Views on the Functionality and Use of the PeerConnect App Among Public Safety Personnel: Qualitative Analysis.

BACKGROUND: Research supports that public safety personnel (PSP) are regularly exposed to potentially psychologically traumatic events and occupational stress, which can compromise their well-being. To help address PSP well-being and mental health, peer support is increasingly being adopted (and developed) in PSP organizations. Peer support apps have been developed to connect the peer and peer supporter anonymously and confidentially, but little is known about their effectiveness, utility, and uptake. OBJECTIVE: We designed this study to evaluate the functionality and use of the PeerConnect app, which is a vehicle for receiving and administering peer support. The app connects peers but also provides information (eg, mental health screening tools, newsfeed) to users; thus, we wanted to understand why PSP adopted or did not adopt the app and the app's perceived utility. Our intention was to determine if the app served the purpose of connectivity for PSP organizations implementing peer support. METHODS: A sample of PSP (N=23) participated in an interview about why they used or did not use the app. We first surveyed participants across PSP organizations in Ontario, Canada, and at the end of the survey invited participants to participate in a follow-up interview. Of the 23 PSP interviewed, 16 were PeerConnect users and 7 were nonusers. After transcribing all audio recordings of the interviews, we used an emergent theme approach to analyze themes within and across responses. RESULTS: PSP largely viewed PeerConnect positively, with the Connect feature being most popular (this feature facilitated peer support), followed by the Newsfeed and Resources. App users appreciated the convenience of the app and felt the app helped reduce the stigma around peer support use and pressure on peer supporters while raising awareness of wellness. PSP who did not use the app attributed their nonuse to disinterest or uncertainty about the need for a peer support app and the web-based nature of the app. To increase app adoption, participants recommended increased communication and promotion of the app by the services and continued efforts to combat mental health stigma. CONCLUSIONS: We provide contextual information about a peer support app's functionality and use. Our findings demonstrate that PSP are open to the use of mental health and peer support apps, but more education is required to reduce mental health stigma. Future research should continue to evaluate peer support apps for PSP to inform their design and ensure they are fulfilling their purpose.

Positive mental health in Canadian adults who have experienced childhood sexual abuse: exploring the role of social support.

PURPOSE: Childhood sexual abuse (CSA) is predictive of poorer mental health, greater psychiatric disorder risk, and lower positive mental health (PMH) during adulthood, outcomes potentially moderated by social support. The current study aimed to explore whether Canadian adults who have experienced CSA differ from those who have not in terms of PMH and social support. Within the CSA sample, it was further investigated whether gender differences exist with respect to PMH and social support, and if particular social support subscales predict PMH. METHOD: Using data from the 2012 Canadian Community Health Survey - Mental Health (CCHS-MH), 1,328 adults between 20 and 64 years reporting CSA were profiled and compared in terms of sociodemographic and socioeconomic factors, using an age, sex, and frequency matched sample of non-CSA adults. Social Provisions Scale (SPS), and the Mental Health Continuum - Short Form (MHC-SF) means were subsequently compared between the CSA and non-CSA samples, and Hierarchical regressions were conducted for CSA males and females separately to examine whether SPS subscales predicted PMH after controlling for age and income. RESULTS: Canadian adults reporting CSA had significantly lower PMH and social support (overall and for particular subscales). For adult CSA females, guidance, social integration, and reassurance of worth predicted higher PMH, while attachment and reassurance of worth predicted higher PMH scores for CSA males. CONCLUSION: Adults who have experienced CSA are at risk for lower PMH and social support. Gender differences are also evident in social support subtypes that predict PMH which have important clinical implications.

Touchscreen learning deficits and normal social approach behavior in the Shank3B model of Phelan-McDermid Syndrome and autism.

SHANK3 is a synaptic scaffolding protein localized in the postsynaptic density and has a crucial role in synaptogenesis and neural physiology. Deletions and point mutations in SHANK3 cause Phelan-McDermid Syndrome (PMS), and have also been implicated in autism spectrum disorder (ASD) and intellectual disabilities, leading to the hypothesis that reduced SHANK3 expression impairs basic brain functions that are important for social communication and cognition. Several mouse models of Shank3 deletions have been generated, varying in the specific domain deleted. Here we report impairments in cognitive function in mice heterozygous for exon 13-16 (coding for the PDZ domain) deletion. The touchscreen pairwise discrimination task was chosen by virtue of its: (a) conceptual and technical similarities to the Cambridge Neuropsychological Test Automated Battery (CANTAB) and NIH Toolbox Cognition Battery used for testing cognitive functions in humans, (b) minimal demand on motor abilities, and (c) capability to measure many aspects of learning and memory and complex cognitive functions, including cognitive flexibility. The similarity between our mouse tasks and human cognitive assays means a high translational validity in future intervention studies using preclinical models. Our study revealed that Shank3B heterozygous mice (+/-) were slower to reach criterion in the pairwise visual discrimination task, and exhibited trends toward making more errors (first trial errors) and more correction errors than wildtype mice (+/+). Open field activity was normal in +/-, ruling out hypo- or hyperactivity as potential confounds in the touchscreen test. Sociability in the three chamber test was also normal in both +/+ and +/-. These results indicate a deficit in discrimination learning in the Shank3B model of PMS and ASD, suggesting that this mouse model is a useful preclinical tool for studying neurobiological mechanisms behind cognitive impairments in PMS and ASD. The current findings are the starting point for our future research in which we will investigate multiple domains of cognition and explore pharmacological interventions.

16p11.2 Deletion mice display cognitive deficits in touchscreen learning and novelty recognition tasks.

