With a high incidence, cancer pain is an unresolved clinical problem right now. Many randomized controlled studies have shown that intrathecal infusion of analgesic drugs is an effective way to relieve pain. Intrathecal drug infusion system provides cli-nicians with exact individualized treatment approach in the effective analgesia, but with minimum side effects. Patients who received in-trathecal analgesic therapy in the early stage would get more benefit. Before implanting intrathecal drug delivery devices, it is needed to test analgesic effect firstly, and the proper implementation of the test period is extremely important. This effectively maintaining time decides whether the patients need intrathecal analgesia system. However, there are many factors that may affect its application in clin-ic. This article focuses on the treatment principle, patient selection, testing, technical problems and complications when applying intra-thecal drug delivery devices.

microRNA(miRNA) ,a class of small noncoding RNAs,negatively regulates gene expression at post-transcriptional level, and is involved in many fundamental biological processes, including development,apoptosis and cell proliferation, p53 is a transcription factor that plays a critical role in the control of cell cycle and apoptosis. Aberrant expression of either miRNA or p53 intimately links to tumorigenesis. This article reviews recent advances in the study of inter-relatioship between miRNA and p53 in tumorigenesis.

Objective To create 3-D models of immediately loaded screw-type dental implants for finite element analysis by computer.Methods Using the commercial code of SolidWorks,3-D models of screw-type dental implants and a segment of mandibular bone were generated.By ABAQUS software,the 3-D implant-bone complex was meshed.The interfacial contact of bone and the implants was defined to be a frictional contact with the initial press-fit stress(by Interference Fit Option) to simulate the contact of immediately loaded implants and bone tissue.Results The finite element models of the immediately loaded screw-type implant were successfully created on the computer.As the interference fit got deeper,the interfacial initial press-fit stress got higher values.Conclusion The finite element models of the immediately loaded screw-type implants can be built with this method.The interfacial status of the primary press-fit stress can be simulated by the Interference Fit Options in the finite element software.

Objective To investigate the effect of methyltransferase inhibitor 5-Aza-dC (5-aza-2’-deoxycytidine) on proliferation and activation of myofibroblasts in arthrofibrosis of the knee. Methods The model of arthrofibrosis of rat knee was firstly established.Myofibroblasts were isolated and cultured from the posterior capsule of rat knee. Cells were identified by immunofluorescence.Myofibroblasts were treated with 2 μmol/L 5-Aza-dC. The expression levels ofα-SMA、col1A1 mRNA and protein in myofibroblasts before and after the treatment with 5-Aza-dC were detected by RT-PCR and Western blotting,respectively.The proliferation rate of these myofibroblasts were detected by MTT method,and the cell cycle was detected by flow cytometry of DNA content in each phase. Results The extension of rat knee in arthrofibrosis model was significantly decreased. α-SMA protein,the representational protein of myofibroblast,was largely expressed in the isolated cells from model knees. The expression levels ofα-SMA、col1A1 mRNA and protein in myofibroblasts were decreased after the treatment with 5-Aza-dC and the growth of myofibroblasts was also slowed down. Conclusion The methyltransferase inhibitor 5-Aza-dC may become a potential therapeutic drug in the treatment of arthrofibrosis of the knee through inhibiting the proliferation of myofibroblasts.

AIM: To investigate the effects of tripchlorolide (TP) on proliferation and autophagy of human lung cancer A549 cells, and explore its mechanism.METHODS: MTT assay was performed to analyze the effect of TP on the viability of human lung cancer A549 cells.The A549 cells were treated with TP, and their autophagy was observed un-der the fluorescence microscope through acridine orange staining.Green fluorescence spots were observed by fluorescence microscopy through GFP-LC3 plasmid transfection experiment.The levels of LC3 and p-ERK in the A549 cells after TP treatment were determined by Western blot.RESULTS: The viability of human lung cancer A549 cells was significantly inhibited by TP in a dose-time dependent manner (P <0.05).The number of the intracellular acidic follicles dyed with bright red fluorescence was significantly increased after TP treatment in A549 cells.The number of green dot-like con-gregate autophagosomes in cell cytoplasm was significantly increased after TP treatment in the A549 cells transfected with GFP-LC3 plasmid, while the normal treatment only induced a few cells with autophagosome formation.At the same time, we did not observe the dot-like congregate autophagosomes after TP treatment in the A549 cells transfected with GFP-control plasmid.Compared with control group, the expression of LC3-II protein was up-regulated in A549 cells after TP treatment (P <0.01).Furthermore, treatment with TP in A549 cells for 48 h also led to a significant upregulation of phosphorylated form of ERK (P <0.01).In contrast, no significant change in the levels of total ERK protein was observed.Compared with 100 nmol/L TP group, TP +3-MA group down-regulated the protein levels of LC3-II (P <0.01) and p-ERK (P <0.01) in the A549 cells.CONCLUSION: TP significantly inhibits the growth of A549 lung cancer cells and induces the
autophagy, which may be correlated with upregulation of p-ERK protein.

