Childhood maltreatment (CM) is one of the best described environmental risk factors for developing any psychiatric disorder, while it also confers increased odds for obesity, cardiometabolic disorders and all-cause mortality. Inflammation has been suggested to mediate the widespread clinical effects of CM. Previously, Ligthart et al. (2016) identified a polyepigenetic signature of circulating CRP levels, a measure of chronic low-grade inflammation, that has been reliably associated with a wide array of complex disorders. The study of this biomarker could dilucidate the mechanistic relationship between CM and psychiatric outcomes.

Thus, CRP-associated epigenetic modifications were explored regarding proximal exposure to CM.

Genomic DNA was extracted from peripheral blood mononuclear cells of 157 children and adolescents (7 to 17 years old). Exposure to CM was assessed following the TASSCV criteria. Genome-wide DNA methylation was assessed by means of the EPIC array. Fifty-two out of the 58 original CRP-associated CpG sites surpassed quality control and were included in the analysis. Age, sex, psychopathological status and cell type proportions were included as covariates.

DNA methylation at 12 out of 52 CpG sites (23%) was significantly associated with exposure to CM (p < .05); 8 of these associations survived correction for multiple testing (q < .05).

This is the first study to date to explore the relationship between childhood maltreatment and an epigenetic signature of chronic low-grade inflammation. Our findings underscore the presence of immune dysregulation early after exposure to CM; further studies are needed to assess the long-term clinical implications of this signature in psychiatric patients.

No significant relationships.

To quantitatively evaluate relationships between infection preventionists (IPs) staffing levels, nursing hours, and rates of 10 types of healthcare-associated infections (HAIs).

An ambidirectional observation in a 528-bed teaching hospital.

All inpatients from July 1, 2012, to February 1, 2021.

Standardized US National Health Safety Network (NHSN) definitions were used for HAIs. Staffing levels were measured in full-time equivalents (FTE) for IPs and total monthly hours worked for nurses. A time-trend analysis using control charts, t tests, Poisson tests, and regression analysis was performed using Minitab and R computing programs on rates and standardized infection ratios (SIRs) of 10 types of HAIs. An additional analysis was performed on 3 stratifications: critically low (2–3 FTE), below recommended IP levels (4–6 FTE), and at recommended IP levels (7–8 FTE).

The observation covered 1.6 million patient days of surveillance. IP staffing levels fluctuated from ≤2 IP FTE (critically low) to 7–8 IP FTE (recommended levels). Periods of highest catheter-associated urinary tract infection SIRs, hospital-onset Clostridioides difficile and carbapenem-resistant Enterobacteriaceae infection rates, along with 4 of 5 types of surgical site SIRs coincided with the periods of lowest IP staffing levels and the absence of certified IPs and a healthcare epidemiologist. Central-line–associated bloodstream infections increased amid lower nursing levels despite the increased presence of an IP and a hospital epidemiologist.

Of 10 HAIs, 8 had highest incidences during periods of lowest IP staffing and experience. Some HAI rates varied inversely with levels of IP staffing and experience and others appeared to be more influenced by nursing levels or other confounders.

People living in precarious housing or homelessness have higher than expected rates of psychotic disorders, persistent psychotic symptoms, and premature mortality. Psychotic symptoms can be modeled as a complex dynamic system, allowing assessment of roles for risk factors in symptom development, persistence, and contribution to premature mortality.

The severity of delusions, conceptual disorganization, hallucinations, suspiciousness, and unusual thought content was rated monthly over 5 years in a community sample of precariously housed/homeless adults (n = 375) in Vancouver, Canada. Multilevel vector auto-regression analysis was used to construct temporal, contemporaneous, and between-person symptom networks. Network measures were compared between participants with (n = 219) or without (n = 156) history of psychotic disorder using bootstrap and permutation analyses. Relationships between network connectivity and risk factors including homelessness, trauma, and substance dependence were estimated by multiple linear regression. The contribution of network measures to premature mortality was estimated by Cox proportional hazard models.

Delusions and unusual thought content were central symptoms in the multilevel network. Each psychotic symptom was positively reinforcing over time, an effect most pronounced in participants with a history of psychotic disorder. Global connectivity was similar between those with and without such a history. Greater connectivity between symptoms was associated with methamphetamine dependence and past trauma exposure. Auto-regressive connectivity was associated with premature mortality in participants under age 55.

Past and current experiences contribute to the severity and dynamic relationships between psychotic symptoms. Interrupting the self-perpetuating severity of psychotic symptoms in a vulnerable group of people could contribute to reducing premature mortality.

