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Objective To investigate the neuroprotective effect of lateral intracerebroventricular injection of Apelin-13 on the YAP expression and the cerebral ischemia/reperfusion (I/R) injury in Wistar rats.Methods Healthy adult male Wistar rats were randomly divided into the sham group, cerebral I/R group and Apelin-13 treatment group.The middle cerebral artery occlusion model was established with ischemia for 1 hour and reperfusion for 24 hours after restricting food and water intake for 12 hours.Apelin-13 was injected into rats' lateral ventricles of Apelin-13 treatment group after reperfusion.Neural function defects was assessed.The volume of infarction was evaluated by TTC staining.The expression levels of YAP were detected by western blot.Results Compared with the cerebral I/R group,the rats in the Apelin-13 treatment group had abetter neurologic score ((2.67±0.33) vs (1.67±0.33) , P＜0.05), the infarction volume was decreased ((30.60± 1.42) ％ vs (23.70± 2.20) ％,P＜0.05) , and YAP expression level was increased in each part of the cerebral tissue(P＜0.05).Conclusion Apelin-13 has a neuroprotective effect,which plays the therapeutic effect by regulating the expression of YAP on cerebral ischemia/ reperfusion (I/R) injury in Wistar rats.

Objective To investigate the molecular genetic changes of anaplastic lymphoma kinase (ALK) gene and c-myc gene in anaplastic large cell lymphoma (ALCL). Methods The structural aberrations and changes of copy numbers in ALK and c-myc genes in 72 paraffin-embedded ALCL specimens were detected by interphase fluorescence in situ hybridization (FISH). Results Among 72 ALCL specimens, ALK protein was expressed in 42, ALK gene translocation was detected in 40 specimens in which extra copies of ALK gene were detected in 17. ALK gene translocation was not found in all 30 ALK negative specimens, but extra copies of ALK gene were detected in 14 cases. The difference of incidence rates of extra copies in ALK gene between ALK positive and ALK negative specimens was not significant (P＞0.05). c-myc gene translocation was not found in any of 72 ALCL specimens, but extra copies were detected in 24 cases.Conclusion Most (75.0%) ALCL have ALK gene aberration, in which ALK gene translocations are most common (55.6%), and the extra copies of ALK gene are relatively common genetic changes (43.1%). The ALK gene aberration is only detected in ALK positive ALCL and the gene translocations are in either ALK positive and negative ALCL. There is no or rare c-myc gene translocation in ALCL, but extra copies of c-myc gene are relatively common (33.3%).

Objective: To investigate the expression change, biological role and action mechanism of long non-coding RNA (lncRNA) LINC00978 in non-small cell lung cancer (NSCLC). Methods: The expression levels of LINC00978 in tumor tissues and serum samples of NSCLC patients were detected by the qRT-PCR. The effects of knockdown and overexpression of LINC00978 on the biological function of A549 cells were determined by the CCK-8, colony formation, Transwell migration and invasion assays. The action mechanisms of LINC00978 in NSCLC were investigated by the flow cytometry, qRT-PCR and western blot, respectively. Results: The expression levels of LINC00978 in the tissues ( t =2.465, P ＜0.05) and serum samples ( t =8.781, P ＜0.01) of NSCLC patients increased. The knockdown of LINC00978 inhibited the proliferation, migration and invasion of A549 cells ( P ＜0.01) and induced cell cycle arrest at G1 phase and apoptosis of A549 cells ( P ＜0.01). The knockdown of LINC00978 downregulated the expression of Cyclin D1 and Bcl-2 , and upregulated the expression of Bax ( P ＜0.05). In addition, the knockdown of LINC00978 inhibited the expression of N-cadherin, Vimentin, Snail, Slug and Twist, and promoted the expression of E-cadherin ( P ＜0.05). The overexpression of LINC00978 had the opposite effect. Conclusion LINC00978 is highly expressed in NSCLC and can promote the occurrence and progression of NSCLC, which may serve as a potential target for the diagnosis and therapy of NSCLC.