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The transparency of two-dimensional (2D) materials to intermolecular interactions of crystalline materials has been an unresolved topic. Here we report that remote atomic interaction through 2D materials is governed by the binding nature, that is, the polarity of atomic bonds, both in the underlying substrates and in 2D material interlayers. Although the potential field from covalent-bonded materials is screened by a monolayer of graphene, that from ionic-bonded materials is strong enough to penetrate through a few layers of graphene. Such field penetration is substantially attenuated by 2D hexagonal boron nitride, which itself has polarization in its atomic bonds. Based on the control of transparency, modulated by the nature of materials as well as interlayer thickness, various types of single-crystalline materials across the periodic table can be epitaxially grown on 2D material-coated substrates. The epitaxial films can subsequently be released as free-standing membranes, which provides unique opportunities for the heterointegration of arbitrary single-crystalline thin films in functional applications.

While the biological substrates of brain and behavioural changes in persons with schizophrenia remain unclear, increasing evidence implicates that inflammation is involved. In schizophrenia, including first-episode psychosis and anti-psychotic naïve patients, there are numerous reports of increased peripheral inflammation, cognitive deficits and neuropathologies such as cortical thinning. Research defining the relationship between inflammation and schizophrenia symptomatology and neuropathology is needed. Therefore, we analysed the level of C-reactive protein (CRP), a peripheral inflammation marker, and its relationship with cognitive functioning in a cohort of 644 controls and 499 schizophrenia patients. In a subset of individuals who underwent MRI scanning (99 controls and 194 schizophrenia cases), we tested if serum CRP was associated with cortical thickness. CRP was significantly increased in schizophrenia patients compared to controls, co-varying for age, sex, overweight/obesity and diabetes (p < 0.006E-10). In schizophrenia, increased CRP was mildly associated with worse performance in attention, controlling for age, sex and education (R =− 0.15, p = 0.001). Further, increased CRP was associated with reduced cortical thickness in three regions related to attention: the caudal middle frontal, the pars opercularis and the posterior cingulate cortices, which remained significant after controlling for multiple comparisons (all p < 0.05). Together, these findings indicate that increased peripheral inflammation is associated with deficits in cognitive function and brain structure in schizophrenia, especially reduced attention and reduced cortical thickness in associated brain regions. Using CRP as a biomarker of peripheral inflammation in persons with schizophrenia may help to identify vulnerable patients and those that may benefit from adjunctive anti-inflammatory treatments.

Over 50% of women experience mood disturbance in the postpartum period, with significant implications for maternal and infant health but identifying those at risk is not easily possible. The essential amino acid, tryptophan (TRP) through its neuroactive metabolites, has been implicated in the pathology of mood disorders. Thus, TRP levels tested in the peripartum period have been proposed as a potential biomarker for subsequent development of postpartum mood disturbances, in particular postpartum depression (PPD). A systematic review and meta-analysis following PROSPERO guidelines [CRD42021252462] was conducted on peer-reviewed, English language studies that measured blood levels of TRP during the postpartum period in women who were also evaluated for postpartum “blues” or PPD. Thirteen studies met the inclusion criteria, of which five studies contained sufficient data to conduct a meta-analysis. Low total TRP levels in postpartum days 1 to 5 were significantly associated with PPD (SMD: -5.39, 95%CI [-7.72, -3.05]). No significant association was found between free TRP levels in the postpartum period and PPD (SMD: -3.43, 95%CI [-7.76, 0.89]). Our findings confirm the necessity for more replicable designed studies regarding TRP and its relationship to postpartum depression. If there were greater clarity regarding TRP metabolism during pregnancy, then the next step would be to consider measuring total plasma TRP levels on postpartum days 1 to 5 to identify women at greater risk of developing PPD.