Different studies have confirmed the association between cannabis use and psychosis and, also, the relationship between age at first cannabis use and age at onset of psychosis (Henquet et al 2005, Barnes et al 2006). In a young psychiatric sample, we aimed to investigate the correlation between cannabis use and the age at onset of psychotic and non-psychotic symptoms and whether this relationship is modulated by the genetic variability at COMT, CNR1 and CHRNA7genes.

The sample comprised 157 Caucasian patients (mean age: 17.01 (3.6)) diagnosed following DSM-IV-TR criteria: 80 patients with schizophrenia-spectrum disorders, 77 patients with affective or conduct disorders. Cannabis use was assessed with UNICA-A and DIGS scales (Nurnberger 1994) and 49% individuals were classified as consumers. SNPs were genotyped using Taqman 5′-exonuclease assays.

We observed a positive relationship between age at first cannabis use and age at onset in, both, schizophrenia-spectrum (β = 1.44 p < 0.001) and other psychiatric disorders (β = 0.56 p < 0.002). An interaction was observed between COMT Val158Met polymorphism and cannabis use specifically within schizophrenia-spectrum disorders’ group (β = −2.72 p = 0.04), with Val/Val genotype carriers showing an earlier age of onset than Val/Met carriers, and these, lower than the Met/Met carriers. No modulation effect of CNR1 or CHRNA7 polymorphisms was observed.

Our results seem to indicate the importance of maturation timing and brain development in which exposition to cannabis occurs. We provide new evidence about the COMT modulation effect on the association between cannabis use and age at onset of symptoms, specifically in individuals affected by schizophrenia-spectrum disorders.

Neurocognitive deficits and schizotypal features are elevated in first-degree relatives of schizophrenia patients. However, the co-aggregation of these indicators is not well known. Some studies have found that neurocognitive deficits and schizotypy increase in severity with the density of family history of schizophrenia. Therefore, we studied in affected families a) whether the status of Presumed Carrier (PC) of the genetic risk for schizophrenia is associated with higher levels of neurocognitive deficits and schizotypic features and b) the relationship between schizotypy and neurocognition.

From an ongoing Catalan Multicentric Family Study on Schizophrenia, 70 families were included in this analysis. 90 non-psychotic parents of schizophrenic patients (age 50.7/8.8; education 10.3/4.04; IQ 96.2/14.6) were defined as PC if they had at least one first (apart of offspring) or second degree relative with schizophrenia spectrum disorders (FIGS), resulting in 17 PC and 73 non-PC. Schizotypic features were assessed with the SCID-II and the SPQ-B. Working memory (WM), executive functioning, sustained attention, verbal fluency and logical memory were also assessed.

PC differed significantly from NPC on verbal working memory, even after controlling for IQ (d=0.8). They did not differ on any of the self-reported or interview measures of schizotypy. The negative schizotypic dimension was associated with more WCST-perseverative errors, and low scores in spatial-WM, verbal fluency and immediate/delayed logical memory.

A large association was found between verbal-WM and the familial background of schizophrenia. Only negative features were associated with some neurocognitive functions, supporting the view of multiple independent dimensions or a pleiotropic expression of risk.

The extent and causes of covariance between schizotypy and neurocognition is not well-known yet. Certain models conceive their association as necessary for the construct validity of schizotypy, whereas others view them as independently contributing to a multivariate endophenotype. It is also not clear whether those at increased genetic risk for schizophrenia present stronger covariance, reflecting an extra latent source of variance. We analysed their association within relatives of schizophrenia patients defined with FIGS as Presumed Carriers -PC- of the genetic risk for schizophrenia, Presumed Non Carriers -PNC-, and controls.

108 healthy relatives of schizophrenia patients and 72 healthy controls were assessed with the SCID-II and completed the SPQ-B. Neurocognitive assessment: Letter-Number Sequencing (LNS), WCST, CPT-IP, verbal fluency, and logical memory.

Partial correlations adjusting for age and education showed that within PC-relatives self-rated negative schizotypy was associated with lower LNS and CPT-IP; positive schizotypy was associated with CPT-IP, and disorganization with memory and failure to maintain set. Schizoid symptoms had an association with failure to maintain set (though not perseveration) and paranoid symptoms with memory. Within PNC-relatives, negative schizotypy was associated with lower verbal fluency and more perseverative errors. Within controls, positive schizotypy was associated with perseverative errors and both positive and negative dimensions were associated with verbal fluency.

Results indicate a wider array of covariation between relatives with presumed higher genetic liability. A consistent pattern of associations between psychotic-like dimensions and the brain functions tapped by neurocognitive tests did not emerge across groups.

