Objective To describe the anatomical variants of infants’internal cerebral veins and their tributaries with MR suscep-tibility weighted imaging,and to evaluate the capability in the visualization of cerebral deep veins.Methods 80 healthy infants were enrolled in this study.All the brain images were obtained by a 3D gradient-echo sequence (Enhanced T2 ? weighted angiography-ES-WAN)on a 3.0T MR,which were reconstructed with minimal intensity projection.The septal vein,thalamostriate vein,internal cerebral vein and anterior caudate nucleus veins were evaluated.4 types (ⅠA,ⅠB,ⅡA,ⅡB)were classified based on their rela-tionship with the septal vein-internal cerebral vein junction and interventricular foramen,and 3 types (Ⅰ,Ⅱ,Ⅲ)based on the drainage patterns of the anterior caudate nucleus veins.Results The septal vein,thalamostriate vein and internal cerebral vein could be clearly and continuously visualized in 100% infants,and the visualization rate of the anterior caudate nucleus veins was 88.1%. TypeⅠA and TypeⅠ were most common in the two classification patterns.Conclusion Infants’internal cerebral veins and their tributaries are able to be clearly shown with the minimal intensity projection in susceptibility weighted imaging,which is a good method to evaluate the cerebral deep veins in infants.

OBJECTIVE: To investigate whether rapamycin treatment starting at 24 h after cerebral ischemia/reperfusion(I/R) has protective effect on brain injury in rats. METHODS: The rat I/R model was established by middle cerebral artery occlusion according to Longa's method. A total of 104 Sprague Dawley rats were randomly divided into sham group, model group, and rapamycin-treated groups (6 h or 24 h after modeling). Neurological function was assessed with neurological severity score (NSS). Triphenyl tetrazolium chloride (TTC) staining and Fluoro-Jade B (FJB) staining were used to examine the infarct volume and neuronal apoptosis, respectively. The expression of p-S6 protein in mTOR signaling pathway was detected by Western blot analysis. RESULTS: Compared with sham group, NSS of the model group was significantly increased and TTC staining indicated obvious infarct area (all <0.01). Furthermore, significantly increased number of FJB-positive cells and p-S6 expression in the penumbra area were shown in the model group (all <0.01). Compared with the model group, both rapamycin-treated groups demonstrated decreased NSS, infarction volume and FJB positive cells as well as p-S6 expression in the penumbra area (<0.05 or <0.01). There was no significant difference between the groups of rapamycin administrated 6 h and 24 h after modeling (all >0.05). CONCLUSIONS Rapamycin treatment starting at 24 h after I/R exhibits protective effect on brain injury in rats.
Animals ; Brain Ischemia ; drug therapy ; Immunosuppressive Agents ; therapeutic use ; Infarction, Middle Cerebral Artery ; drug therapy ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; prevention & control ; Sirolimus ; therapeutic use ; Treatment Outcome

Objective To investigate the effect of programmed death ligand-1(PD-L1)overexpression on epithelial mesenchymal transformation(EMT)in endometrial cancer cells and its possible mechanism.Methods Ishikawa/PD-L1,a PD-L1 stable overexpression cell line constructed in the laboratory and the control Ishikawa/EV were used.The efficiency of PD-L1 overexpression was detected by qPCR and Western blot assay.The cell migration ability and invasion activity were detected by scratch assay and Transwell assay.The EMT-related protein and the phosphorylation level of nuclear transcription factor-κB(NF-κB)were detected by Western blot.Results Compared with the control group,the migration ability and invasion activity of Ishikawa/PD-L1 were significantly enhanced,and the expression of E-cadherin was significantly down-regulated,whereas vimentin,N-cadherin and p-p65 were significantly increased.Conclusion PD-L1 can promote EMT by inducing the activation of NF-κB pathway,and thus enhance the migration and invasion ability of endometrial cancer cells.