Medical microrobots can be made personal by 3D printing them from patient blood–derived biomaterials.

Long-term effects of the COVID-19 pandemic on autistic individuals and their families are recently emerging. This study investigated these effects in 40 mother-child dyads by measuring the behavioral problems of autistic individuals (via Aberrant Behavior Checklist) and their mothers’ anxiety levels (via Beck Anxiety Inventory) during the pre-pandemic period, one month after, and one year after its onset. One year into the pandemic, aberrant behaviors of autistic individuals worsened only for those whose mothers had high anxiety levels. The continued negative impact of the COVID-19 pandemic on the behavior of autistic individuals is related to their mother’s anxiety level, highlighting the need to support maternal mental health in families with individuals with autism.

Background: Borderline Personality Disorder (BPD) is a complex psychiatric condition with multifactorial origins, with a high proportion of patients reporting early trauma. Stressors such as adverse childhood experiences (ACEs) can shape the epigenetic landscape including DNA methylation (DNAm) and act on gene expression. DNAm is increasingly being investigated as a molecular link between environmental exposures such as ACE and psychiatric outcomes. Differential DNAm of the gene PR domain zinc finger protein 8 (PRDM8), a histone methyltransferase, has recently been reported to be sensitive to early life trauma. Its role in BPD, especially in the context of ACE, remains to be elucidated. Methods: This study investigated DNAm patterns of PRDM8 in peripheral blood and saliva obtained from BPD patients undergoing Dialectic Behavioral Therapy (DBT) compared to healthy control (HC) participants. Associations with ACE and BPD symptom severity were assessed, and therapy-related changes in DNAm were examined. Results: At baseline, BPD patients demonstrated significant hypomethylation of PRDM8 in blood relative to the HC group. Following DBT, a nominally significant increase in DNAm was observed, aligning with inversely correlated symptom severity. No significant differences in saliva were detected. ACE was not associated with PRDM8 DNAm. Conclusions: Our findings suggest that PRDM8 DNAm might be associated with BPD and therapeutic intervention but not with ACE. Together with prior research, the results underscore the importance of future investigation of gene–environment interactions and the functional significance of PRDM8 regulation in the pathophysiology of BPD.

Adult mental disorders (aMD), including borderline personality disorder (BPD), major depressive disorder (MDD), and social anxiety disorder (SAD), share adverse childhood experiences (ACEs) as an environmental risk factor. Epigenetic mechanisms, including DNA methylation (DNAm), may mediate the biological link between early adversity and psychiatric risk. SIAH3, implicated in stress-related and mitochondrial pathways, has been previously associated with both ACE and aMD. This study examined SIAH3 DNAm in adults with BPD, MDD, or SAD, relative to healthy control participants (HC), testing effects of diagnosis, ACE exposure, and their interaction across the pooled sample and within each diagnostic group. Both aMD diagnosis and high ACE exposure showed trends toward SIAH3 hypomethylation, and a significant diagnosis × ACE interaction emerged, with inconclusive post-hoc tests. Disorder-specific analyses revealed heterogeneous patterns: in BPD, high ACE showed a trend toward hypermethylation in unadjusted models; in MDD, interaction effects were marginal and not robust to covariate adjustment; in SAD, significant main effects and a diagnosis × ACE interaction were observed, with high ACE associated with lower DNAm exclusively in HC. These findings suggest disorder-specific epigenetic responses to ACE, positioning SIAH3 as a potential molecular link between early life stress, mitochondrial function, and aMD.

Background The peripartum period encompasses physiological, endocrine, and immunological adaptations that ensure maternal health and fetal development. Notably, the molecular correlates of these adaptations in healthy women remain limited, particularly at the transcriptomic level. This study aimed to identify systemic transcriptomic differences between late pregnancy and the early postpartum period in a large cohort of healthy women. Methods RNA sequencing was performed on 112 samples from peripheral blood collected at gestational week 38 (gw38; n = 40) and postpartum week 8 (ppw8; n = 72). The transcriptome was compared while adjusting for age and BMI. Additional covariate-adjusted analyses were performed considering cell-type composition, sex of the fetus, and gestational length. Results A total of 293 differentially expressed genes (DEGs) were identified when comparing ppw8 vs. gw38, with the majority being downregulated in the postpartum period. The postpartum phase was marked by the lower expression of genes involved in erythropoiesis and innate, granulocyte-driven immunity, as well as higher levels of adaptive, antibody-mediated defense transcripts. The directionality and functional patterns of DEGs were largely preserved, while accounting for shifts in cellular heterogeneity from pregnancy to postpartum, alongside the emergence of DEGs in cell-intrinsic regulatory pathways. Conclusions Our results reveal systemic transcriptomic differences from late pregnancy to postpartum, particularly a shift from innate to adaptive immune signatures as well as hematopoietic processes, cellular and metabolic pathways. These findings provide reference data for further understanding of peripartum adaptation and establish a molecular baseline for future investigations into perinatal biology and related disorders.

Background: Estrogens and progestogens exert widespread regulatory effects on gene and protein expression through receptor binding and epigenetic regulation. The systemic epigenetic effects of these steroids are poorly understood. Moreover, the effects of menstrual cycle phase and hormonal contraceptive use on epigenome-wide DNA methylation in relation to depressive symptoms have not been systematically investigated. Methods: Peripheral blood samples were collected from 116 healthy females aged 18-33 years while using hormonal contraceptives or naturally cycling at the early follicular or periovulatory phase at baseline and follow-up. The hormonal milieu changed only for starters and discontinuers between two sampling points, whereas participants in the naturally cycling groups provided samples at the same menstrual cycle phase at both time points. Linear mixed models were fitted to examine the relationship between hormonal contraceptive use, hormonal group trajectories, and DNA methylation levels across the whole methylome. Differentially methylated CpG sites and regions were further examined in relation to circulating endogenous and synthetic hormone concentrations as well as depressive symptom levels. Results: Groups representing different hormonal milieus of the early follicular and periovulatory phases, continuous contraceptive use, as well as initiation and discontinuation of contraceptive use, were associated with differential methylation at several CpG sites and regions, including loci annotated to RUNX1 , STAT3 and LCN8 . These DNA methylation signatures showed significant correlations with circulating synthetic hormone concentrations, but not with depressive symptoms and endogenous hormone levels. Conclusion: This study revealed epigenome-wide DNA methylation correlates of hormonal contraceptive use and trajectories across hormonal groups. While highlighting a potential relationship between synthetic sex hormones and peripheral DNA methylation, the findings warrant replication in larger cohorts and clinical studies to further understand the biological mechanism behind the interaction between sex hormones and women’s mental health.