Background Perinatal depression is common: on average, more than 13% of women suffer from physician-diagnosed disorder and 20% report symptoms bearing clinical relevance. Maternal depression not only significantly impacts women’s quality of life but also increases the offspring’s risk of negative developmental outcomes, including mental disorders, through a combination of maternal alterations in in-utero biology and postnatal rearing factors during the early period of life. The HappyMums project aims to improve our understanding of perinatal depression by identifying the factors that robustly predict risk and resilience in mothers and their offspring, determining underlying neurobiological mechanisms, and, finally, testing the efficacy of potential interventions. Methods HappyMums will use data from a large collection of cohorts and registries containing biological, clinical, socio-demographic, environmental, and lifestyle data. It will pool unique human samples of maternal blood, placenta, chorionic villi and amniotic fluid, analyzing these data alongside pre-clinical samples of brain, blood and placental tissue from models of prenatal stress in mice and livebearing fish for correlative analyses. HappyMums will develop a mobile application (App) to collect multiple data types from women for early screening and monitoring of depressive symptoms. Conclusion The findings generated by HappyMums will be clinically relevant as they will increase the knowledge on perinatal depression, with unprecedented benefits for the offspring and the society as a whole.

Early life stress, especially when experienced during the prenatal period or childhood, affects the brain developmental trajectories leading to an enhanced vulnerability for stress-related psychiatric disorders later in life. Although both clinical and preclinical studies clearly support this association, the biological pathways deregulated by such exposure, and the effects of early life stress in shaping the neurodevelopmental trajectories, have so far been poorly investigated. By using the prenatal stress (PNS) model, a well-established rat model of early life stress, we performed transcriptomic analyses in the prefrontal cortex of rats exposed or not to PNS and sacrificed at different postnatal days (PNDs 21, 40, 62). We first investigated the mechanisms and pathways affected by exposures to PNS that may contribute to the long-lasting vulnerability of developing altered behaviours in adulthood (at PND62). Moreover, by focusing on transcriptomic changes, we evaluated the effects of PNS in shaping brain trajectories with the aim to identify the most critical temporal window of vulnerability, when biological alterations are already present, but clear symptoms not manifested yet. In adult rats (PNDs 62), PNS modulates 389 genes which resulted to be involved mainly in the stress and inflammatory system response. Moreover, when we looked at temporal trajectories in term of gene expression, we found the most significant effects of PNS during adolescence (between PND40 versus 21) with an effect on pathways related to stress, inflammation and metabolism that was then maintained until adulthood. Our data suggest that molecules belonging to the stress, inflammatory and metabolic systems may serve as biomarkers of risk to allow the identification of adolescents that have been exposed to adversities and are at high risk to develop mental illness later in life, and that thus could benefit from early preventive interventions with novel pharmacological or non pharmacological interventions able to target these biological systems. PND 40 versus PND 21 we found the GP6 Signalling Pathway , Actin Cytoskeleton Signalling , Integrin Signalling and cAMP-mediated Signalling ; whereas among the most significant pathways modulated at PND 62 vs PND 40 we found Nuclear factor erythroid 2-related factor 2 (NRF2)-mediated Oxidative Stress Response, Triacylglycerol Biosynthesis, Osteoarthritis Pathway and Liver X Receptor (LXR)/ Retinoid X Receptor (RXR) Activation.

Major Depressive Disorder (MDD) has a prevalence of 11% by the end of adolescence and 90% of adolescents live in low and middle income countries (LMIC). Hence, identifying biomarkers to early identify adolescents at risk of developing the disorder is of paramount importance. A risk-stratified cohort of 150 adolescents was recruited in Porto Alegre (Brazil) by using the risk score developed by the IDEA (Identifying Depression Early in Adolescence) project. The cohort is comprised of 50 adolescents with a current diagnosis of MDD, 50 at high- and 50 at low-risk of developing MDD. Genome-wide gene expression analysis was performed and raw data processed for bioinformatic analysis. The comparison between depressed and high-risk adolescents showed the highest difference in terms of genes differentially modulated (FC > |1.2|, p<0.05); the pathways analysis showed the modulation of biological signatures associated with inflammation and immune system in the MDD group compared with both high- and low-risk groups. Alteration in inflammatory pathways are associated with the presence of MDD in adolescence but have not been observed in adolescents at risk of MDD.

Wadsley-Roth (W-R) structured oxides featured with wide channels represent one of the most promising material families showing compelling rate performance for lithium-ion batteries. Herein, we report an in-depth study on the fast and extensive intercalation chemistry of phosphorus stabilized W-R phase PNb9O25 and its application in high energy and fast-charging devices. We explore the intercalation geometry of PNb9O25 and identify two geometrical types of stable insertion sites with the total amount much higher than conventional intercalation-type electrodes. We reveal the ion transportation kinetics that the Li ions initially diffuse along the open type III channels and then penetrate to edge sites with low kinetic barriers. During the lithiation, no remarkable phase transition is detected with nearly intact host phosphorous niobium oxide backbone. Therefore, the oxide framework of PNb9O25 keeps almost unchanged with all the fast diffusion channels and insertion cavities well-maintained upon cycling, which accomplishes the unconventional electrochemical performance of W-R structured electrodes.