Chromosomal 16p11.2 deletion syndrome frequently presents with intellectual disabilities, speech delays, and autism. Here we investigated the Dolmetsch line of 16p11.2 heterozygous (+/-) mice on a range of cognitive tasks with different neuroanatomical substrates. Robust novel object recognition deficits were replicated in two cohorts of 16p11.2+/- mice, confirming previous findings. A similarly robust deficit in object location memory was discovered in +/-, indicating impaired spatial novelty recognition. Generalizability of novelty recognition deficits in +/- mice extended to preference for social novelty. Robust learning deficits and cognitive inflexibility were detected using Bussey-Saksida touchscreen operant chambers. During acquisition of pairwise visual discrimination, +/- mice required significantly more training trials to reach criterion than wild-type littermates (+/+), and made more errors and correction errors than +/+. In the reversal phase, all +/+ reached criterion, whereas most +/- failed to reach criterion by the 30-d cutoff. Contextual and cued fear conditioning were normal in +/-. These cognitive phenotypes may be relevant to some aspects of cognitive impairments in humans with 16p11.2 deletion, and support the use of 16p11.2+/- mice as a model system for discovering treatments for cognitive impairments in 16p11.2 deletion syndrome.

In tribute to Bob Blanchard: Divergent behavioral phenotypes of 16p11.2 deletion mice reared in same-genotype versus mixed-genotype cages.

Mouse models offer indispensable heuristic tools for studying genetic and environmental causes of neuropsychiatric disorders, including autism. Development of useful animal models of complex human behaviors depends not only on extensive knowledge of the human disease, but also on a deep understanding of animal behavior and ethology. Robert and Caroline Blanchard pioneered a number of elegant social paradigms in rodents. Their early work led to systematic delineations of rodent naturalist defensive behaviors,which were proven to be highly useful models of human psychiatric disorders, including fear and anxiety. Their work using the Visible Burrow System to study social stress in rats represented an unprecedented approach to study biological mechanisms of depression. In recent years, their extensive knowledge of mouse behavior and ethology enabled them to quickly become leading figures in the field of behavioral genetics of autism. To commemorate Robert Blanchard's influences on animal models of human psychiatric disorders, here we describe a study conceptualized and led by Mu Yang who was trained as a graduate student in the Blanchard laboratory in the early 2000s. This investigation focuses on social housing in a genetic mouse model of 16p11.2 deletion syndrome. Heterozygous deletions and duplications of a segment containing about 29 genes on human chromosome 16 appear in approximately 0.5­1% of all cases of autism. 16p11.2 deletion syndrome is also associated with intellectual disabilities and speech impairments. Our previous studies showed that a mouse model of 16p11.2 deletion syndrome exhibited deficits in vocalizations and novel object recognition, as compared to wildtype littermate control cagemates. In the spirit of Bob Blanchard's careful attention to the role of social dominance in rodent behaviors, we became interested in the question of whether behavioral outcomes of a mutation differ when mutants are housed in mixed genotype cages, versus housing only mutants together in one group cage, and only wildtype littermates together in another group cage after weaning. 16p11.2 deletion presented a particularly good model organism to investigate this question, because the heterozygotes are smaller than their wildtype littermates, and may therefore become subordinate to their larger cagemates.Wildtype and heterozygotes were housed with cagemates of the same genotype (same-genotype cage) or with cagemates of the opposite genotype (mixed-genotype cage). Current results replicated social vocalization and object recognition deficits that we previously found in heterozygotes living in mixed-genotype cages. In contrast, heterozygotes that lived in same-genotype cages emitted normal numbers of vocalizations during male­female interactions, and displayed normal novel object recognition, indicating that the deletion per se was not sufficient to cause cognitive or social deficits. Social approach, same-sex social interaction, anxiety-related behavior, depression-related behavior, and open field exploration were not different between genotypes, and were not affected by housing in mixed versus in same-genotype cages. These findings suggest that elements of the home cage social environment could interact with genotype to impact aspects of disease phenotypes. Current findings are discussed as potentially reflecting behavioral deficits resulted from social stress, as inspired by a seminal paper by Bob and Caroline Blanchard [1].

16p11.2 Deletion Syndrome Mice Display Sensory and Ultrasonic Vocalization Deficits During Social Interactions.

Recurrent deletions and duplications at chromosomal region 16p11.2 are variably associated with speech delay, autism spectrum disorder, developmental delay, schizophrenia, and cognitive impairments. Social communication deficits are a primary diagnostic symptom of autism. Here we investigated ultrasonic vocalizations (USVs) in young adult male 16p11.2 deletion mice during a novel three-phase male-female social interaction test that detects vocalizations emitted by a male in the presence of an estrous female, how the male changes its calling when the female is suddenly absent, and the extent to which calls resume when the female returns. Strikingly fewer vocalizations were detected in two independent cohorts of 16p11.2 heterozygous deletion males (+/-) during the first exposure to an unfamiliar estrous female, as compared to wildtype littermates (+/+). When the female was removed, +/+ emitted calls, but at a much lower level, whereas +/- males called minimally. Sensory and motor abnormalities were detected in +/-, including higher nociceptive thresholds, a complete absence of acoustic startle responses, and hearing loss in all +/- as confirmed by lack of auditory brainstem responses to frequencies between 8 and 100 kHz. Stereotyped circling and backflipping appeared in a small percentage of individuals, as previously reported. However, these sensory and motor phenotypes could not directly explain the low vocalizations in 16p11.2 deletion mice, since (a) +/- males displayed normal abilities to emit vocalizations when the female was subsequently reintroduced, and (b) +/- vocalized less than +/+ to social odor cues delivered on an inanimate cotton swab. Our findings support the concept that mouse USVs in social settings represent a response to social cues, and that 16p11.2 deletion mice are deficient in their initial USVs responses to novel social cues.