The aim of this study was to detect MTA2 expression in pancreatic ductal adenocarcinoma (PDA) and to analyze its association with prognosis of PDA patients. MTA2 mRNA and protein expression were determined by real-time quantitative reverse transcriptase-polymerase chain reaction and immunohistochemistry in specimens of primary cancer and their adjacent noncancerous tissues in PDA patients. We found that MTA2 mRNA and protein expression levels were both significantly upregulated in PDA lesions compared with adjacent noncancerous tissues. Immunohistochemistry showed that high MTA2 expression was correlated with poor tumor differentiation, TNM stage, and lymph node metastasis. Kaplan-Meier survival analysis showed that patients with high expression levels of MTA2 showed lower overall survival rate than those with low expression levels. Multivariate analysis showed that high MTA2 protein expression was an independent prognostic factor for PDA patients. Our study suggests that overexpression of MTA2 may play an important role in the progression of PDA and MTA2 expression may serve as a biomarker for poor prognosis for PDA.

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Post-traumatic stress disorder (PTSD)-associated cognitive dysfunction significantly disturbs patients' quality of life and will to live. However, its underlying mechanism is as yet unknown. Recent researches indicate that blood-brain barrier (BBB) breakdown is responsible for early cognitive dysfunction. Microglia might participate in remodeling of BBB-associated tight junction and regulating BBB integrity. Nevertheless, it is unclear whether microglia activation and BBB injury involve in PTSD-associated cognitive dysfunction. Hence, we established an animal model of PTSD, single prolonged stress (SPS), and investigated permeability changes in the hippocampus and further explored the effects of microglia on BBB remodeling. The Y maze was used to assess the changes of cognitive function. The sodium fluorescein (NaFlu) assay and western blotting analysis were employed to detect BBB integrity changes. Minocycline was administered to inhibit microglial activation. Immunofluorescence stains were used to assess the activation states in microglia. The results showed that SPS-exposed rats exhibited poorer cognitive performance, higher passage of NaFlu, and lower expression of tight junction proteins (occludin and claudin 5) in the hippocampus on the day after SPS, but no difference on the 7th day. Inhibition of microglial activation by minocycline attenuated poor cognitive performance and BBB impairment including the extravasation of NaFlu and protein levels of the tight junction. Taken together, the present study indicates that BBB impairment may underlie the shared pathological basis of PTSD and cognitive dysfunction. Microglial activation may involve in BBB remodeling at the early stage of SPS.