Evidence shows that depression is associated with hypothalamic–pituitary–adrenal (HPA) axis hyperactivation, although such findings are not entirely unequivocal. In contrast, various psychiatric conditions, including atypical depression, are associated with hypocortisolism. Another line of research has demonstrated that personality is associated with HPA axis alteration. It is thus hypothesized that different personality pathology in depression would be associated with distinct cortisol reactivity.Eighty-seven outpatients with DSM-IV major depressive disorder were recruited. Personality was assessed by the temperament and character inventory (TCI). HPA axis reactivity was measured by the combined dexamethasone (DEX)/corticotropin-releasing hormone (CRH) test. According to our previous studies, two subgroups were considered based on their cortisol responses to the DEX/CRH test: incomplete-suppressors whose cortisol response was exaggerated and enhanced-suppressors whose cortisol response was blunted.The analysis of covariance, controlling for age, gender and symptom severity, revealed that incomplete-suppressors scored significantly higher on cooperativeness than enhanced-suppressors (p=0.002). A multivariate stepwise logistic regression analysis predicting the cortisol suppression pattern from the seven TCI dimensions, controlling for age, gender and symptom severity, revealed that lower cooperativeness (p=0.001) and higher reward dependence (p=0.018) were significant predictors toward enhanced suppression.The neuroendocrine challenge test was administered only once, based on a simple test protocol.Our findings suggest that (personality-related) subtypes of depression might be differentiated based on the different pattern of cortisol reactivity. Future studies are warranted to further characterize the HPA axis alteration in relation to various subtypes of depression.

The data presented in this paper is related to the research article entitled “Synthesis, Spectroscopy, Electrochemistry and DFT of Electron-Rich Ferrocenylsubphthalocyanines” [1] where electrochemical redox data and cyclic voltammograms at only a scan rate of 0.10 V s−1 of four ferrocenylsubphthalocyanine dyads Fc(CH2)nCO2BSubPc(H)12 (n = 0, 1 or 3) and FcCO(CH2)2CO2BSubPc(H)12, are presented. This data article provides extensive electrochemical redox data and cyclic voltammograms at various scan rates from 0.05 up to 5.00 V s−1 to illustrate the effect of the different scan rates on the electrochemical behaviour of the four ferrocenylsubphthalocyanine dyads.

Buildings consume a considerable share of global energy, mostly from non-renewable sources, and emit a substantial amount of CO2. As this is not aligned with sustainable development goals one of the main changes needed is to make buildings more energy efficient by insulating them from the ambient environment. This article discusses the factors affecting the type and quantity of insulating materials in a residential building made using prefabricated Structural Insulated Panels (SIPs), and designed to require near zero space conditioning. A life cycle assessment approach is used to find the most effective level of insulation. The analysis shows it is not appropriate to use the same type of SIPs in different locations, as some relevant factors are context-dependent. The factors considered in this analysis were the design goals, climate characteristics, and most importantly the current and projected profile of the energy used for manufacturing materials and for operating the building. It is important these factors are studied together, as individual investigations can be misleading.

Immunological dysregulation has been suggested to be involved in the pathogenesis of schizophrenia. Accumulating evidences further implicate that activated inflammatory processes may be particularly relevant for the precipitation of negative and cognitive symptoms of schizophrenia. Toll-like receptor 2 (TLR2) plays an important role in innate immunity by sensing a variety of pathogens and inducing an acquired immunity. In the present study, we investigated whether the coding region of single nucleotide polymorphisms (SNPs) of the TLR2 gene was associated with schizophrenia as well as with clinical symptoms in schizophrenia patients. The study population consisted of 286 Korean schizophrenia patients and 305 Korean control subjects. The assessment of the Scale for the Assessment of Negative Symptoms was used to evaluate the negative symptoms of schizophrenia; the operational criteria checklist was used to measure general psychopathology. We selected two cSNPs [rs3804099 (Asn199Asn) and rs3804100 (Ser450Ser)] considering their heterozygosity and minor allele frequency. SNP genotyping was conducted using direct sequencing. We did not find any significant associations between SNPs and schizophrenia in the genotype and allelic frequencies. On the other hand, in the analysis of cognitive symptoms, rs3804099 showed significant differences in schizophrenia patients with poor concentration in the dominant model (TC/CC vs. TT, p = 0.0099). Also, rs3804100 showed a significant association with poor concentration in the co-dominant (TC vs. TT, p = 0.014) and the dominant models (TC/CC vs. TT, p = 0.0035). We obtained no significant support for the association of the TLR2 gene with susceptibility to schizophrenia in the Korean population. However, our results provide possibility that C allele of rs3804099 and rs3804100 may be associated with poor concentration in schizophrenia patients. Further studies with larger samples are required to confirm our results.

Xia-Gibbs syndrome (Mental retardation, autosomal dominant 25; MRD25) [MIM 615829] is a rare autosomal dominant disease characterized by mental retardation, developmental delay, speech delay, structural brain anomalies, hypotonicity, protuberant eyes, visual problems, laryngomalacia and snoring. Since the first description in 2014, fewer than 50 patients with Xia-Gibbs syndrome have been noticed in the literature. We describe here 2 years 2 months old girl with developmental delay, brain anomalies, laryngomalacia and craniosynostosis. Whole-Exome Sequencing (WES) analyses in patient showed a heterozygous NM_001029882: c.4370 A>G; p. (Asp1457Gly) mutation in AHDC1. Craniosynostosis rarely observed in the patients described to date, and west syndrome-like EEG pattern, constipation and electrolyte imbalance observed for the first time were present in our patient. Further reports and in-vivo/in-vitro works will make possible knowing of the genetic and clinical background of this disease.