Experience can shape cortical circuits, especially during critical periods for plasticity. In visual cortex, imbalance of activity from the two eyes during the critical period shifts ocular dominance (OD) towards the more active eye. Inhibitory circuits are crucial in this process: OD plasticity is absent in GAD65KO mice that show diminished inhibition. This defect can be rescued by application of benzodiazepines, which increase GABAergic signalling. However, it is unknown how such changes in inhibition might disrupt and then restore OD plasticity. Since NMDA dependent synaptic plasticity mechanisms are also known to contribute to OD plasticity, we investigated whether NMDA receptor levels and function are also altered in GAD65KO. There are reduced NR2A levels and slower NMDA currents in visual cortex of GAD65KO mice. Application of benzodiazepines, which rescues OD plasticity, also increases NR2A levels. Thus it appears as if OD plasticity can be restored by adding a critical amount of excitatory transmission through NR2A-containing NMDA receptors. Together, these observations can unify competing ideas of how OD plasticity is regulated: changes in either inhibition or excitation would engage homeostatic mechanisms that converge to regulate NMDA receptors, thereby enabling plasticity mechanisms and also ensuring circuit stability.

Purpose. A natural disaster negatively affects children's emotional and behavioral adjustment. The purpose of this paper was to examine the prevalence, symptoms, and correlates of PTSD after the occurrence of Typhoon Rusa.Method. 261 elementary school children living in Kimcheon, which was a devastated rural area in South Korea by Typhoon Rusa, were selected. Data were collected 4 months after the disaster using the PTSD Reaction Index categories recommended by Frederick, severity of PTSD.Results. 12.3% of the children had either moderate or severe PTSD symptoms; 22.7% reported mild symptoms; and the remaining 65% had sub-clinical symptoms of PTSD. The most frequent symptom was recurrenct fear(67.0%). 13% to 17.2% of children exhibited difficulty in concentration, sleep disturbance, and guilt feeling. The regression model of severity of PTSD was composed of the level of exposure to traumatic experiences, grade in school, gender, negative coping style, and social support, and explained 34.3% for PTSD symptoms. Exposure to traumatic experiences was the strongest factor of all predictors. Conclusion.Emotional support from friends and coping style were correlated with PTSD severity. School-based interventions that emphasizes coping with disaster related problems and problem-solving may prove to be useful, and may aid in building close and supportive ties with teachers, classmates, and friends.Key Words: Children, PTSD, Natural disaster informing efforts have been limited. Up to date, there have not been any studies in South Korea about posttraumatic stress disorder in children who have experienced such a disaster.Several investigations have reported the incidence of PTSD symptoms and diagnosis in children. In a large sample of school-age children who experienced a forest fire, over 50% of their parents reported PTSD symptoms at 2 months after the accident, and 33% of them reported PTSD symptoms after 2 years (McFarlane, 1987). However, most studies have not directly focused on the presence or absence of the diagnosis of PTSD and it is still unclear whether children who were exposed to disaster experience all of the PTSD symptoms.The essential feature of PTSD is developing characteristic symptoms after a traumatic event (Green, 1991). These symptoms involve the following three clusters: persistent re-experiencing of the stressor (e.g., recurrent thoughts or dreams of the disaster), persistent avoidance of reminders of the event and numbing of general responsiveness (e.g., avoidance of disaster-related activities, and feeling of detachment), and persistent symptoms of hyper-arousal (e.g., experience difficulties in sleeping or concentrating). When children are repetitively exposed to traumatic events, generalized nightmares, psychosomatic symptoms (e.g., headaches, stomach aches), and foreboding omens may occur.This study was done to identify the PTSD symptoms of children caused by a natural disaster and diverse factors that are related to these symptoms by examining 261 elementary school children in Kimcheon, 4 month...

Atopic dermatitis (AD) is a common allergic disease, imposing large social and economic burdens worldwide. Atopic dermatitis is characterized by eczematous skin lesions and immunoglobulin E (IgE) hypersecretion. We investigated the role of JNK1 on the development of AD in mice. The vitamin D3 analogue MC903, a psoriasis therapeutic drug, was used to induce AD-like symptoms in wild-type (WT) and JNK1-/- mice. The symptoms of AD were less severe in JNK1-/- mice compared with WT mice. JNK1-/- mice showed less ear thickening and infiltration of eosinophils and mast cells in AD-like lesions than did WT mice when treated with MC903. MC903-treated JNK1-/- mice also showed significantly lower level of serum IgE, which was elevated in MC903-treated WT mice. Splenocytes isolated from MC903-treated WT and JNK1-/- mice were stimulated with anti-CD3 and anti-CD28 monoclonal antibodies. Splenocytes from JNK1-/- mice produced lower levels of T-helper (Th2) cytokines (interleukin-4 and -13) and transcription factor GATA-binding protein 3, and produced increased levels of the Th1 cytokines interferon-γ and transcription factor T-box expressed in T cells. Our results indicate that JNK1 plays an important role in the pathogenesis of AD and may be a useful target for therapies to ameliorate AD.

The soy isoflavone daidzein is bioconverted to 7,8,4'-trihydroxyisoflavone (7,8,4'-THIF) by microorganisms. Here, we investigated the matrix metalloproteinase (MMP)-1 inhibitory properties of 7,8,4'-THIF that arise through the suppression of UVB-induced MMP-1 expression. 7,8,4'-THIF reduced UVB-induced MMP-1 expression at the transcriptional level in primary human dermal fibroblasts and inhibited UVB-induced transcriptional activity of AP-1, a major activator of MMP-1 expression. Additionally, it was observed that the mitogen-activated protein kinase (MAPK) pathway, a crucial signalling cascade for MMP-1 expression, was suppressed by 7,8,4'-THIF. Protein kinase C iota (PKCι) was suspected to be a direct target of 7,8,4'-THIF. The direct interaction between 7,8,4'-THIF and PKCι was confirmed using pull-down assays and immobilized metal ion affinity-based fluorescence polarization assays. Finally, we observed that 7,8,4'-THIF inhibited UVB-induced MMP-1 expression in a human skin equivalent model. Taken together, these results suggest that 7,8,4'-THIF, a bioconversion product of daidzein, suppresses UVB-induced MMP-1 expression.