[Effects of surface treatment on the phase and fracture strength of yttria- and magnesia-stabilized zirconia implants].

OBJECTIVE: To evaluate the effects of surface treatment on the phase and fracture strength of yttria-and magnesia-stabilized and its mechanisms. METHODS: One-piece cylindrical screw-type implants were fabricated with yttria-stabilized tetragonal zirconia polycrystal (Y-TZP) and magnesia partially stabilized zirconia (Mg-PSZ) using computer aided design (CAD)/computer aided manufacture (CAM) technique.They were divided into three groups: (1) placed in water for 1 h after final sintering (control group), (2) sandblasting using 110 µm Al2O3 particles, (3) sandblasting plus etching with hydrofluoric acid for 1 h.The surface morphology and roughness of the implants were evaluated.Tetragonal to monoclinic transformation was measured on the surface by X-ray diffraction.Static tests of the zirconia implants were carried out at room temperature following the International Standards Organization (ISO)14801:2014 Standard. RESULTS: Both sandblasting alone and sandblasting plus acid etching significantly increased surface roughness (Ra) of Mg-PSZ and Y-TZP implants (P < 0.01), with sandblasting plus acid etching exhibited the highest surface roughness.No monoclinic band was detected in Mg-PSZ surface.Compared with the control group, the surface monoclinic content of Mg-PSZ had no obvious change after surface treatments.However, strong monoclinic bands appeared in surface modified Y-TZP.Monoclinic content of Y-TZP was higher than that of control group (1.55%) after both sandblasting alone (16.44%) and sandblasting plus acid etching (7.68%).For Mg-PSZ implants, fracture strengths of sandblasting group and sandblasting plus acid etching group were (294.1±3.3) N and (331.3±26.4) N respectively, which were lower than that of control group (458.4±48.7) N with significant differences (P < 0.01).For Y-TZP implants, fracture strength of control group was (827.3±101.6) N.Compared with control group, sandblasting group showed significantly higher fracture strength (P=0.03), which was (1 162.9±116.5) N.While sandblasting plus acid etching group had a fracture strength of (867.2±171.0) N, with no significant difference with control group (P>0.99). CONCLUSION: Sandblasting improved the fracture strength of Y-TZP implants.For the Mg-PSZ implants manufactured in this study, surface treatments with sandblasting and sandblasting plus acid etching resulted in a decrease of fracture strength.

[Effects of femtosecond laser treatment on surface characteristics and flexural strength of zirconia].

OBJECTIVE: To evaluate the effects of femtosecond laser treated microgrooved surface on microscopic topography, phase transformation, and three-points flexural strength of zirconia, and to provide reference for surface microstructure optimization of zirconia implant. METHODS: According to different surface treatment methods, 57 computer aided design/computer aided manufacture (CAD/CAM) zirconia bars (20.0 mm×4.0 mm×1.4 mm) were evenly divided into three groups: sintered group, no treatment after sintering, taken as control; sandblasted group, sandblasted with 110 µm aluminium oxide (Al2O3) after sintering; microgrooved group, femtosecond laser fabricated microgrooves with 50 µm width, 30 µm depth, and 100 µm pitch. Surface microscopic topography was observed with scanning electron microscope (SEM) and 3D laser microscope. Further, surface roughness in each group and microgroove size were measured. Crystal phase was analyzed with X-ray diffraction. Specimens were subjected to three- points flexural strength test, and Weibull distribution was used to analyze their strength characteristics. RESULTS: SEM showed that sintered surface was flat with clear grain structure; sandblasted surface exihibited bumps and holes with sharp margins and irregular shape; microgrooves were regularly aligned without evident defect, and nano-scale particles were observed on the surface inside of the microgrooves. Ra value of microgrooved group [(9.42±0.28)] µm was significantly higher than that of sandblasted group [(1.04±0.03) µm] and sintered group [(0.60±0.04) µm], and there was statistical difference between sandblasted group and sintered group (P < 0.001). The microgroove size was precise with (49.75±1.24) µm width, (30.85±1.02) µm depth, and (100.58±1.94) µm pitch. Crystal phase analysis showed that monoclinic volume fraction of sandblasted group (18.17%) was much higher than that of sintered group (1.55%), while microgrooved group (2.21%) was similar with sintered group. The flexural strength of sandblasted group (986.22±163.25) MPa had no statistical difference with that of sintered group (946.46±134.15) MPa (P=0.847), but the strength in microgrooved group (547.92±30.89) MPa dropped significantly compared with the other two groups (P < 0.001). Weibull modulus of sintered, sandblasted, microgrooved groups were 7.89, 6.98, and 23.46, respectively. CONCLUSION: Femtosecond laser was able to form micro/nanostructured microgrooves on zirconia surface, which deleteriously affected the flexural strength of zirconia.

