PTSD may be as prevalent and persistent in disaster victims in China as in those elsewhere. Prompt and effective postdisaster intervention could mitigate the impact of initial exposure and reduce the probability of PTSD occurrence. Caution should be used in comparing rates of postdisaster PTSD identified by using different diagnostic criteria.

This study aims to observe longitudinal change of quality of life (QOL) and psychological wellbeing in a community sample affected by an earthquake and to examine the relationship between QOL and disaster exposure, post-disaster support and other related variables. The subjects, from two villages at different distances from the epicenter, were assessed using the brief version of the World Health Organization Quality of Life Assessment (WHOQOL-BREF) and three subscales of a symptoms checklist at 3 months (n = 335) and 9 months (n = 253) after the earthquake, respectively. Exposure to the earthquake was associated with multidimensional impairment in QOL, including physical, psychological and environmental domains at 3 months, and psychological and environmental domains at 9 months. The victims also suffered significantly more psychological distress in terms of depression, somatization and anxiety. At both assessment points the group that experienced lower initial exposure but then received less post-disaster help reported poorer QOL and psychological well-being. The two victim groups also differed significantly in changing trend along time. The group that received more support showed a general improvement in post-disaster well-being from 3 months to 9 months. The results confirm that post-disaster variables could be as important to post-disaster psychosocial outcomes as variables of predisaster vulnerability and disaster per se. A comprehensive and prospective assessment of disaster effects is imperative for the better organization of disaster relief programs and psychosocial interventions.

Neurofibromatosis type 1 (NF1) is a common autosomal dominant tumor predisposition syndrome in which affected individuals develop astrocytic brain tumors (gliomas). To determine how the NF1 gene product (neurofibromin) regulates astrocyte growth and motility relevant to glioma formation, we have used Nf1-deficient primary murine astrocytes. Nf1 À/À astrocytes exhibit increased protein translation and cell proliferation, which are mediated by Rasdependent hyperactivation of the mammalian target of rapamycin (mTOR) protein, a serine/threonine protein kinase that regulates ribosomal biogenesis, protein translation, actin cytoskeleton dynamics, and cell proliferation. In this study, we show that Nf1-deficient astrocytes have fewer actin stress fibers and exhibit increased cell motility compared with wildtype astrocytes, which are rescued by pharmacologic and genetic mTOR inhibition. We further show that mTORdependent regulation of actin stress fiber formation, motility, and proliferation requires rapamycin-sensitive activation of the Rac1 GTPase but not elongation factor 4E-binding protein 1/S6 kinase. Nf1 À/À astrocytes also exhibit increased protein translation and ribosomal biogenesis through increased expression of the nucleophosmin (NPM) nuclear-cytoplasmic shuttling protein. We found that NPM expression in Nf1

Spontaneous intracerebral hemorrhage (ICH) is often a fatal event. In a patient who survives the initial ictus, the resulting hematoma within brain parenchyma can trigger a series of events that lead to secondary insults and severe neurological deficits. Great efforts have been focused on searching for new approaches to help patients recover neurological function after ICH. Previous studies indicate that mesenchymal stem cells (MSCs) grafted into the ischemic rat brain can improve neurological function. However, there is no report regarding whether MSCs can be used in the same way to improve the neurological function after ICH. We generated the ICH model by injecting collagenase VII into rat brain. Subsequently, 5-bromo-2-deoxyuridine (BrdU)-labeled mesenchymal stem cells were delivered into the brain through carotid artery, cervical vein or lateral ventricle. The distribution and differentiation of MSCs were investigated by methods of immunohistochemistry. We found that MSCs were able to differentiate into neural cells in vitro as well as in the rat brain after ICH. The injected MSCs were able to migrate into hippocampus, blooding foci and ipsilateral cortex. In the hippocampus, MSCs differentiated into neurons; but in surrounding bleeding foci, they differentiated into neurons and astrocytes. In the ipsilateral cortex, MSCs differentiated into neurons, astrocytes and oligodendrocytes. Notably, the motor function of the rats in the carotid artery (CA) group and the lateral ventricle (LV) group improved significantly. Collectively, our study indicates that MSCs are able to differentiate into neural cells in the rat brain after ICH and can significantly improve motor function.