Molecular medicine reports
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Transplantion of neural stem cells (NSCs) has shown promise for the treatment of traumatic brain injury (TBI). Although the functional mechanisms underlying transplant‑mediated recovery following TBI have yet to be determined, previous studies demonstrated that transplanted NSCs may respond to the release of specific neurotransmitters, and/or the production of factors that promote neuronal growth. Therefore, we hypothesize that the direct transplantation of NSCs into the injured brain enhanced the expression of synaptic protein and regeneration-associated protein, which may be responsible for promoting functional recovery in a rat model of TBI. ⋯ RT-PCR and Western blot analysis demonstrated that the expression of synaptophysin (SYP) and regeneration‑associated protein (GAP43) in the injured brain of NSC-transplanted rats was significantly increased compared to the saline control rats during the experimental period. These data suggest that NSCs transplanted directly into the injured brain are capable of surviving, differentiating into neurons and promoting functional recovery in a rat model of TBI. Engrafted NSCs increase the expression of SYP and GAP43 in the injured brain of NSC-transplanted rats, which is suggested as one of the mechanisms underlying the improved functional recovery on motor behavior due to the transplantation of NSCs following TBI.
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In the present study, we investigated the antinociceptive effect of herpes simplex virus type 1 (HSV-1) amplicon vector-mediated human proenkephalin (hPPE) on chronic constriction injury (CCI)-induced neuropathic pain in rats. Male Sprague-Dawley rats were intrathecally administered normal saline (NS), pHSVIRES-lacZ (SHZ) or recombinant HSV-1 amplicon vector pHSVIRES-hPPE-lacZ (SHPZ), respectively. Once a week for 5 weeks after the intrathecal (i.t.) administration, the expression levels of hPPE mRNA and leu‑enkephalin (L-EK) were determined. ⋯ The antinociceptive effect of SHPZ reached its peak 3 weeks after i.t. administration and was maintained for 5 weeks. In the rats administered vehicle or SHZ, there were no significant differences between the PWMT or PWTL and the thresholds before i.t. administration. These results indicate that a single i.t. administration of HSV-1 amplicon vector-mediated hPPE attenuated CCI-induced hypersensitivity in rats.
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Let-7g miRNAs, short non-coding RNAs approximately 21 nucleotides long, repress protein translation by binding to the 3'UTR of target mRNAs. Aberrant expression of let-7g is associated with the poor prognosis of lung cancer patients. Compared to normal lung cells, let-7g expression is absent in non-small cell lung cancer (NSCLC) cells. ⋯ In this study, we evaluated the potential role of precursor (pre)-let-7g in lung cancer cell metastasis, focusing on the two targets of let-7g, HMGA2 and K-Ras. We found that pre-let-7g inhibited the migration of A549 lung cancer cells through HMGA2-mediated E2F1 down-regulation. Thus, our results suggest that pre-let-7g could be used as a suitable target for the suppression of lung cancer cell migration.
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The presence of HER 2/neu has been reported in gastric cancer, but its impact on patient survival remains unclear. The purpose of this study was to investigate the expression of HER 2/neu in gastric cancer. A total of 218 paired resected gastric cancer and corresponding normal specimens were collected. ⋯ However, HER 2/neu expression was correlated with poorer overall survival (p<0.001). In multivariate analysis, HER 2/neu expression was a significant independent prognostic predictor of gastric cancer (p<0.001), and was associated with poor survival in gastric cancer patients. These data indicate that HER 2/neu may play a major role in the therapeutic management of gastric cancer.
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High-mobility group box 1 (HMGB1) plays a role in inflammatory and immune-mediated diseases. This study investigated the role of HMGB1 in colonic inflammation. Colitis was induced by orally feeding mice 4.5% dextran sulfate sodium (DSS) for up to 7 days. ⋯ Immunohistochemical study of the colons showed that the tissues of mice treated with DSS had a higher expression of HMGB1 and its receptor - the receptor for advanced glycation end products - than normal controls, especially in inflammatory infiltrates. The anti-HMGB1 antibody ameliorated tissue damage. In conclusion, HMGB1 is an important mediator of colonic inflammation, and suppression of this protein partially protects against colonic inflammation.