Functional connectivity between the ventral anterior cingulate and amygdala during implicit emotional conflict regulation and daily-life emotion dysregulation.

Emotional conflict adaptation involving ventral anterior cingulate cortex (ACC) suppression of the amygdala is thought to be important in emotion regulation, with evidence of impaired implicit emotion regulation in emotional distress disorders. However, it is unclear how this impairment is associated with daily-life emotion dysregulation in emotional distress disorders. In the current study, female participants with an emotional distress disorder (N = 27) were scanned with MRI while completing an implicit emotion conflict regulation task that involved identifying the facial expression of an image while ignoring an overlaid congruent or incongruent affect label. Participants then completed two weeks of ambulatory assessment of daily-life emotion dysregulation. Consistent with previous research on comorbid emotional distress disorders (Etkin and Schatzberg, 2011), there was no behavioral effect of emotional conflict adaptation (p = .701) but a significant effect of congruent adaptation (p = .006), suggesting impairment is specific to implicit emotional conflict regulation. Additionally, there was no neural evidence of emotional conflict adaptation in the ventral ACC and amygdala (ps > .766). Further, in our primary psychophysiological interactions analyses, we examined ventral ACC-amygdala functional connectivity. As hypothesized, increased ventral ACC-amygdala functional connectivity for emotional conflict adaptation was associated with increased daily-life affective instability (p = .022), but not mean daily-life negative affect (p = .372). Overall, results provide behavioral and neural evidence of impaired implicit emotional conflict adaptation in individuals with emotional distress disorders and suggests that this impairment is related to daily-life affective instability in these disorders.

Endometriosis: A Malignant Fingerprint.

BACKGROUND: Endometriosis is complex, but identifying the novel biomarkers, inflammatory molecules, and genetic links holds the key to the enhanced detection, prediction and treatment of both endometriosis and endometriosis related malignant neoplasia. Here we review the literature relating to the specific molecular mechanism(s) mediating tumorigenesis arising within endometriosis. METHODS: Guidance (e.g. Cochrane) and published studies were identified. The Published studies were identified through PubMed using the systematic review methods filter, and the authors' topic knowledge. These data were reviewed to identify key and relevant articles to create a comprehensive review article to explore the molecular fingerprint associated with in endometriosis-driven tumorigenesis. RESULTS: An important focus is the link between C3aR1, PGR, ER1, SOX-17 and other relevant gene expression profiles and endometriosis-driven tumorigenesis. Further studies should also focus on the combined use of CA-125 with HE-4, and the role for OVA1/MIA as clinically relevant diagnostic biomarkers in the prediction of endometriosis-driven tumorigenesis. CONCLUSIONS: Elucidating endometriosis' molecular fingerprint is to understand the molecular mechanisms that drive the endometriosis-associated malignant phenotype. A better understanding of the predictive roles of these genes and the value of the biomarker proteins will allow for the derivation of unique molecular treatment algorithms to better serve our patients.