Though cognitive abilities in adulthood are largely influenced by individual genetic background, they have also been shown to be importantly influenced by environmental factors. Some of these influences are mediated by epigenetic mechanisms. Accordingly, polymorphic variants in the epigenetic gene DNMT3B have been linked to neurocognitive performance. Since monozygotic (MZ) twins may show larger or smaller intrapair phenotypic differences depending on whether their genetic background is more or less sensitive to environmental factors, a twin design was implemented to determine if particular polymorphisms in the DNMT3B gene may be linked to a better (worse) response to enriched (deprived) environmental factors.

Applying the variability gene methodology in a sample of 54 healthy MZ twin pairs (108 individuals) with no lifetime history of psychopathology, two DNMT3B polymorphisms were analyzed in relation to their intrapair differences for either intellectual quotient (IQ) or working memory performance.

MZ twin pairs with the CC genotype for rs406193 SNP showed statistically significant larger intrapair differences in IQ than CT pairs.

Results suggest that DNMT3B polymorphisms may explain variability in the IQ response to either enriched or impoverished environmental conditions. Accordingly, the applied methodology is shown as a potentially valuable tool for determining genetic markers of cognitive plasticity. Further research is needed to confirm this specific result and to expand on other putative genetic markers of environmental sensitivity.

The present study aimed to examine the prevalence of child abuse across the continuum of psychosis.

The sample consisted of 198 individuals divided in three groups: (1) 48 FEP patients, (2) 77 individuals scoring high in Community Assessment of Psychic Experiences (CAPE), classified as “High CAPE” group and (3) 73 individuals scoring low, classified as “Low CAPE” group. Childhood abuse was assessed using self-report instruments. Chi2 tests and logistic regression models controlling by sex, age and cannabis were used to perform three comparisons: (i) FEP vs. Low CAPE; (ii) FEP vs. High CAPE and (iii) High CAPE vs. Low CAPE.

The frequency of individuals exposed to childhood abuse for FEP, High CAPE and Low CAPE groups were 52.1%, 41.6% and 11%, respectively. FEP and High CAPE group presented significantly higher rates of childhood abuse compared to Low CAPE group, however, no significant differences were found between FEP and High CAPE groups regarding the frequency of childhood abuse.

There is an increasing frequency of childhood abuse from low subclinical psychosis to FEP patients. However, childhood abuse is equally common in FEP and at risk individuals.

To test whether firstly, different parental rearing components were associated with different dimensions of psychiatric symptoms in adulthood, secondly BDNF-Val66Met polymorphism moderated this association and thirdly, this association was due to genetic confounding.

Perceived parental rearing according to Parental Bonding Instrument (PBI), psychiatric symptoms evaluated with the Brief Symptom Inventory (BSI) and the BDNF-Val66Met polymorphism were analyzed in a sample of 232 adult twins from the general population.

In the whole sample, paternal care was negatively associated with depression. Maternal overprotection was positively associated with paranoid ideation, obsession-compulsion and somatization. Gene-environment interaction effects were detected between the BDNF-Val66Met polymorphism and maternal care on phobic anxiety, paternal care on hostility, maternal overprotection on somatization and paternal overprotection also in somatization. In the subsample of MZ twins, intrapair differences in maternal care were associated with anxiety, paranoid ideation and somatization.

Met carriers were, in general, more sensitive to the effects of parental rearing compared to Val/Val carriers in relation to anxiety and somatization. Contra-intuitively, our findings suggest that high rates of maternal care might be of risk for Met carriers regarding anxiety. Results from analyses controlling for genetic confounding were in line with this finding.

Glutamatergic neurotransmission dysfunction has classically been related to the aetiology of psychotic disorders. A substantial polygenic component shared across these disorders has been reported and molecular genetics studies have associated glutamatergic-related genes, such as d-amino acid oxidase activator (DAOA) and regulator of G-protein signalling 4 (RGS4) with the risk for psychotic disorders. Our aims were to examine: (i) the relationship between DAOA and RGS4 and the risk for psychotic disorders using a family-based association approach, and (ii) whether variations in these genes are associated with differences in patients’ cognitive performance.

The sample comprised 753 subjects (222 patients with psychotic disorders and 531 first-degree relatives). Six SNPs in DAOA and 5 SNPs in RGS4 were genotyped. Executive cognitive performance was assessed with Trail Making Test B (TMT-B) and Wisconsin Card Sorting Test (WCST). Genetic association analyses were conducted with PLINK, using the transmission disequilibrium test (TDT) for the family-based study and linear regression for cognitive performance analyses.