Background Adolescent refugees are at high risk of developing mental disorders but are often not recognised early. This pilot study aimed to identify early putative risk factors associated with psychological symptoms in newly resettled refugee youth at potential risk of subsequently developing mental disorders. Methods Newly resettled adolescent refugees were recruited through English language schools in Melbourne, Australia. Participants were assessed with the MINI-Kid, Achenbach Youth Self-Report and Reaction of Adolescents to Traumatic Stress scale. Parents completed a mental health screening separately. Linear regression models were used to identify predictive factors associated with symptom ratings. Results Seventy-eight, ostensibly well, refugee adolescents ( mean age  = 15.0 ± 1.6 years) resettled in Australia for 6.1 ± 4.2 months were assessed. Levels of anxiety, depression and post-traumatic stress symptoms were considerably lower than in mainstream population data. Prior displacement was a key determinant of symptomatology. Transitory displacement, irrespective of duration, was associated with elevated scores for depression ( t (47) = -4.05, p  < 0.0001), avoidance/numbing ( U  = 466, p  < .05) and total trauma ( U  = 506, p  < .05) symptoms. Older age was a unique predictor of depression ( F (1,74) = 8.98, p  < .01), internalising ( F (1,74) = 6.28, p  < .05) and total ( F (1,74) = 4.10, p  < .05) symptoms, whilst parental depression symptoms ( t  = 2.01, p  < 0.05), displacement ( t  = 3.35, p  < 0.01) and, expectedly, trauma exposure ( t  = 3.94, p  < 0.001) were unique predictors of post-traumatic stress symptoms. Conclusions Displaced status, older age, and parental symptoms predicted psychological symptoms in adolescent refugees in an initial relatively asymptomatic post-resettlement phase. The early recognition of at-risk refugee youth may provide an opportunity for preventative mental health interventions.

IntroductionGlobally, studies have consistently demonstrated the harmful mental and physical health impacts of immigration detention, with high levels of distress documented among detained asylum seekers and refugees (ASR). However, the consequences of immigration detention over time on the psychological and physical health of ASR are unclear and poorly quantified.Methods and analysisThis prospective, mixed-methods cohort study will recurrently assess and describe the health profiles of adult ASR with an experience of Australian Government-sponsored immigration detention greater than 28 days. ASR ≥18 years old released from immigration detention will be assessed at 0, 3, 6 and 12 months and annually thereafter for up to 10 years, contingent on resourcing. Five self-report scales and a structured psychiatric interview will assess the primary outcome of depression, anxiety, post-traumatic stress, pain intensity and severity, somatic symptoms, functional impairment, physical health conditions associated with detention and engagement in available treatment of this cohort. Additionally, pre-existing health records will be accessed to identify current and previous health status and assess changes in these health indices. Quantitative findings will be triangulated with a qualitative phenomenological thematic analysis of interviews to determine additional psychosocial factors associated with the outcomes.Ethics and disseminationThe study protocol was approved by the Monash Health Human Research Ethics Committee (HREC/73614/MonH-2021-251322). Results will be reported at conferences, in peer-reviewed publications and to all relevant stakeholder groups.

How early in life stress-immune related environmental factors increase risk predisposition to schizophrenia remains unknown. We examined if pro-inflammatory changes perturb the brain epidermal growth factor (EGF) system, a system critical for neurodevelopment and mature CNS functions including synaptic plasticity. We quantified genes from key EGF and immune system pathways for mRNA levels and eight immune proteins in post-mortem dorsolateral prefrontal (DLPFC; Brodmann’s Area (BA) 46) and orbitofrontal (OFC; BA11) cortices from people with schizophrenia, mood disorders and neurotypical controls. In BA46, 64 genes were differentially expressed, predominantly in schizophrenia, where attenuated expression of the MAPK-ERK, NRG1-PI3K-AKT and mTOR cascades indicated reduced EGF system signalling, and similarly diminished immune molecular expression, notably in TLR, TNF and complement pathways, along with low NF-κB1 and elevated IL12RB2 protein levels were noted. There was nominal evidence for altered convergence between ErbB-PI3K-AKT-mTOR and TLR pathways in BA46 in schizophrenia. Comparatively minimal changes were noted in BA11. Overall, distinct pathway gene expression changes may reflect variant pathological processes involving immune and EGF system signalling between schizophrenia and mood disorder, particularly in DLPFC. Further, the abnormal convergence between innate immune signalling and candidate EGF signalling pathways may indicate a pathologically important interaction in the developing brain in response to environmental stressors.

The similarities between the depressive symptoms of Major Depressive Disorders (MDD) and Bipolar Disorders (BD) suggest these disorders have some commonality in their molecular pathophysiologies, which is not apparent from the risk genes shared between MDD and BD. This is significant, given the growing literature suggesting that changes in non-coding RNA may be important in both MDD and BD, because they are causing dysfunctions in the control of biochemical pathways that are affected in both disorders. Therefore, understanding the changes in non-coding RNA in MDD and BD will lead to a better understanding of how and why these disorders develop. Furthermore, as a significant number of individuals suffering with MDD and BD do not respond to medication, identifying non-coding RNA that are altered by the drugs used to treat these disorders offer the potential to identify biomarkers that could predict medication response. Such biomarkers offer the potential to quickly identify patients who are unlikely to respond to traditional medications so clinicians can refocus treatment strategies to ensure more effective outcomes for the patient. This review will focus on the evidence supporting the involvement of non-coding RNA in MDD and BD and their potential use as biomarkers for treatment response.

