Objective To study the change of expression of c-fos and c-jun when using IN-1 alone or combination with NT-3 after spinal cord injury. Methods 120 adult health Sprague-Dawley (SD) rats were random divided into three groups, including control group, IN-1 group, and IN-1 combination with NT-3 group. All rats were killed at the scheduled time and its myeloid tissues were taken out. In each group, the expression of c-fos and c-jun gene was detected by using reverse transcription- polymerase chain reaction technique ( RT-PCR ). Result The transcriptional levels of c-fos decreased and c-jun increased when using IN-1 alone, and the levels changed more when using IN-1 combination with NT-3. The peak of c-fos reached to 0. 974 ±0. 126 in control group, 0. 834 ±0. 047 in IN-1 group, and 0. 698 ±0. 052 in IN-1 combination with NT-3 group, and the peak of c-jun reached 0. 642 ±0. 048, 0. 712 ±0. 050, and 0. 814 ±0. 041, respectively. Conclusion One of the mechanisms of IN-1 and NT-3 to protect the spinal cord might be through inhibiting the expression of c-fos and enhancing the expression of c-jun.

Architectural changes with Tianyi cloud storage of China Telecom were made to the up/ down loading of the image-text mega data created in the picture archiving and communication systems (PACS)of the hospital.Thanks to the changes, the data volume uploaded by the PACS of the hospital reached 160G per day, with average upload speed up to 5.3M/second;supporting online query of all image-text data of patients.The authors hold cloud storage technology as safe and reliable, and such other merits as supporting data encryption, automatic offsite redundancy, almost online real-time read/write access,almost infinite extendibility, fast self-healing and off-site disaster-tolerant backup.

To investigate the microRNA (miR)-150 expression level in human osteosarcoma cell lines (Saos-2, MG-63) and its function in cell proliferation, and to explore the potential molecular mechanisms. 
 Methods: MiR-150 expression levels in human osteosarcoma cell lines (Saos-2, MG-63) and normal osteoblast cell line (NHOst) were detected by relative quantitative real-time PCR (qRT-PCR). MiR-150 was overexpressed in Saos-2 and MG-63 cells by lentivirus infection. Cell proliferation rates were monitored by MTS assay. RUNX2 and β-actin protein levels were examined by Western blot. Inhibitory effect of miR-150 on binding RUNX2 3'-UTR was detected by Dual-Luciferase assay.
 Results: MiR-150 expression level is lower in human osteosarcoma cell lines (Saos-2, MG-63) compared to the normal osteoblast cell line (NHOst) (0.23±0.02 and 0.32±0.03 vs 1.00±0.02), which showed statistical significance (P<0.01). After lentivirus infection, miR-150 level increased in Saos-2 (P<0.01) and MG-63 cells (P<0.01). Overexpression of miR-150 decreased cell proliferation and RUNX2 protein level in Saos-2 and MG-63 cells. The binding of miR-150 to RUNX2 3'-UTR decreased luciferase activity by 69% in Saos-2 cells (P<0.05) and 59% in MG-63 cells (P<0.05). Administration of exogenous RUNX2 recovered the cell proliferation in miR-150 overexpressed Saos-2 and MG-63 cell lines (P<0.01).
 Conclusion: MiR-150 inhibites proliferation in human osteosarcoma cell lines through binding to RUNX2 3'-UTR, resulting in the reducion of RUNX2 protein level.
3' Untranslated Regions ; Actins ; metabolism ; Bone Neoplasms ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; genetics ; Core Binding Factor Alpha 1 Subunit ; drug effects ; genetics ; pharmacology ; physiology ; Gene Expression Regulation, Neoplastic ; drug effects ; genetics ; Humans ; MicroRNAs ; pharmacology ; Osteoblasts ; physiology ; Osteosarcoma ; genetics ; physiopathology