1Med Inform Internet Med 2004 Mar 29: 65-74
TitleSuicide risk factors and suicide vulnerability in various major psychiatric disorders.
AbstractThere are many known suicide risk factors (SRF) common to major psychiatric disorders, but their impact on suicide vulnerability remains unclear. We used FALCON (Fuzzy Adaptive Learning Control Network) to evaluate those impacts.
Staff psychiatrists completed computerized suicide risk scales (CSRS-III) including 21 SRF for 612 patients. Diagnoses were: schizophrenia, schizoaffective, major depression, anxiety disorder, bipolar affective disorder, personality disorder, organic brain syndromes, delusional disorder and other diagnoses. An optimal trained FALCON was obtained by running the network 10 times with 552 CSRS-III, validating with the balance. Medically serious suicide attempts (the vulnerability factor) served as the target variable. The significance of each variable in the trained network was determined by the magnitude of the change in output as affected by the consecutive change in all points of the variable input, then calculating the mean variance of all cases. The direction of influence was determined by the input on the entire scale of each variable, point by point, across all cases, then calculating the mean of all outputs.
The impact and direction of influence of the various SRF differed for each diagnosis.
Evaluation of the individual patient with his/her specific impact profile, determination of direction of influence of the corresponding SRF's may assist in increasing the accuracy of individual suicide risk assessment.
SCZ Keywordsschizophrenia, schizophrenic
2J. Cell Biol. 2013 Nov 203: 643-56
TitleDysbindin is a potent inducer of RhoA-SRF-mediated cardiomyocyte hypertrophy.
AbstractDysbindin is an established schizophrenia susceptibility gene thoroughly studied in the context of the brain. We have previously shown through a yeast two-hybrid screen that it is also a cardiac binding partner of the intercalated disc protein Myozap. Because Dysbindin is highly expressed in the heart, we aimed here at deciphering its cardiac function. Using a serum response factor (SRF) response element reporter-driven luciferase assay, we identified a robust activation of SRF signaling by Dysbindin overexpression that was associated with significant up-regulation of SRF gene targets, such as Acta1 and Actc1. Concurrently, we identified RhoA as a novel binding partner of Dysbindin. Further phenotypic and mechanistic characterization revealed that Dysbindin induced cardiac hypertrophy via RhoA-SRF and MEK1-ERK1 signaling pathways. In conclusion, we show a novel cardiac role of Dysbindin in the activation of RhoA-SRF and MEK1-ERK1 signaling pathways and in the induction of cardiac hypertrophy. Future in vivo studies should examine the significance of Dysbindin in cardiomyopathy.
SCZ Keywordsschizophrenia, schizophrenic