Serum miR-200c expression level as a prognostic biomarker for gastric cancer.

The aim of the present study was to analyze the serum expression level of microRNA-200c (miR-200c) in gastric cancer (GC) patients and to determine the relationship between this expression and clinicopathological features and survival. Serum samples were obtained from 98 patients with GC between February 2008 and January 2013. Quantitative RT-PCR was used to assess miR-200c expression levels in serum samples. Survival curves were plotted using the Kaplan-Meier method, and differences between survival curves were compared by the log rank test. The Cox proportional hazard regression model was used to analyze the risk factors for GC. Relative serum miR-200c level was found to be significantly higher in patients with GC than healthy controls. Mean serum miR-200c level was 97.43 ± 26.16 in the GC group and 20.79 ± 14.61 in the control group (P < 0.0001). Serum miR-200c level was also significantly associated with tumor grade (P = 0.01) and TNM stage (P = 0.009). Kaplan-Meier survival curves demonstrated that the overall survival rate was significantly lower in the patients with high serum miR-200c level than in those with low levels (27.9 vs 55.9%, P = 0.007). In addition, multivariate analysis confirmed that the hazard risk (HR) of death was significantly higher in patients with high serum miR-200c expression levels compared with low expression levels (HR = 4.01, 95%CI = 2.67-10.02, P = 0.006). The relative expression of serum miR-200c in GC patients was significantly higher compared to healthy controls, and it may prove to be useful in assessing the prognosis of GC.

Effects of miR-132 on proliferation and apoptosis of pancreatic cancer cells via Hedgehog signaling pathway.

OBJECTIVE: Micro ribonucleic acids (miRNAs) and Hedgehog (Hh) signaling pathway play key roles in the proliferation, migration and invasion of tumor cells. The aim of this study was to investigate the role of miR-132 and Hh signaling pathway in the proliferation and apoptosis of pancreatic cancer cells, and to investigate the possible underlying mechanism. MATERIALS AND METHODS: The expressions of miR-132 and Shh (a ligand of Hh) in clinical pancreatic cancer specimens and pancreatic cancer cell lines were determined by qRT-PCR. Meanwhile, the correlation between the two molecules was analyzed. Pancreatic cancer cell line (MiaPaCe-2a) was transfected with miR-132 mimics and inhibitor. The effects of miR-132 up- and down-regulation on the expressions of miR-132, Shh, Cyclin-D1, cleaved Caspase-3 and cleaved Caspase-9 were detected. In addition, the exact role of miR-132 in the proliferation, apoptosis and distribution of MiaPaCe-2a cells were investigated. RESULTS: The expression level of miR-132 in pancreatic cancer specimens and pancreatic cancer cell lines was significantly elevated when compared with that of control group. Meanwhile, miR-132 expression was negatively correlated with the expression level of Shh. Moreover, transfection with miR-132 mimics evidently up-regulated miR-132 expression. Moreover, miR-132 up-regulation significantly decreased the mRNA and protein expressions of Shh, facilitated the proliferation of MiaPaCe-2a cells, reduced the protein expressions of Cyclin-D1, cleaved Caspase-3 and cleaved Caspase-9, and suppressed cell apoptosis. On the contrary, miR-132 inhibitor transfection significantly inhibited the proliferative activity of MiaPaCe-2a cells, decreased the proportion of cells in G1 phase, and increased the proportion of cells in G2/M phase. CONCLUSIONS: MiR-132 promotes proliferation and inhibits apoptosis of pancreatic cancer cells through Hh signaling pathway.

miR-409 down-regulates Jak-Stat pathway to inhibit progression of liver cancer.

