Women's experiences of trauma, the psychosocial impact and health service needs during the perinatal period.

BACKGROUND: Traumatic events are associated with psychological and physical health problems for women in the perinatal period (i.e., pregnancy-12-months after childbirth). Despite the negative impact of trauma on perinatal women, the long-term impact of such diverse trauma and women's experience during the perinatal period remains understudied. METHODS: This study explored two research questions: 1) What are the psychological experiences of perinatal women who have experienced interpersonal traumatic events? And 2) What are the service needs and gaps expressed by women relating to perinatal medical protocols and psychological services? These questions were addressed via in-depth semi-structured qualitative interviews with nine perinatal women (one pregnant and eight postpartum) residing in central Canada who reported experiencing interpersonal traumatic events occurring from adolescence to the perinatal period. Recruitment and data collection occurred from October 2020 to June 2021. Interviews were audio-recorded, transcribed, and analyzed according to constructivist grounded theory. RESULTS: The emergent grounded theory model revealed the central theme of the role of prior trauma in shaping women's perinatal experiences, with four related main themes including perinatal experiences during the COVID-19 pandemic, the role of social support in women's perinatal experiences, the barriers that women experienced while seeking psychological and medical services prior to the perinatal period and during the perinatal period, and the specific needs of perinatal women with a history of interpersonal trauma. CONCLUSIONS: Findings of this research highlight the negative and long-lasting impact of traumatic events experienced on women's psychological health and psychosocial functioning during the perinatal period, as well as perinatal women's unmet psychological and medical service needs. A call to action for perinatal researchers and clinicians is imperative in furthering this important area of research and practicing person-centered and trauma-informed care with this population.

Congenital neurodevelopmental anomalies in pediatric and young adult cancer.

Congenital anomalies that are diagnosed in at least 120,000 US infants every year are the leading cause of infant death and contribute to disability and pediatric hospitalizations. Several large-scale epidemiologic studies have provided substantial evidence of an association between congenital anomalies and cancer risk in children, suggesting potential underlying cancer-predisposing conditions and the involvement of developmental genetic pathways. Electronic medical records from 1,107 pediatric, adolescent, and young adult oncology patients were reviewed. The observed number (O) of congenital anomalies among children with a specific pediatric cancer subtype was compared to the expected number (E) of anomalies based on the frequency of congenital anomalies in the entire study population. The O/E ratios were tested for significance using Fisher's exact test. The Kaplan-Meier method was used to compare overall and neurological malignancy survival rates following tumor diagnosis. Thirteen percent of patients had a congenital anomaly diagnosis prior to their cancer diagnosis. When stratified by congenital anomaly subtype, there was an excess of neurological anomalies among children with central nervous system tumors (O/E = 1.56, 95%CI 1.13-2.09). Male pediatric cancer patients were more likely than females to have a congenital anomaly, particularly those <5 years of age (O/E 1.35, 95%CI 0.97-1.82). Our study provides additional insight into the association between specific congenital anomaly types and pediatric cancer development. Moreover, it may help to inform the development of new screening policies and support hypothesis-driven research investigating mechanisms underlying tumor predisposition in children with congenital anomalies.

Rax is a selector gene for mediobasal hypothalamic cell types.

The brain plays a central role in controlling energy, glucose, and lipid homeostasis, with specialized neurons within nuclei of the mediobasal hypothalamus, namely the arcuate (ARC) and ventromedial (VMH), tasked with proper signal integration. Exactly how the exquisite cytoarchitecture and underlying circuitry becomes established within these nuclei remains largely unknown, in part because hypothalamic developmental programs are just beginning to be elucidated. Here, we demonstrate that the Retina and anterior neural fold homeobox (Rax) gene plays a key role in establishing ARC and VMH nuclei in mice. First, we show that Rax is expressed in ARC and VMH progenitors throughout development, consistent with genetic fate mapping studies demonstrating that Rax+ lineages give rise to VMH neurons. Second, the conditional ablation of Rax in a subset of VMH progenitors using a Shh::Cre driver leads to a fate switch from a VMH neuronal phenotype to a hypothalamic but non-VMH identity, suggesting that Rax is a selector gene for VMH cellular fates. Finally, the broader elimination of Rax throughout ARC/VMH progenitors using Six3::Cre leads to a severe loss of both VMH and ARC cellular phenotypes, demonstrating a role for Rax in both VMH and ARC fate specification. Combined, our study illustrates that Rax is required in ARC/VMH progenitors to specify neuronal phenotypes within this hypothalamic brain region. Rax thus provides a molecular entry point for further study of the ontology and establishment of hypothalamic feeding circuits.