This cross-sectional study assesses the frequency and thoroughness of reporting of sociodemographic variables in randomized clinical trials published in 5 high-impact health journals from January 2014 to July 2020.

Postsecondary students confront many stressors that may contribute to the emergence of mental illness. 1 Longitudinal data suggest that rates of mental illnesses are increasing among Canadian postsecondary students, with more students reporting self-harm, suicidal ideation and suicide attempts over time. 1 When a student presenting at a university-affiliated health clinic is assessed to be at imminent risk of harm, legislative tools may be used to mandate emergent psychiatric assessment. In Ontario, Canada, under the province's Mental Health Act, 2 a "Form 1 Application by Physician for Psychiatric Assessment" can be completed to initiate this process. When a Form 1 is issued, students must be transferred to a designated hospital facility for evaluation.Although robust data are lacking, the annual number of student mental health transfers on some Ontario university campuses has increased substantially since 2014. 3 However, the processes for such transfers are an underresearched topic, part of a larger gap in research surrounding the conveyance of people experiencing a mental health crisis to hospital from communitybased points of care. [4][5][6][7][8] There is substantial heterogeneity in transfer processes when a Form 1 is completed for students pre-senting at university health clinics in Ontario. In particular, the involvement of police and use of physical restraints for transfers vary between institutions 8,9 and have been the subject of media scrutiny. 3,[10][11][12] These issues are important questions confronting health care professionals. 9 Some have argued for police involvement and use of restraints on the basis that they provide a type of safety to patients themselves, to health care professionals and to those transporting patients to hospital. 13 Opponents of routine police involvement and restraint use contend that such practices are traumatizing and stigmatizing, and perpetuate the criminalization of people with mental illness. [7][8][9][14][15][16][17] Given

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Background 17β‐estradiol loss is related to Alzheimer’s disease (AD) risk factors, including disordered sleep and associative memory decrements (Gervais et al., 2017; Rentz et al., 2017). Women have higher risk for AD than men, and those with mid‐life 17β‐estradiol loss due to surgical menopause, including bilateral salpingo‐oophorectomy (BSO) before age 48, have even higher risk (Rocca et al., 2007). Our learning objective was to investigate whether sleep and associative memory in women with BSO (mean age 44‐46) would be comparable to those with spontaneous/natural menopause (SM; mean age 57), and whether 17β‐estradiol‐based hormone therapy (ET) might mitigate these effects. Method We assessed sleep using the average of three nights of portable polysomnography (Temec) in women with BSO either taking ET (BSO+ET; n=16), or not (BSO; n=18), and in older spontaneously menopausal women (SM; n=14). Using EEG (Fp1‐Fp2), we obtained sleep staging automatically (Neurobit Technologies). Participants also completed a face‐name associative memory task during functional magnetic resonance imaging. Recognition accuracy and brain activation during encoding were measured. Result BSO exhibited reduced sleep efficiency compared to BSO+ET. For BSO, there was no relationship between percent of total sleep time in N3 and hippocampal activation during associative encoding, even though percent of total sleep time in N3 was negatively associated with hippocampal activation during associative encoding in BSO+ET. For all groups, including BSO, lower latency to consolidated N3 correlated with better associative memory accuracy. There were no group differences in associative memory accuracy. In contrast to BSO, SM showed significantly longer latency to consolidated N3 than BSO+ET. Conclusion Younger women with BSO have comparable sleep to older women in SM. In younger women with BSO, ET improves sleep efficiency. Further, while associative memory may be disrupted by increased latency to consolidated N3 in all women, BSO and BSO+ET showed similar associative memory accuracy and latency to consolidated N3. Only BSO+ET exhibited a significant correlation between hippocampal activity during associative encoding and time spent in N3, indicating that ET may support the negative relationship between N3 and hippocampal function. Overall, ET in younger women with BSO potentially ameliorates poor sleep and associative memory decrements.

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Background: Women bear the greatest burden of Alzheimer's disease (AD), and early (<45y) ovarian hormone deprivation via surgical menopause further increases risk (Rocca et al., 2007). Given that sleep disturbance is implicated in AD progression (Lim et al., 2013), an important area of investigation is determining whether

Background Women bear the greatest burden of Alzheimer’s disease (AD) with menopause‐associated estrogen (E) loss becoming increasingly implicated. Surgical menopause <45 years of age (via bilateral salpingo‐oophorectomy, BSO) is thought to further increase the risk (Rocca et al., 2007). Neurodegeneration and atrophy in medial temporal lobe (MTL) structures including the perirhinal (PRC) and entorhinal (ERC) cortices occur in the very early stages of AD (e.g. Khan et al., 2013; Wolk et al., 2017). Further, sleep disturbance is also implicated in AD progression (Lim et al., 2013). Unknown is whether BSO‐associated sleep disturbance contributes to reduced memory performance and MTL atrophy via sleep disturbance, and whether E2 supplementation influences this relation. Our study aimed to determine the effect of early hormone deprivation (via BSO) on MTL volume, visual recognition memory, and whether this is correlated with sleep disturbance. Method Demographic and cognitive measures were administered to women with an oophorectomy <45 years who were either taking estradiol‐based hormone therapy (BSO+E2: n=19), or not taking E2 (BSO no E2: n=15). Data was also collected from age‐matched premenopausal women (AMC: n=27). High‐resolution T2‐weighted scans were acquired using a Siemens 3T Prisma scanner, and hippocampal subfields, PRC, ERC, and parhippocampal cortex were manually segmented (Olsen et al., 2017) in FSLView. The interference match‐to‐sample (IMTS) task was used to asses and recognition memory (Watson et al., 2013). Sleep was assessed using an at‐home polysomnography device (Vitaport‐5/REMbo‐234, Temec Technologies). Result Relative to AMCs, the BSO no E2 group had smaller volumes in the dentate gyrus, CA2, and CA3 (DGCA23) (p<.05, d=1.03). Relative to BSO+E2 women with BSO no E2 had reduced recognition memory performance (p<.05; d=1.36) and their sleep was more disrupted, indicated by increased sleep latency (p<.05, d=.71), and cortical arousals ( p<.05, d=.87]. DGCA23 volume and nighttime arousals were correlated negatively (r=‐.503, p<.05). Conclusion Our findings demonstrate that HPC, recognition memory, and sleep are sensitive to E2 loss and suggest that reduced HPC volume relates to disrupted sleep. Taken together these findings begin to explicate the path from early menopause to late‐life dementia and the importance of E2 for women’s brain health.

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