Trajectories of Posttraumatic Growth and Their Associations With Quality of Life After the 2011 Tohoku Earthquake and Tsunami.

The 2011 Tohoku earthquake and tsunami in Japan was an extraordinarily stressful incident that caused harmful psychological reactions, such as posttraumatic stress disorder (PTSD), among affected individuals. However, a proportion of exposed individuals experienced posttraumatic growth (PTG), characterized by a noticeable degree of personal strength, spirituality, life appreciation, perception of new possibilities in life, and enhanced relationships with others. Some researchers have argued that these positive reactions may be an illusory change related to coping with traumatic events. We examined trajectory patterns related to PTG Inventory (PTGI) subscales to elucidate the existence of both real and illusory growth regarding quality of life (QoL), utilizing group-based trajectory models. Three online questionnaires were distributed at 6 months (N = 2,554; M age = 47.04 years, SD = 12.62), 12 months (N = 887; M age = 48.11 years, SD = 12.43), and 42 months (N = 560; M age = 48.86 years, SD = 12.25) postdisaster. Participants responded to items related to demographic characteristics, disaster experiences, posttraumatic stress symptoms, PTG, and QoL. Three main PTG trajectories emerged, characterized by growth, no growth, and illusory growth, with QoL as a time invariant covariate. Compared with the growth trajectory, the odds ratios (ORs) for no growth ranged from 2.27 to 5.04; for illusory growth, the ORs ranged from 2.09 to 4.67. To our knowledge, this was the first study to report growth trajectories related to PTGI subscales and their underlying differences in psychological mechanisms and processes following the 2011 Tohoku earthquake and tsunami.

Chronic exposure to stress hormones promotes transformation and tumorigenicity of 3T3 mouse fibroblasts.

Epinephrine and norepinephrine are produced during psychological stress and can directly bind to cells to induce DNA damage. These effects may have more long-lasting consequences such as DNA mutations resulting in an increased potential for cellular transformation and/or tumor progression. This study examined the molecular effects of a chronic (24 h) in vitro exposure to these stress hormones on murine 3T3 cells. Long exposures (24 h) in dose-response experiments with norepinephrine or epinephrine induced significant increases in DNA damage in treated cells compared to that of untreated controls as measured by the alkaline comet assay. Pre-treatment with a blocking agent (the ß-adrenergic receptor antagonist propranolol) eliminated this increase in damage. In addition, both norepinephrine and epinephrine increased cellular transformation, as assessed by growth in soft agar, and 3T3 cells pre-treated with either norepinephrine or epinephrine induced a more rapid onset of tumors and more aggressive tumor growth in nude mice. In summary, incubation of 3T3 cells with catecholamines results in long-term DNA damage as measured by increased transformed phenotypes and tumor progression, indicating that they are important mediators of stress effects on genomic instability and vulnerability to tumor formation.