Neurophysiological Markers Related to Negative Self-referential Processing Differentiate Adolescent Suicide Ideators and Attempters.

Background: Adolescent suicide is a major public health concern, and presently, there is a limited understanding of the neurophysiological correlates of suicidal behaviors. Cognitive models of suicide indicate that negative views of the self are related to suicidal thoughts and behaviors, and this study investigated whether behavioral and neural correlates of self-referential processing differentiate suicide ideators from recent attempters. Methods: Adolescents with depression reporting current suicidal ideation and no lifetime suicide attempts (suicide ideators, n = 30) and past-year suicide attempts (recent attempters, n = 26) completed a self-referential encoding task while high-density electroencephalogram data were recorded. Behavioral analyses focused on negative processing bias (i.e., tendency to attribute negative information as being self-relevant) and drift rate (i.e., slope of reaction time and response type that corresponds to how quickly information is accumulated to make a decision about whether words are self-referent). Neurophysiological markers probing components reflecting early semantic monitoring (P2), engagement (early late positive potential), and effortful encoding (late late positive potential) also were tested. Results: Adolescent suicide ideators and recent suicide attempters reported comparable symptom severity, suicide ideation, and mental disorders. Although there were no behavioral differences, compared with suicide ideators, suicide attempters exhibited greater P2 amplitudes for negative versus positive words, which may reflect enhanced attention and arousal in response to negative self-referential stimuli. There were no group differences for the early or late late positive potential. Conclusions: Enhanced sensory arousal in response to negative stimuli-that is, attentional orienting to semantic, emotional, and self-relevant features-differentiates adolescent suicide attempters from ideators and thus may signal risk for suicidal behavior.

Functional integration of acute myeloid leukemia into the vascular niche.

Vascular endothelial cells are a critical component of the hematopoietic microenvironment that regulates blood cell production. Recent studies suggest the existence of functional cross-talk between hematologic malignancies and vascular endothelium. Here we show that human acute myeloid leukemia (AML) localizes to the vasculature in both patients and in a xenograft model. A significant number of vascular tissue-associated AML cells (V-AML) integrate into vasculature in vivo and can fuse with endothelial cells. V-AML cells acquire several endothelial cell-like characteristics, including the upregulation of CD105, a receptor associated with activated endothelium. Remarkably, endothelial-integrated V-AML shows an almost fourfold reduction in proliferative activity compared with non-vascular-associated AML. Primary AML cells can be induced to downregulate the expression of their hematopoietic markers in vitro and differentiate into phenotypically and functionally defined endothelial-like cells. After transplantation, these leukemia-derived endothelial cells are capable of giving rise to AML. These novel functional interactions between AML cells and normal endothelium along with the reversible endothelial cell potential of AML suggest that vascular endothelium may serve as a previously unrecognized reservoir for AML.