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Social defeat, the subjective experience of viewing oneself as a failure or social outsider, is associated with various psychiatric disorders. Recent studies suggest that social defeat may play an important role in the development of psychotic disorders. This study examined the role of social defeat in the relationship between childhood trauma and paranoid ideation, a symptom of psychosis, in non-psychotic mental disorders. Psychiatric patients (N = 199) completed the Korean version of the Childhood Trauma Questionnaire, the Korean version of the Defeat Scale, and Restructured Clinical Scale 6 (Ideas of Persecution) of the Korean version of the Minnesota Multiphasic Personality Inventory-2. A partial correlation analysis revealed that childhood trauma was significantly related to social defeat and paranoid ideation after controlling for age and gender. Structural equation modeling confirmed that the relationship between childhood trauma and paranoid ideation was partially mediated by social defeat. Thus, social defeat is a possible psychological mechanism underlying the association between childhood trauma and paranoia.

Introduction: An increasing body of evidence suggests that development of coronary artery disease (CAD) is probably affected by a variety of lifestyle factors. However, most studies have not assessed comprehensive lifestyle factors including well-being psychological factors simultaneously, therefore relative contribution of each factors is obscure. Hypothesis: A variety of lifestyle factors including defect in well-being psychological factors may contribute to development of CAD through interacting muturally. Methods and Results: A case-control, cross-sectional study analyzing comprehensive lifestyle factors of patients with acute coronary syndrome (ACS) and healthy control was conducted. 92 patients with ACS (73 male; 53.2 yr; 30 acute MI, 62 unstable angina) and 69 healthy control (43 male; 48.7yr) were recruited. For dietary analysis, food frequency questionnaire (FFQ) and 2 days of 24 hour dietary recall were used. Anxiety, depression, stress, job stress, and hostility were analyzed to assess psychological ill-being factors. Primary and secondary control strategies, health-related quality of life (HRQoL), and satisfaction degree in 7 life domains such as marriage, leisure, standard of living, job, family, sex life, and self were analyzed to assess well-being factors. Univariate analysis showed that ACS group vs. control group had more current/ex-smoker and exercised less (all, p Conclusions: Defects in well-being psychological factors rather than ill-being factors are closely associated with ACS. A variety of lifestyle factors, especially, poor satisfaction in 7 life domains, use of primary control strategy, greater intake of sea foods and sweets, smoking, and poor exercise are independent predictors of ACS. Therefore preventive intervention trial of ACS should include modification of comprehensive lifestyle factors including defects in well-being factors.

Background and Objectives: Increasing evidence supports that psychological factors may be related to development of coronary artery disease (CAD). Although psychological well-being, ill-being, and control strategy factors may play a significant role in CAD, rarely have these factors been simultaneously examined previously. We assessed comprehensive psychological factors in patients with acute coronary syndrome (ACS). Subjects and Methods: A total of 85 ACS patients (56 unstable angina, 29 acute myocardial infarction; 52.6±10.2 years; M/F=68/17) and 63 healthy controls (48.7±6.7 years, M/F=43/20) were included. Socio-demographic information, levels of psychological maladjustment, such as anxiety, hostility, and job stress, health-related quality of life (HRQoL), and primary and secondary control strategy use were collected through self-report questionnaires. Results: There was no significant difference between the ACS group and control group in levels of anxiety, hostility, and job stress. Howev er, ACS patients had significantly lower scores on the general health perception and bodily pain subscales of HRQoL than the control group. The ACS group, as compared with the controls, tended to use primary control strategies more, although not reaching statistical significance by univariate analysis. Multivariate logistic regression analysis after adjusting age and gender identified the physical domain of HRQoL {odds ratio (OR)=0.40}, primary control strategy (OR=1.92), and secondary control strategy (OR=0.53) as independent predictors of ACS. Conclusion: Poor HRQoL and primary control strategy, proactive behaviors in achieving ones’ goal, may act as risk factors for ACS, while secondary control strategy to conform to current situation may act as a protective factor for ACS. (Korean Circ J 2015;45(2):117-124)

While the results of animal studies have shown that perfluorinated compounds (PFCs) can modulate concentrations of thyroid hormones in blood, limited information is available on relationships between concentrations of PFCs in human blood serum and fetal thyroid hormones. The relationship between concentrations of PFCs in blood and fetal thyroid hormone concentrations or birth weight, and ratios of major PFCs between maternal and fetal serum were determined. Concentrations of PFCs were measured in blood serum of pregnant women (n = 44), fetal cord blood serum (n = 43) and breast milk (n = 35). Total concentrations of thyroxin (T4), triiodothyronin (T3) and thyroid stimulating hormone (TSH) in blood serum were also quantified. The ratios of major PFCs in maternal versus fetal serum were 1:1.93, 1.02, 0.72, and 0.48 for perfluorotridecanoic acid (PFTrDA), perfluorooctanoic acid (PFOA), perfluorohexane sulfonate (PFHxS), and perfluorooctane sulfonate (PFOS), respectively. Fetal PFOS, PFOA, PFTrDA and maternal PFTrDA were correlated with fetal total T4 concentrations, but after adjusting for major covariates, most of the relationships were no longer statistically significant. However, the significant negative correlations between maternal PFOS and fetal T3, and maternal PFTrDA and fetal T4 and T3 remained. Since thyroid hormones are crucial in the early development of the fetus, its clinical implication should be evaluated. Given the observed trans-placental transfer of PFCs, efforts should be also made to elucidate the exposure sources among pregnant women.

The Hebei Spirit oil spill episode (December 7, 2007) has affected the western coastal area of South Korea; however, there is limited information on the potential toxicity of the oil spill to the ecosystem or humans. The potential toxicity of sediments collected from the affected area (n = 22) 2 years after the spill was evaluated. Acute lethal toxicity tests using Vibrio fischeri and Moina macrocopa and tests for genotoxicity and alteration of steroidogenesis using chicken DT40 cells and H295R cells, respectively, were conducted. Both crude and weathered oil extracts were evaluated in order to link the observed toxicity in the sediment extracts to the oil spill. Whereas toxicity to bacteria and daphnids was observed in only two elutriate samples, 10 of the 22 sediment extracts showed genotoxic potential in DT40 cells. The mechanisms of genotoxicity involved nucleotide excision repair (XPA(-/)), homologous recombination (RAD54(-/-)), and translesion synthesis pathways (REV3(-/-)). In addition, nine sediment extracts caused significantly greater production of E2 in H295R cells, and significant up-regulation of CYP19, CYP11B2, and 3βHSD2 by sediment extracts was observed. The pattern of toxicities observed in both crude and weathered oil samples was similar to that observed in the sediment extracts. The genotoxicicity and endocrine-disruption potential of the sediment extracts suggest a need for long-term followup for such toxicity in humans and wildlife in this area.