OBJECTIVE: To elucidate the influence of microRNA-409 and the Jak-Stat pathway on the development of liver cancer. PATIENTS AND METHODS: The quantitative Real-time polymerase chain reaction (qRT-PCR) method was used to detect the expression of microRNA-409 in hepatocarcinoma, paracancerous tissues and normal liver tissues, and the correlation between its expression and clinicopathological parameters of patients was analyzed, with the area under the microRNA-409 curve (AUC) being detected. The level of microRNA-409 in different liver cancer cells was detected by qPCR. Then it was overexpressed or knock-downed in the liver cancer cells by cell transfection technique. The cell apoptosis and viability after inhibition or overexpression of microRNA-409 were evaluated by propidium iodide (PI) staining and cell counting kit-8 (CCK-8) assay. Subsequently, Jak2 and Stat3 mRNA levels were detected by qPCR in hepatocarcinoma and paracancerous tissues, with their protein levels analyzed by Western blot after microRNA-409 was inhibited or up-regulated. At last, CCK-8 assay was performed to evaluate the effect of Jak2 on cell viability. RESULTS: Compared with paracancerous and normal liver tissues, the level of microRNA-409 was remarkably reduced in hepatocarcinoma tissues and was negatively correlated with tumor stage, tumor size and overall survival time of patients with liver cancer. Meanwhile, microRNA-409 expression in hepatoma cell lines was also strikingly lower than that in normal liver cells. After overexpression of microRNA-409 in HHCC, cell viability significantly decreased while apoptosis increased, and opposite results were shown in HepG2 cells after miR409 was knock-downed. In liver cancer tissues, the levels of Jak2 and Stat3 were significantly higher than those in adjacent tissues. Additionally, up-regulating microRNA-409 reduced the level of Jak2 and Stat3 protein, while down-regulating it elevated them. In addition, Jak2 could reverse the inhibitory effect of microRNA-409 on the proliferation of hepatoma cells. CONCLUSIONS: Highly-expressed microRNA-409 can down-regulate the Jak-Stat signaling pathway and inhibit cell proliferation to slow down the progression of liver cancer.

LncRNA LOC554202 promotes proliferation and migration of gastric cancer cells through regulating p21 and E-cadherin.

OBJECTIVE: To explore whether long noncoding RNA (lncRNA) LOC554202 could regulate proliferative and migratory abilities of gastric cancer (GC) cells. MATERIALS AND METHODS: Expression level of LOC554202 in GC cell lines HGC-27 and MGC-803, as well as normal gastric mucosal cell line GES-1 was detected by quantitative real-time polymerase chain reaction (qRT-PCR). LOC554202 knockdown or overexpression in HGC-27 and MGC-803 cells was achieved by transfection of LOC554202-siRNA or pcDNA-LOC554202, respectively. Cell cycle in GC cells was accessed by flow cytometry. Migratory ability of GC cells was determined by wound healing assay and transwell assay. Finally, protein expressions of p21 and E-cadherin in GC cells were detected by Western blot. RESULTS: LOC554202 expression was higher in GC cells than that of gastric mucosal cells (p<0.01). Overexpression of LOC554202 in MGC-803 cells enhanced proliferative and migratory abilities, but decreased protein expressions of p21 and E-cadherin (p<0.01). On the contrary, LOC554202 overexpression in HGC-27 cells decreased proliferative and migratory abilities, but increased protein expressions of p21 and E-cadherin (p<0.01). CONCLUSIONS: LncRNA LOC554202 is highly expressed in GC cells. It could promote proliferative and migratory abilities by downregulating expression levels of p21 and E-cadherin in GC cells.

MiR-210 knockdown promotes the development of pancreatic cancer via upregulating E2F3 expression.

OBJECTIVE: The aim of this study was to explore the role of microRNA-210 (miR-210) and E2F3 in the development of pancreatic cancer and to investigate the possible underlying mechanism. PATIENTS AND METHODS: The expression level of miR-210 in pancreatic cancer tissues, para-cancerous tissues, and normal pancreatic tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between miR-210 expression and pathological indicators of pancreatic cancer was analyzed. Meanwhile, the expression of miR-210 in pancreatic cancer cells and normal pancreatic ductal epithelial cells was detected by qRT-PCR. After transfection with miR-210 mimics and inhibitor, the viability and cell cycle of pancreatic cancer cells were detected by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The binding condition of miR-210 and E2F3 was verified by Dual-Luciferase reporter gene assay. RESULTS: MiR-210 was lowly expressed in pancreatic cancer tissues than that of para-cancerous tissues. The expression of miR-210 was negatively correlated with TNM stage and tumor size of pancreatic cancer. In vitro experiments showed that the miR-210 was downregulated in pancreatic cancer cells than that of normal pancreatic ductal epithelial cells. Meanwhile, overexpression of miR-210 arrested cell cycle decreased cell viability and downregulated E2F3 expression in pancreatic cancer cells. Dual-Luciferase reporter gene assay indicated that E2F3 bound to mi-210. Further experiments confirmed that E2F3 was negatively regulated by miR-210. CONCLUSIONS: MiR-210 knockdown promotes cell proliferation by upregulating E2F3 expression, thereby promoting the progression of pancreatic cancer.