Two experiments were conducted in order to examine the relationship between alexithymia and: 1) family environment; 2) discomfort and ambivalence experiencing and expressing emotion; and 3) dissociation. Research participants in both experiments were college students. We examined the ability to identify and communicate emotion using the Toronto Alexithymia Scale. In Experiment 1, we found that alexithymia was significantly correlated with ambivalence concerning expression of emotion (measured using the Ambivalence over Emotional Expressiveness Questionnaire) and with discomfort concerning negative emotional states (measured using a new instrument called the Emotional Experience Discomfort Scale). Higher levels of alexithymia were associated with retrospective reports of diminished family expressiveness (measured using the Expressiveness subscale of the Family Environment Scale) and with feeling less emotionally safe during childhood (measured using a new instrument called the Childhood Experiences Questionnaire). In Experiment 2, we found that alexithymia was significantly correlated with dissociative experiences (measured using the Dissociative Experiences Scale). However, alexithymia and dissociation differed in the way they were associated with retrospective reports of different aspects of family expressiveness (measured using the Family Expressiveness Questionnaire). High levels of dissociation were associated with increased negative dominant family communication. In contrast, high levels of alexithymia were associated with low levels of positive family communication.

Black Americans are disproportionately affected by dementia. To expand our understanding of mechanisms of this disparity, we look to Alzheimer's disease (AD) biomarkers. In this review, we summarize current data, comparing the few studies presenting these findings. Further, we contextualize the data using two influential frameworks: the National Institute on Aging–Alzheimer's Association (NIA‐AA) Research Framework and NIA's Health Disparities Research Framework. The NIA‐AA Research Framework provides a biological definition of AD that can be measured in vivo. However, current cut‐points for determining pathological versus non‐pathological status were developed using predominantly White cohorts—a serious limitation. The NIA's Health Disparities Research Framework is used to contextualize findings from studies identifying racial differences in biomarker levels, because studying biomakers in isolation cannot explain or reduce inequities. We offer recommendations to expand study beyond initial reports of racial differences. Specifically, life course experiences associated with racialization and commonly used study enrollment practices may better account for observations than exclusively biological explanations.

Background-Acute ethanol is known to affect cells and organs but the underlying molecular mechanisms are poorly explored. Recent developments highlight the potential importance of mitogen activated protein kinases, MAPKs (i.e. ERK1/2, p38 and JNK1/2) signaling, and histone modifications (i.e. acetylation, methylation and phosphorylation) in the actions of ethanol in hepatocytes. We have therefore investigated significance of these molecular steps in vivo using a model in which rats were acutely administered ethanol intraperitoneally (IP).

Summary ERβ is regarded as a “tumor suppressor” in breast cancer due to its anti-proliferative effects. However, unlike ERα, ERβ has not been developed as a therapeutic target in breast cancer due to loss of ERβ in aggressive cancers. In a small molecule library screen for ERβ stabilizers, we identified Diptoindonesin G (Dip G) which significantly increases ERβ protein stability, while decreasing ERα protein levesl. Dip G enhances the transcription and anti-proliferative activities of ERβ, while attenuating the transcription and proliferative effects of ERα. Further investigation revealed that instead of targeting ER, Dip G targets the CHIP E3 ubiquitin ligase shared by ERα and ERβ. Thus, Dip G is a dual functional moiety that reciprocally controls ERα and ERβ protein stability and activities via an indirect mechanism. The ERβ stabilization effects of Dip G may enable the development of ERβ-targeted therapies for human breast cancers.

The epigenetic histone modification by ethanol is emerging as one of the mechanisms for its deleterious effects in the liver. In this context, we have investigated the role of histone H3 phosphorylation at Ser10 (P-H3-Ser10), and Ser28 (P-H3-Ser28) in liver after acute ethanol treatment in vivo. Ethanol was administered intraperitoneally in male Sprague-Dawley rats. Ethanol dose-response (1-5 g/kg body weight) and time-course (1-4 h) experiments were conducted, and various parameters were monitored. Steatosis and necrosis (serum alanine aminotransferase) of the liver increased in 4 h, suggesting liver injury. There were differences between P-H3-Ser10 and P-H3-Ser28 at 1 h, with the latter being more sensitive to lower ethanol doses. It was noteworthy that phosphorylation of both serines disappeared at the highest dose used (5 g/kg). We also examined phosphoacetylation of histone H3 at K9S10 and observed a dramatic increase. The changes in histone H3 phosphorylation and phosphoacetylation were also accompanied with expression of early response genes (c-fos, c-jun, mitogen-activated protein kinase phosphatase-1). Chromatin immunoprecipitation assays in samples from 1.5 and 4 h of ethanol administration indicated that increased histone H3 phosphorylation at Ser28 was associated with the promoters of c-jun and plasminogen activator inhibitor-1. In conclusion, this study demonstrates for the first time that in vivo exposure of liver to acute ethanol induced phosphorylation and phosphoacetylation of histone H3, and these modifications are differentially involved in the mRNA expression of genes.