These findings imply that treatment strategies for individuals at UHR for psychosis should be comprehensive, promoting resilience as well as targeting the reduction of positive and negative symptoms to foster social reintegration and recovery.
Mental adjustment and coping affect the physical outcome and survival as well as quality of life in cancer patients. The Mini-Mental Adjustment to Cancer (Mini-MAC) scale is a new refined, economical and reliable self-rating instrument measuring cognitive and behavioral responses to cancer. The aim of this study was to evaluate the psychometric properties of the Mini-MAC in Korean cancer patients. A total of 208 cancer patients recruited from the Yonsei Cancer Center were assessed with the Mini-MAC and the Hospital Anxiety and Depression Scale (HADS). Principal component analysis with varimax rotation for the Korean version of Mini-MAC (K-Mini-MAC) confirmed four factors. Three had psychometric properties similar to Helpless-Hopeless (HH), Anxious Preoccupation (AP) and Cognitive Avoidance (CA) of the original Mini-MAC. A novel factor, named Positive Attitude, included items of both Fatalism (FA) and Fighting Spirit (FS) from the original version. The five subscales from the original version (AP, HH, FS, FA and CA) and Positive Attitude had acceptable internal reliabilities in our sample (Cronbach's alpha coefficient 0.50-0.86; correlation coefficient of test-retest 0.68-0.88). For the validity, significant interscale correlation was observed in the original five subscales and Positive Attitude. Each subscale including Positive Attitude was also significantly related to Depression and Anxiety of HADS. As a whole, the K-Mini-MAC was a reliable, valid and acceptable tool for Korean cancer patients. These findings can provide information about the cross-cultural validity of Mini-MAC scale's factor structure. Cultural differences were also discussed.
Resilience to aversive events has a central role in determining whether stress leads to the development of depression. mGluR5 has been implicated in the pathophysiology of depression, but the effect of mGluR5 activity on stress resilience remains unexplored. We found that mGluR5(-/-) (also known as Grm5(-/-)) mice displayed more depression-like behaviors (for example, learned helplessness, social withdrawal and anhedonia) than control mice following exposure to various stressful stimuli. Lentiviral 'rescue' of mGluR5 in the nucleus accumbens (NAc) decreased these depression-like behaviors in mGluR5(-/-) mice. In the NAc, ΔFosB, whose induction promotes stress resilience, failed to be upregulated by stress in mGluR5(-/-) mice. Notably, targeted pharmacological activation of mGluR5 in the NAc increased ΔFosB expression. Our findings point to an essential role for mGluR5 in promoting stress resilience and suggest that a defect in mGluR5-mediated signaling in the NAc may represent an endophenotype for stress-induced depression.
ObjectiveAlthough the relationship between obsessive compulsive disorder (OCD) and impulsivity has long been debated, impulsivity has not been systematically examined in clinical samples of OCD. Meanwhile, recent findings suggest that impulsivity is multi-dimensional construct that can be examined through several constructs. Therefore, this study is aimed to evaluate multiple facets of impulsivity in OCD.MethodThe recruitment includes 80 OCD and 76 healthy control participants. Participants completed a test battery comprising three behavioral tasks of stop signal task (SST), delay discounting task (DDT) and balloon analog risk test (BART), and one self-report measure of the Barratt Impulsiveness scale (BIS-11).ResultsOCD subjects showed significantly lower stop signal reaction time of SST reflecting higher action impulsivity and higher delay discounting parameter of DDT suggesting increased choice impulsivity but significantly lower adjusted mean pump of BART implying lower risk taking propensity of BART than healthy control.ConclusionIncreased Action and choice impulsivity, and decreased risk taking propensities were found in OCD. These findings seem to be consistent with clinical characteristics of OCD such as greater preference for or avoid risky situations (avoidance), inability to wait tension relief may provoke safety behaviors (compulsion) and inability to stop already started behaviors (repetition).
DNA methylation patterns at specific cytosine-phosphate-guanine (CpG) sites predictably change with age and can be used to derive "epigenetic age", an indicator of biological age, as opposed to merely chronological age. A relatively new estimator, called "DNAm GrimAge", is notable for its superior predictive ability in older populations regarding numerous age-related metrics like time-to-death, time-to-coronary heart disease, and time-to-cancer. PTSD is associated with premature mortality and frequently has comorbid physical illnesses suggestive of accelerated biological aging. This is the first study to assess DNAm GrimAge in PTSD patients. We investigated the acceleration of GrimAge relative to chronological age, denoted "AgeAccelGrim" in combat trauma-exposed male veterans with and without PTSD using crosssectional and longitudinal data from two independent well-characterized veteran cohorts. In both cohorts, AgeAccelGrim was significantly higher in the PTSD group compared to the control group (N = 162, 1.26 vs −0.57, p = 0.001 and N = 53, 0.93 vs −1.60 Years, p = 0.008), suggesting accelerated biological aging in both cohorts with PTSD. In 3-year follow-up study of individuals initially diagnosed with PTSD (N = 26), changes in PTSD symptom severity were correlated with AgeAccelGrim changes (r = 0.39, p = 0.049). In addition, the loss of CD28 cell surface markers on CD8 + T cells, an indicator of T-cell senescence/exhaustion that is associated with biological aging, was positively correlated with AgeAccelGrim, suggesting an immunological contribution to the accelerated biological aging. Overall, our findings delineate cellular correlates of biological aging in combat-related PTSD, which may help explain the increased medical morbidity and mortality seen in this disease. Members of the PTSD Systems Biology Consortium are listed in Supplementary information.
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