Objective To investigate the improvement of ischemic hypoxic injury of brain after the transplantation of bone marrow mesenchymal stem cells (BMSCs).Methods Rats were randomly (random number) divided into sham operation group,cardiac arrest group and BMSCs treatment group (n =10 in each group).The model of cardiac arrest was induced by asphyxia.One hour after restoration of spontaneous circulation (ROSC),green fluorescent protein labeled BMSCs were transplanted via tail vein injection.At 3 and 7 days after transplantation,frozen sections of hippocampus was stained with hematoxylin-eosin (HE).The rest of brain tissue was weighed by an electronic balance.Brain water content (％) was calculated as (wet weight-dry weight) / wet weight × 100％.Results ①BMSCs were observed in hippocampus at 3 and 7 days after transplantation under fluorescent microscopy.②Compared with sham operation group and BMSCs treatment group,brain water content in cardiac arrest group was higher (all P ＜ 0.05).HE staining results showed that BMSCs transplantation could lessen hypoxia ischemia damage on brain.Conclusions BMSCs reduced the neurons damage induced by cardiac arrest and promoted neurological function recovery.

Objective: To explore the mechanism of miR-19a-3p regulating cell adhesion molecule 2 (CADM2) to inhibit the proliferation and metastasis of renal carcinoma cells via the AKT signaling pathway. Methods: A total of 42 patients with renal cancer admitted to Department of Nephrology, the First Affiliated Hospital of Suzhou University from April 2012 to November 2017 were enrolled to collect samples of surgically resected renal carcinoma tissues and paracancerous tissues. Expression of miR-19a-3p was detected in renal carcinoma tissues and 4 types of renal carcinoma cell lines such as 786-O by quantitative Real-time polymerase chain reaction (qPCR). The effects of miR-19a-3p knockdown on proliferation, invasion and epithelial mesenchymal transition (EMT) of renal carcinoma 786-O cells were evaluated by CCK-8 assay, Transwell assay and immunofluorescence, respectively. Subsequently, dual luciferase reporter assay was used to verify whether CADM2 was a target gene of miR-19a-3p. Furthermore, Wb was applied to detect the regulatory effect of miR-19a-3p onAKT signaling pathway through CADM2. Results: miR-19a-3p expression was significantly up-regulated in renal carcinoma tissues and cell lines (all P<0.01). Knockdown of miR-19a-3p could inhibit proliferation, invasion and EMT process of 786-O cells; furthermore, the results indicated that CADM2 was a direct target of miR-19a-3p and its expression was down-regulated (P <0.05 or P<0.01). Additionally, knockdown of miR-19a-3p obviously suppressed proliferation, migration and EMT process of 786-O cells via up-regulating CADM2 and blocking AKT pathway (all P<0.05 or P<0.01), thus alleviating the occurrence and development of renal carcinoma. Conclusion: The study demonstrates that miR-19a-3p has a high expression level in renal carcinoma tissues; knockdown of miR-19a-3p could significantly inhibit the proliferation, migration and EMT process of renal carcinoma tissues, and its mechanism may be associated with miR-19a-3p/CADM2/AKT axis.