HepG2 cells were incubated with dexamethasone,glucocorticoid receptor (GR) antagonist RU486,and pioglitazone for 24 or 48 h.Glucose concentration in culture medium was detected.The results showed that 10 μmol/L RU486 blocked the surge of glucose concentration by 48 h of dexamethasone treatment and the glucose concentration in RU486 + pioglitazone group was higher than pioglitazone group( P＜0.05 ),suggesting that the cross talk between PPARγ and GR may exist in hepatic glucose metabolism.

Background and purpose: Ovarian cancer is the common gynecological cancer, and the drug resistance of anti-tumor drug was one of major reasons for therapy failure, some studies considered that there is a closed relationship between Gankyrin and drug resistance. In this study, we investigated the effects and mechanisms of Gankyrin silencing on reversing the cisplatin resistance of ovarian cancer drug-resistant SKOV3/DDP cell line. Methods:The expression of Gankyrin in SKOV3 and SKOV3/DDP cells was measured by real-time PCR assay, MTS assay was employed to determine the effect of Gankyrin on SKOV3/DDP sensitivity to cisplatin, apoptosis rate and intracellular concentration of rhodamine-123 (Rh-123) were determined by lfow cytometry, the expression of multi-drugs resistant protein MDR1, Caspase-3/8, Survivin and Bcl-2 were determined by Western blot and real-time PCR. The phosphorylation of AKT and expression of p53, NF-κB and PTEN were analyzed by Western blot assay. Results:The expression of Gankyrin was increased in SKOV3/DDP cells, Gankyrin silencing was able to increase the cisplatin sensitivity of SKOV3/DDP. Before and after gene silencing, the reverse folds (RF) to cisplatin were 1.81 and 2.45, respectively, the intracellular levels of Rh-123 were 1.73 and 2.42 fold, the apoptosis rates were 2.23 and 4.23 fold,the expressions of MDR1, Survivin and Bcl-2 were downregulated, the mRNA expressions of MDR1 were 62.8%and 21.6%, the mRNA expressions of Survivin were 24.5%and 10.3%, the mRNA expressions of Bcl-2 were 47.5%and 18.4%, the levels of Caspase-3/8, p53 and PTEN were elevated, phosphorylation of AKT and expression of NF-kB were downregulated compared with control group. Conclusion:Gankyrin silencing was able to reverse the cisplatin resistance of SKOV3/DDP cells by inhibiting the drug eflfux and promoting cell apoptosis, the PTEN/AKT/NF-κB/p53 may be the key pathway.

Neurolytic celiac plexus block (NCPB) is an effective method used to alleviate upper abdominal pain or back pain caused by pancreatic cancer and other malignancies. NCPB can relieve cancer pain to improve the quality of life and cause fewer side effects than conventional analgesic drugs. This article systemically reviewed NCPB methodology and research progress in clinical appli-cations.

Changes in heart rate of fetal is function regulating performance of the circulatory system and the central nervous system, it is significant to detect heart rate of fetus in perinatal fetal. This paper puts forward the fetal heart rate detection method based on short time Fourier transform and blind source separation. First of all, the mixed ECG signal was preprocessed, and then the wavelet transform technique was used to separate the fetal ECG signal with noise from mixed ECG signal, after that, the short-time Fourier transform and the blind separation were carried on it, and then calculated the correlation coefficient of it, Finally, An independent component that it has strongest correlation with the original signal was selected to make FECG peak detection and calculated the fetal instantaneous heart rate. The experimental results show that the method can improve the detection rate of the FECG peak (R), and it has high accuracy in fixing peak(R) location in the case of low signal-noise ratio.
Electrocardiography ; Fetus ; Heart Rate, Fetal ; Humans

14-3-3σ,an vital tumor suppressor which is regulated by p53,plays a key role in cell cycle regulation, apoptosis, migration and proliferation, affecting tumor formation, invasion and metastasis. The methylation inactivation of 14-3-3σ is widely recognized as one of the mechanisms of tumorigenesis,and be associated with the metastasis of NPC.