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.

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.

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.

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.

Tyrosine kinase receptors mediate many critical cellular functions that contribute to tumor progression and metastasis.Recepteur d'origine nantais(RON)belongs to a subfamily of receptor tyrosine kinases(RTK)with unique expression patterns and biological activities.RON is activated by a serum-derived growth factor macrophage stimulating protein(MSP),primarily expressed in cells of epithelial origin.RON activation induced cell transformation,growth,migration and matrix invasion.We review RON molecular structure,activation,and carcinogenic mechanism related.It will contribute to cancel treatment and to discuss RON expression in the tumor.

To study the general characteristics of cancer pain and to improve cancer pain diagnosis and treatment lev-el by prospective and open cross-sectional assessment of the clinical characteristics of patients with moderate to severe cancer pain. Methods:Patients with moderate to severe cancer pain were observed upon initial admission to the hospital from December 2012 to De-cember 2013. We assessed pain intensity, location, characteristics, and predisposing and mitigating factors and classified the pain by pathophysiology. Results:A total of 310 patients with moderate (101 cases, 32.58%) and severe (209 cases, 67.42%) pains were as-sessed. The top five cancers identified were lung cancer (102 cases, 32.90%), colorectal cancer (30 cases, 9.68%), pancreatic cancer (27 cases, 8.71%), breast cancer (24 cases, 7.74%), and gastric cancer (20 cases, 6.54%). These patients reported 533 cancer pain locations, including waist (132 cases), abdominal (125 cases), chest (88 cases), lower limb (71 cases), shoulder, neck, and upper limb (47 cases), pelvis (33 cases), perineal area (23 cases), and head and face (14 cases). The pain location of the pancreatic cancer was 90.63%consis-tent with the primary tumor site. The pathophysiology of the pain was classified as follows:bone pain (145 cases, 27.20%), visceral pain (138 cases, 25.89%), soft tissue pain (126 cases, 23.64%), and neuropathic pain (124 cases, 23.27%). The incidence of visceral pain in pancreatic cancer was 92.59%. Conclusion:A variety of common malignancies could cause moderate to severe pain, especially lung cancer. The clinical manifestation of pancreatic cancer pain is visceral pain. The location of this cancer was consistent with the pri-mary tumor site. No apparent specificity was observed in other cancer types.

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.

Objective:To observe the effect of ischemic preconditioning(IP)on hepatocellular apoptosis caused by ischemia-reperfus ion(IR)injury and expression of apoptosis regulatory genes(Survivin,HIF-1?)protein,to explore the protective mechanisms of IP on IR injury in rat liver.Methods:Ninty SD rats were randomly divided into sham operation(SO)group,ischemia-reperfusion(IR)group,ischemic preconditioning(IP)group.In SO group,the hepatoduodenal ligament of rat was only pulled and separated,and then closed the abdomen;IR group subjected to 30 minutes of ischemia;IP group was achieved by ischemia for 5 minutes,followed by reperfusion for 5 minutes before continuous to ischemia for 30 minutes.Ten rats of each group were killed after reperfusion for 2,6,12,24 hours respectively,then liver tissues were taken out.The rats in SO group were killed after operation for 2 hours.To detect the Apotosis index(A)Iand Survivin,HIF-1? protein levels.Results:AI of hepotocytes significantly increased in IR group and IP group than that in SO group(P

The role of central catecholamine (CA) and angiotensin Ⅱ (AⅡ) in one-kidney Grollman hypertensive rats was investigated. Arterial blood pressure was measured by indirect tail-plethysmography, and the contents of norepinephrine(NE), epinephrine(E) and AⅡ in hypothalamus and medulla oblongata were determined by means of fluorimetry and immunoradioassay respectively. The results showed that during the maintenance period of one-kidney Grollman hypertension the brain contents of NE E and AⅡ were significantly higher than that of the age-matched sham-wrapped rats. Separate intracerebroventricular injections of 6-OHDA and captopril not only induced significant decline of arterial blood pressure but also induced reduction of NE, E and AⅡ in the brain areas. Besides, the arterial baroreflex sensitivity in one-kidney Grollman hypertensive rats was markedly decreased. It suggests that the increase of NE, E and AⅡ and the decrease of the arterial baroreflex sensitivity may play an important role in one-kidney Geallmon hyportension.