Association between F2-isoprostanes and self-reported stressors in pregnant americans of African and European ancestry.

Background: Poor birth outcomes such as preterm birth/delivery disproportionately affect African Americans compared to White individuals. Reasons for this disparity are likely multifactorial, and include prenatal psychosocial stressors, and attendant increased lipid peroxidation; however, empirical data linking psychosocial stressors during pregnancy to oxidative status are limited. Methods: We used established scales to measure five psychosocial stressors. Maternal adverse childhood experiences, financial stress, social support, anxiety, and depression were measured among 50 African American and White pregnant women enrolled in the Stress and Health in Pregnancy cohort. Liquid chromatography-tandem mass spectrometry was used to measure biomarkers of oxidative stress (four urinary F2-isoprostane isomers), to estimate oxidative status. Linear regression models were used to evaluate associations between psychosocial stressors, prenatal oxidative status and preterm birth. Results: After adjusting for maternal obesity, gestational diabetes, and cigarette smoking, African American women with higher oxidative status were more likely to report higher maternal adverse childhood experience scores (ß = 0.16, se = 1.07, p-value = 0.024) and depression scores (ß = 0.05, se = 0.02, p = 0.014). Higher oxidative status was also associated with lower gestational age at birth (ß = -0.13, se = 0.06, p = 0.04) in this population. These associations were not apparent in Whites. However, none of the cross-product terms for race/ethnicity and social stressors reached statistical significance (p > 0.05). Conclusion: While the small sample size limits inference, our novel data suggest that psychosocial stressors may contribute significantly to oxidative stress during pregnancy, and preterm birth or delivery African Americans. If replicated in larger studies, these findings would support oxidative stress reduction using established dietary or pharmacological approaches present a potential avenue to mitigate adverse effects of psychosocial stressors on birth outcomes.

Childhood and Adulthood Trauma Associate With Cognitive Aging Among Black and White Older Adults.

Sociocontextual factors powerfully shape risk for age-related cognitive impairment, including excess risk burdening medically underserved populations. Lifecourse adversity associates with cognitive aging, but harms are likely mitigable. Understanding population-salient relationships and sensitive periods for exposure is crucial for targeting clinical interventions. OBJECTIVE: The authors examined childhood and adulthood traumatic events in relation to cognition among Black and White older adults in the Health and Retirement Study (HRS). PARTICIPANTS: Participants (N = 13,952) aged 55+ had complete lifetime trauma and cognitive testing data at the 2006/08, 2010/12, and/or 2014/16 waves. MEASURES: Trauma indices comprised childhood and adulthood event counts. Outcomes included baseline performance and trajectories on the Telephone Interview for Cognitive Status. DESIGN: Main and nonlinear trauma effects were modeled via linear regression, and overall contributions assessed with omnibus likelihood ratio tests. RESULTS: Black participants (N = 2,345) reported marginally lower adulthood trauma exposure than White participants (N = 11,607) with no other exposure differentials observed. In White participants only, greater childhood trauma exposure predicted worse baseline cognition but slower change over time. Across race, adulthood trauma robustly associated with baseline cognition. Relationships were frequently nonlinear: low but nonzero trauma predicted highest cognitive scores, with much poorer cognition observed as trauma exposure increased. Relationships between adulthood trauma and trajectory were limited to the White sample. CONCLUSION: Traumatic experiences, particularly in adulthood, may impact late-life cognitive health if not addressed. Findings highlight foci for clinical researchers and providers: adverse life events as a source of cognitive risk, and identification of community-specific resources that buffer behavioral, physical, and mental health sequelae of previous and incident trauma.

A developmental approach to diversifying neuroscience through effective mentorship practices: perspectives on cross-identity mentorship and a critical call to action.

Many early-career neuroscientists with diverse identities may not have mentors who are more advanced in the neuroscience pipeline and have a congruent identity due to historic biases, laws, and policies impacting access to education. Cross-identity mentoring relationships pose challenges and power imbalances that impact the retention of diverse early career neuroscientists, but also hold the potential for a mutually enriching and collaborative relationship that fosters the mentee's success. Additionally, the barriers faced by diverse mentees and their mentorship needs may evolve with career progression and require developmental considerations. This article provides perspectives on factors that impact cross-identity mentorship from individuals participating in Diversifying the Community of Neuroscience (CNS)-a longitudinal, National Institute of Neurological Disorders and Stroke (NINDS) R25 neuroscience mentorship program developed to increase diversity in the neurosciences. Participants in Diversifying CNS were comprised of 14 graduate students, postdoctoral fellows, and early career faculty who completed an online qualitative survey on cross-identity mentorship practices that impact their experience in neuroscience fields. Qualitative survey data were analyzed using inductive thematic analysis and resulted in four themes across career levels: (1) approach to mentorship and interpersonal dynamics, (2) allyship and management of power imbalance, (3) academic sponsorship, and (4) institutional barriers impacting navigation of academia. These themes, along with identified mentorship needs by developmental stage, provide insights mentors can use to better support the success of their mentees with diverse intersectional identities. As highlighted in our discussion, a mentor's awareness of systemic barriers along with active allyship are foundational for their role.

A case of fatal familial insomnia: diagnostic and therapeutic approaches.

Fatal Familial Insomnia (FFI) is an uncommon but fatal genetic condition that is characterized by severe progressive insomnia, dysautonomia, neuropsychiatric changes, and gait instability. Diagnostic workup includes genetic testing, EEG, MRI imaging of the brain, polysomnography, and CSF analysis. MRI brain imaging may be notable for areas of restricted diffusion in the thalamus. Therapeutic approaches are centered on symptom management, predominantly for insomnia. It is important for clinicians to consider FFI in patients presenting with progressive insomnia, cognitive deficits, and gait instability, and to direct patients and families toward genetic counseling and palliative care services.

Direct Oral Anticoagulant Agents: Pharmacologic Profile, Indications, Coagulation Monitoring, and Reversal Agents.

Vitamin K antagonists (VKAs), such as warfarin, have been used for thromboprophylaxis and for the treatment of thromboembolic events in patients with nonvalvular atrial fibrillation for over 60 years. The increasing use of direct oral anticoagulants (DOACs) in recent years has shown greater advantages and safer use over VKA, including reduced bleeding, fewer drug interactions, no food interactions, a quick onset and offset of activity, and predictable dose-response properties. Despite their advantages, there are a couple of major limitations that raise concerns among clinicians, including the need for more coagulation assays to monitor their effects and more specific reversal antidotes in life-threatening circumstances of bleeding. This review will discuss the important characteristics of the 5 Food and Drug Administration-approved DOACs (including anticoagulation monitoring for each) and the specific and nonspecific reversal agents to DOAC-associated bleeding.