[Early efficacy of three dimensional printed anatomical biomimetic cervical artificial disc replacement in the treatment of cervical degenerative diseases].

Objective: To investigate the efficacy and safety of a new cervical artificial disc prosthesis in the treatment of cervical degenerative diseases. Methods: The clinical data of 18 patients with single-level cervical degenerative diseases who underwent three dimensional printed anatomical bionic cervical disc replacement at Department of Spinal Surgery,Honghui Hospital,Xi'an Jiaotong University from May 2019 to July 2020 were analyzed retrospectively. There were 7 males and 11 females,aged (45±8) years old(range:28 to 58 years).The surgical segment was located at C3－4 level in 2 cases, C4－5 level in 5 cases, C5－6 level in 9 cases, and C6－7 level in 2 cases.The clinical and radiographic outcomes were recorded and compared at preoperative,postoperative times of one month and twelve months.The clinical assessments contained Japanese orthopedic association (JOA) score,neck disability index (NDI) and visual analogue scale (VAS).Imaging assessments included range of motion (ROM) of cervical spine, prosthesis subsidence and prosthesis anteroposterior migration.Repeated measurement variance analysis was used for comparison between groups,and paired t test was used for pairwise comparison. Results: All patients underwent the operation successfully and were followed up for more than 12 months.Compared with preoperative score,the JOA score,NDI and VAS were significantly improved after surgery (all P<0.01).There was no significant difference in postoperative ROM compared with 1-and 12-month preoperative ROM (t=1.570,P=0.135;t=1.744,P=0.099). The prosthesis subsidence was (0.29±0.13) mm (range: 0.18 to 0.50 mm) at 12-month postoperatively.The migration of prosthesis at 12-months postoperatively were (0.71±0.20) mm (range: 0.44 to 1.08 mm).There was no prosthesis subsidence or migration>2 mm at 12-month postoperatively. Conclusion: Three dimensional printed anatomical biomimetic cervical artificial disc replacement has a good early clinical effect in the treatment of cervical degenerative diseases, good mobility can be obtained while maintaining stability.

MiR-145 changes sensitivity of non-small cell lung cancer to gefitinib through targeting ADAM19.

OBJECTIVE: The aim of this study was to investigate the role of micro-ribonucleic acid (miR)-145 in acquired resistance of non-small cell lung cancer (NSCLC) to gefitinib, and to explore its potential mechanism. MATERIALS AND METHODS: PC-9 cells were continuously stimulated with low-concentration of gefitinib to induce the formation of acquired gefitinib-resistant PC-9/G cells. The sensitivity of PC-9 and PC-9/G cells to gefitinib was detected via Cell Counting Kit-8 (CCK-8) assay. The expressions of miR-145 and adamalysin-19 (ADAM19) in PC-9 and PC-9/G cells were detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) and Western blotting. Subsequently, PC-9 and PC-9/G cells were transfected with miR-145 mimics and miR-145 NC, respectively. The changes in ADAM19 expression were detected via qRT-PCR and Western blotting. The changes in the sensitivity of cells to gefitinib after transfection were explored via CCK-8 assay. Moreover, the influences of miR-145 transfection on cell apoptosis, invasion and migration were detected via flow cytometry, wound healing assay and transwell assay, respectively. Target gene and acting site of miR-145 were verified via Dual-Luciferase reporter gene assay. Furthermore, targeted regulation of miR-145 on ADAM19 was verified by in vitro cellular experiments. RESULTS: The sensitivity of PC-9/G cells to gefitinib was significantly lower than that of PC-9 cells, with nearly 15-fold difference in half maximal inhibitory concentration (IC-50) (p<0.05). QRT-PCR results indicated that miR-145 expression in PC-9/G cells was significantly decreased (p<0.01). The results of Western blotting showed that the expression level of ADAM19 in PC-9/G cells was markedly higher than that of PC-9 cells. The overexpression of miR-145 could remarkably reduce the expression level of ADAM19 in PC-9/G cells, increase the sensitivity of PC-9/G cells to gefitinib, and inhibit cell invasion and metastasis. The detection of Luciferase activity revealed that miR-145 could bind to the 3'-untranslated region (UTR) of ADAM19 gene and negatively regulate the protein expression. CONCLUSIONS: MiR-145 improves the sensitivity of acquired gefitinib-resistant cells to gefitinib. Meanwhile, it inhibits cell invasion and metastasis through negative regulation on ADAM19. Furthermore, the low-expression of miR-145 may become a biomarker and therapeutic target for acquired resistance to gefitinib.

Dehydroepiandrosterone reduced lipid droplet accumulation via inhibiting cell proliferation and improving mitochondrial function in primary chicken hepatocytes.

Dehydroepiandrosterone (DHEA) possesses fat-reducing effect, while little information is available on whether DHEA regulates cell proliferation and mitochondrial function, which would, in turn, affect lipid droplet accumulation in the broiler. In the present study, the lipid droplet accumulation, cell proliferation, cell cycle and mitochondrial membrane potential were analysis in primary chicken hepatocytes after DHEA treated. The results showed that total area and counts of lipid droplets were significantly decreased in hepatocytes treated with DHEA. The cell viability was significantly increased, while cell proliferation was significantly inhibited in a dose dependent manner in primary chicken hepatocytes after DHEA treated. DHEA treatment significantly increased the cell population in S phase and decreased the population in G2/M in primary chicken hepatocytes. Meanwhile, the cyclin A and cyclin-dependent kinases 2 (CDK2) mRNA abundance were significantly decreased in hepatocytes after DHEA treated. No significant differences were observed in the number of mitochondria, while the mitochondrial membrane permeability and succinate dehydrogenase (SDH) activity were significantly increased in hepatocytes after DHEA treated. In conclusion, our results demonstrated that DHEA reduced lipid droplet accumulation by inhibiting hepatocytes proliferation and enhancing mitochondrial function in primary chicken hepatocytes.