The haplotype GAGACT at DAOA was under-transmitted to patients (P = 0.0008), indicating its association with these disorders. With regards to cognitive performance, the DAOA haplotype GAGGCT was associated with worse scores in TMT-B (P = 0.018) in SZ patients only. RGS4 analyses did not report significant results.

Our findings suggest that the DAOA gene may contribute to the risk for psychotic disorders and that this gene may play a role as a modulator of executive function, probably through the dysregulation of the glutamatergic signalling.

The identification of new genetic variants underlying psychosis is crucial to improve its molecular diagnosis and to determine the disease etiology, which is necessary to develop new therapeutic targets.

To identify novel rare genetic variants associated to mental disorders, using whole exome sequencing (WES).

Two families with high prevalence of mental disease were genotyped using WES. The first family has 5 members affected, the mother with a bipolar disorder, three sons, two with schizophrenia and one with schizoaffective disorder, and a cousin with major depression and psychotic symptoms. The second family is constituted by 38 members affected by major mental diseases in three generations. Key affected members of each family were genotyped by WES. Shared rare variants, with allelic frequencies below 0.5% in general population, were identified among the affected members of the family. The segregation of those variants was confirmed by Sanger sequencing.

In family 1, thirty-seven genetic variants related to neurodevelopment were identified. Two of those variants in the genes TRIP12 and RNF25 segregated with psychosis. In family 2, seven rare genetic variants contained in genes related to neurodevelopment were identified. A mutation in the gene ARHGAP19 segregated with psychosis.

Three new genes have been found to be associated with psychosis. TRIP12 and RNF25 encode two E3-ubiquitin ligases which modulate the Wnt pathway, mutations in which lead to neurodevelopmental defects. ARHGAP19 encodes a GTPase which regulates the RhoA protein, involved in the regulation of the cytoskeleton.

The authors have not supplied their declaration of competing interest.

Parasomnias are a category of sleep disorders in which abnormal events occur during sleep, due to inappropriately timed activation of physiological systems.

we report the case of a 41-year-old female who has no psychiatric history. The patient went to emergency department because when she was starting to sleep, in the first state of sleep, she felts a sensation of paralysis in all her body, with incapacity for breathing, chest oppression and tactile hallucinations like something or someone was touching her entire body. Due to that, the patient awoke frightened, with high levels of anxiety, with heart palpitations, shortness of breath, trembling, choking feeling, sweating, nausea and fear of dying. When the patient arrived to the emergency department, she was suffering a panic attack, thinking that she could have some kind of neurological disease or she was suffering a heart attack.after treating the panic attack with 1 mg of lorazepam, all the symptoms subsided gradually.

in this case report, we present a patient with a new-onset parasomnia, with hypnagogic hallucinations and a panic attack at the awakening. It is known that stress factors are closely associated with parasomnias, as we can see in this case because the patient was moving and she was sleeping in a new place.

Parasomnias are very frequently present in general population and they can trigger intense anxiety status that can lead to panic attacks.

The authors have not supplied their declaration of competing interest.

There is consistent evidence that theory of mind (ToM) is impaired in schizophrenia (SZ); however, it remains unclear whether such deficits are trait- or state-dependent. We evaluated ToM in patients with schizophrenia spectrum disorders (SSDs), their healthy first-degree relatives, and controls to test its suitability as an endophenotypic marker. We also studied the modifying effect of markers of clinical and genetic liability to SZ (schizotypy and genetic variability in the oxytocin receptor gene: OXTR) on ToM in healthy individuals.

The sample included 38 stable SSD patients, 80 unaffected first-degree relatives, and 81 controls. ToM was assessed using the Hinting Task (HT) and schizotypy via the Schizotypal Personality Questionnaire-Brief (SPQ-B), which generates interpersonal (SPQ-IP), cognitive-perceptual (SPQ-CP), and disorganization (SPQ-D) scores. The polymorphism rs53576 of OXTR was genotyped.

Patients presented poorer HT performance than relatives and controls (p = 0.003 and p < 0.001). High SPQ-IP and SPQ-CP scores correlated with poorer ToM performance in relatives (p = 0.010 and p = 0.030), but not in controls. OXTR was not associated with HT scores, but it showed a modifying effect within controls; high SPQ-CP was related to HT poorer performance conditional to GG genotype (p = 0.007).

ToM deficits were present in patients but not in unaffected relatives or controls. However, our data indicate the usefulness of clinical and genetic liability markers to characterize differences in ToM abilities within healthy individuals. Then, the observed link between ToM and SZ liability suggests the putative role of ToM as an endophenotypic marker. Nevertheless, new analyses in larger samples are needed.