The Experienced Self and Other Scale: A technique for assaying the experience of one's self in relation to the other

This study tests the construct validity of the Experienced Self and Other Scale (E-SOS), which is a self report measure that assesses the experience of one's self in relation to others. Statistical analyses were conducted using Exploratory factor analysis with an orthogonal rotation, and Confirmatory factor Analysis. The internal consistency was determined using Cronbach's alpha coefficient for each subscale from the factor analysis. Bivariate correlations, as well as multiple linear regression analyses, were used to assess the relationship between the E-SOS and other measures. Three hundred and twenty-seven subjects completed the E-SOS. The factor analysis resulted in a five-factor structure explaining 49.02% of the total variance and with a high internal reliability. While results indicated no relationship between the E-SOS and Psychological Mindedness Scale, the E-SOS subscales were significantly correlated with the corresponded NEO-FFI factors, as well as with the RSQ factors. Preliminary analyses suggest a promising future for the E-SOS as an approach to measuring one experience of self

The Experienced Self and Other Scale: A technique for assaying the experience of one’s self in relation to the other

The construct “self” appears in diverse forms in theories about what it is to be a person. As the sense of “self” is typically assessed through personal reports, differences in its description undoubtedly reflect significant differences in peoples’ apperception of self. This report describes the development, reliability, and factorial structure of the Experience of Sense of Self (E-SOS), an inventory designed to assess one’s perception of self in relation to the person’s perception of various potential “others.” It does so using Venn diagrams to depict and quantify the experienced overlap between the self and “others.” Participant responses to the instrument were studied through Exploratory Factor Analysis. This yielded a five-factor solution: 1) Experience of Positive Sensation; 2) Experience of Challenges; 3) Experience of Temptations; 4) Experience of Higher Power; and 5) Experience of Family. The items comprising each of these were found to produce reliable subscales. Further research with the E-SOS and suggestions for its use are offered.     DOI:10.2458/azu_jmmss_v4i2_shvi

Toward a translational approach to targeting the endocannabinoid system in posttraumatic stress disorder: A critical review of preclinical research

Despite the lack of clinical research, marijuana and synthetic cannabinoids have been approved to treat posttraumatic stress disorder (PTSD) in several states in the United States. This review critically examines preclinical research on the endocannabinoid system (ECS) in order to evaluate three key questions that are relevant to PTSD: (1) Does ECS dysfunction impact fear extinction? (2) Can stress-related symptoms be prevented by ECS modulation? (3) Is the ECS a potential target for enhancing PTSD treatment? Disruption of the ECS impaired fear extinction in rodents, and ECS abnormalities have been observed in PTSD. Targeting fear memories via the ECS had mixed results in rodents, whereas augmented cannabinoid receptor activation typically facilitated extinction. However, the translational value of these findings is limited by the paucity and inconsistency of human research. Further investigation is necessary to determine whether incorporating cannabinoids in treatment would benefit individuals with PTSD, with cautious attention to risks

Greater hippocampal volume is associated with PTSD treatment response

Previous research associates smaller hippocampal volume with posttraumatic stress disorder (PTSD). It is unclear, however, whether treatment affects hippocampal volume or vice versa. Seventy-six subjects, 40 PTSD patients and 36 matched trauma-exposed healthy resilient controls, underwent clinical assessments and magnetic resonance imaging (MRI) at baseline, and 10 weeks later, during which PTSD patients completed ten weeks of Prolonged Exposure (PE) treatment. The resilient controls and treatment responders (n=23) had greater baseline hippocampal volume than treatment non-responders (n=17) (p=0.012 and p=0.050, respectively), perhaps due to more robust fear-extinction capacity in both the initial phase after exposure to trauma and during treatment

PTSD remission after prolonged exposure treatment is associated with anterior cingulate cortex thinning and volume reduction

Background: Brain structures underlying posttraumatic stress disorder (PTSD) have been a focus of imaging studies, but associations between treatment outcome and alterations in brain structures remain largely unexamined. We longitudinally examined the relation of structural changes in the rostral anterior cingulate cortex (rACC), a previously identified key region in the PTSD fear network, to outcome of prolonged exposure (PE) treatment. Method: The sample included 78 adults (53 women): 41 patients with PTSD and 37 trauma-exposed healthy volunteers (TE-HCs). Patients underwent a 10-week course of PE treatment and completed pre- and posttreatment assessments and magnetic resonance imaging (MRI) structural scans. TE-HCs also underwent assessment and MRI at baseline and 10 weeks later. PE remitters (n = 11), nonremitters (n = 14), and TE-HCs, were compared at baseline on demographic and clinical characteristics and ACC structure. Remitters, nonremitters, and TE-HCs were compared for pre- to posttreatment clinical and structural ACC change, controlling for potential confounding variables. Results: There were no baseline differences in structure between PTSD and TE-HCs or remitters and nonremitters. Following treatment, PTSD remitters exhibited cortical thinning and volume decrease in the left rACC compared with PTSD nonremitters and TE-HCs. Conclusions: These results, while in need of replication, suggest that PE treatment for PTSD, by extinguishing maladaptive trauma associations, may promote synaptic plasticity and structure change in rACC. Future research should explore possible underlying mechanisms

MIF inhibits the formation and toxicity of misfolded SOD1 amyloid aggregates: implications for familial ALS

Abstract Mutations in superoxide dismutase (SOD1) cause amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease caused by the progressive loss of motor neurons in the brain and spinal cord. It has been suggested that toxicity of mutant SOD1 results from its misfolding, however, it is yet unclear why misfolded SOD1 accumulates specifically within motor neurons. We recently demonstrated that macrophage migration inhibitory factor (MIF)—a multifunctional protein with cytokine/chemokine activity and cytosolic chaperone-like properties—inhibits the accumulation of misfolded SOD1. Here, we show that MIF inhibits mutant SOD1 nuclear clearance when overexpressed in motor neuron-like NSC-34 cells. In addition, MIF alters the typical SOD1 amyloid aggregation pathway in vitro, and, instead, promotes the formation of disordered aggregates, as measured by Thioflavin T (ThT) assay and transmission electron microscopy (TEM) imaging. Moreover, we report that MIF reduces the toxicity of misfolded SOD1 by directly interacting with it, and that the chaperone function and protective effect of MIF in neuronal cultures do not require its intrinsic catalytic activities. Importantly, we report that the locked-trimeric MIFN110C mutant, which exhibits strongly impaired CD74-mediated cytokine functions, has strong chaperone activity, dissociating, for the first time, these two cellular functions. Altogether, our study implicates MIF as a potential therapeutic candidate in the treatment of ALS