of PAI-2 are more resistant to hypochlorite-induced inactivation of its protease inhibitory activity. Holdase-type extracellular chaperone activity plays a putative non-canonical role for PAI-2. Our data demonstrate that glycosylated PAI-2 more efficiently inhibits the aggregation of Alzheimer’s disease and preeclampsia-associated amyloid beta peptide (Aβ), compared to non-glycosylated PAI-2 in vitro. However, hypochlorite-induced modification of non-glycosylated PAI-2 dramatically enhances its holdase activity by promoting the formation of very high-molecular-mass chaperone-active PAI-2 oligomers. Both PAI-2 forms protect against Aβ-induced cytotoxicity in the SH-SY5Y neuroblastoma cell line in vitro. In the villous placenta, PAI-2 is localised primarily to syncytiotrophoblast with wide interpersonal variation in women with preeclampsia and in gestational-age-matched controls. Although intracellular PAI-2 and Aβ staining localised to different placental cell types, some PAI-2 co-localised with Aβ in the extracellular plaque-like aggregated deposits abundant in preeclamptic placenta. Thus, PAI-2 potentially contributes to controlling aberrant fibrinolysis and the accumulation of misfolded proteins in states characterised by oxidative and proteostasis stress, such as in Alzheimer’s disease and preeclampsia