Background There is no screening tool for major depressive disorder (MDD) or post-traumatic stress disorder (PTSD) in asylum-seekers or refugees (ASR) that can be readily administered by non-mental health workers. Hence, we aimed to develop a brief, sensitive and rapidly administrable tool for non-mental health workers to screen for MDD and PTSD in ASR. Methods The screening tool was developed from an extant dataset ( n  = 121) of multiply screened ASR and tested prospectively ( N  = 192) against the M.I.N.I. (Mini International Neuropsychiatric Interview) structured psychiatric interview. Rasch, Differential Item Functioning and ROC analyses evaluated the psychometric properties and tool utility. Results A 9-item tool with a median administration time of six minutes was generated, comprising two ‘immediate screen-in’ items, and a 7-item scale. The prevalence of PTSD &/or MDD using the M.I.N.I. was 32%, whilst 99% of other diagnosed mental disorders were comorbid with one or both of these. Using a cut-score of ≥2, the tool provided a sensitivity of 0.93, specificity of 0.75 and predictive accuracy of 80.7%. Conclusions A brief sensitive screening tool with robust psychometric properties that was easy to administer at the agency of first presentation was developed to facilitate mental health referrals for asylum-seekers and new refugees.

We retrospectively investigated moral injury and mental health related to immigration detention on Nauru. Participants conveyed the impact of deprivation, lack of agency, violence, and dehumanization. Evaluations of their experiences fit with conceptualizations of moral injury. Immigration detention is associated with detrimental mental health outcomes but little is known about the underlying psychological processes. Moral injury, the experience of transgression of moral beliefs, may play an important role. Our aim was to explore moral injury appraisals and associated mental health outcomes related to immigration detention on Nauru. In this retrospective study, we conducted in-depth interviews with 13 individuals who had sought refuge in Australia and, due to arriving by boat, had been transferred to immigration detention on Nauru. At the time of the study, they lived in Australia following medical transfer. We used reflexive thematic analysis to develop themes from the data. Major themes included 1) how participants' home country experience and the expectation to get protection led them to seek safety in Australia; 2) how they experienced deprivation, lack of agency, violence, and dehumanization after arrival, with the Australian government seen as the driving force behind these experiences; and 3) how these experiences led to feeling irreparably damaged. The participant statement 'In my country they torture your body but in Australia they kill your mind.' conveyed these three key themes in our analysis. Our findings suggest that moral injury may be one of the processes by which mandatory immigration detention can cause harm. Although refugees returned to Australia from offshore detention may benefit from interventions that specifically target moral injury, collective steps are needed to diminish deterioration of refugee mental health. Our results highlight the potentially deleterious mental health impact of experiencing multiple subtle and substantial transgressions of one's moral frameworks. Policy makers should incorporate moral injury considerations to prevent eroding refugee mental health.

Differential expression of neuregulin-1 ( NRG1 ) mRNA isoforms and proteins has been reported in schizophrenia, primarily in post-mortem brain tissue. In this study, we examined 12 NRG1 SNPs, eight NRG1 mRNA isoforms (type I, type I (Ig2) , type II, type III, type IV, EGFα, EGFβ, pan-NRG1) in whole blood, and NRG1-β1 protein in serum of clozapine-treated schizophrenia patients ( N  = 71) and healthy controls ( N  = 57). In addition, using cultured peripheral blood mononuclear cells (PBMC) from 15 healthy individuals, we examined the effect of clozapine on NRG1 mRNA isoform and protein expression. We found elevated levels of NRG1 mRNA, specifically the EGFα ( P  = 0.0175), EGFβ ( P  = 0.002) and type I (Ig2) ( P  = 0.023) containing transcripts, but lower NRG1-β1 serum protein levels ( P  = 0.019) in schizophrenia patients compared to healthy controls. However, adjusting for smoking status attenuated the difference in NRG1-β1 serum levels ( P  = 0.050). Examination of clinical factors showed NRG1 EGFα ( P  = 0.02) and EGFβ ( P  = 0.02) isoform expression was negatively correlated with age of onset. However, we found limited evidence that NRG1 mRNA isoform or protein expression was associated with current chlorpromazine equivalent dose or clozapine plasma levels, the latter corroborated by our PBMC clozapine exposure experiment. Our SNP analysis found no robust expression quantitative trait loci. Our results represent the first comprehensive investigation of NRG1 isoforms and protein expression in the blood of clozapine-treated schizophrenia patients and suggest levels of some NRG1 transcripts are upregulated in those with schizophrenia.