[en] Conductive ceramic thin film thermocouples were investigated for application to silicon carbide fiber reinforced silicon carbide ceramic matrix composite (SiC/SiC CMC) components. High temperature conductive oxides based on indium and zinc oxides were selected for testing to high temperatures in air. Sample oxide films were first sputtered-deposited on alumina substrates then on SiC/SiC CMC sample disks. Operational issues such as cold junction compensation to a 0 °C reference, resistivity and thermopower variations are discussed. Results show that zinc oxides have an extremely high resistance and thus increased complexity for use as a thermocouple, but thermocouples using indium oxides can achieve a strong, nearly linear response to high temperatures. - Highlights: ► Oxide thin film thermocouples tested for SiC/SiC ceramic matrix composites (CMCs) ► In₂O₃, N:In₂O₃, ZnO, AlZnO sputtered and tested on Al₂O₃ and CMC substrates ► ZnO, AlZnO have high resistance, complex temperature response. ► In₂O₃, N:In₂O₃ conductive at room temperature, more linear temperature response

[en] In the present study, the mechanisms of fatigue crack initiation and propagation, and of coating failure under thermal loads that simulate those in diesel engines are investigated. Surface cracks initiate early and grow continuously under thermal low cycle fatigue (LCF) and high cycle fatigue (HCF) stresses. It is found that, in the absence of interfacial oxidation, the failure associated with LCF is closely related to coating sintering and creep at high temperatures. Significant LCF and HCF interactions have been observed in the thermal fatigue tests. The fatigue crack growth rate in the ceramic coating strongly depends on the characteristic HCF cycle number, N*_HCF which is defined as the number of HCF cycles per LCF cycle. The crack growth rate is increased from 0.36 μm/LCF cycle for a pure LCF test to 2.8 μm/LCF cycle for a combined LCF and HCF test at N*_HCF about 20 000. A surface wedging model has been proposed to account for the HCF crack growth in the coating systems. This mechanism predicts that the HCF damage effect increases with heat flux and thus with increasing surface temperature swing, thermal expansion coefficient and elastic modulus of the ceramic coating, as well as with the HCF interacting depth. Good correlation has been found between the analysis and experimental evidence. (orig.)

[en] Objective: To explore the effect of recombinant adenovirus vector mediated mutant IκBα (mIκBα) combined with radiation on the hepatocarcinoma. Methods: Limited dilution method was used to test the virus titer in 293 cells. The HCC9204 cells were infected with MOI 10,20,30 and 50 for 48 h, respectively. The expression of p65 and mIκBα protein was analyzed by Western blot. Transfected HCC9204 cells and controls were treated with 4 Gy γ rays. The inhibition rate of HCC9204 cells was examined by MTT. Rat models of HCC9204 was constructed. AdmIκBα plasmids were injected into tumor tissue and the tumors were administered with 6 Gy γ irradiation 48 hours later. Tumor growth at different time points was recorded during 28 days. Results: The titer of AdmIκBΑ is 1.252 x 10⁹ pfu/ml. The expression of mIκBα protein was increased with titer of AdmIκBα, and p65 protein began to decrease when MOI was 10, and reached the lowest when MOI was 50, they were all dose-dependent. The proliferation of HCC9204 cell lines were suppressed, as was more significant combined with radiation, and the effect was in a viral dose-dependent manner. From days 7 to 28 after AdmIκBα gene and radiotherapy, the tumor growth was significantly slower than after irradiation or gene therapy alone. Conclusions: Recombinant adenoviral-mediated mIκBα gene, combined with irradiation, can increase the cell-killing effect. It is better than that of either one alone. (authors)

[en] Objective: To study the effect of PUMA gene mediated by recombinant adenovirus vector combined with radiation on the pancreatic carcinoma. Methods: The PANC-1 cells were infected with Ad- PUMA (MOI=10, 50 and 100, respectively) for 48 h. The expression of PUMA mRNA and protein was detected by RT-PCR and Western blot, respectively. PANC-1 cells were divided into 4 groups: control group, transfection group, irradiation group and combined treatment group. The cell growth inhibition rate and apoptotic rate of PANC-1 cells were assessed by MTT assay and flow cytometry. Human pancreatic carcinomas were transplanted subcutaneously in nude mice, which were randomized into 4 groups: control group, transfection group, irradiation group and combined treatment group. Tumor growth rate and apoptotic index at different time points were recorded in 35 days. Results: The expression of PUMA mRNA and protein was increased with the increase of MOI of Ad-PUMA, which was does-dependant (MOI=10, mRNA=0.46± 0.02, protein=0.75± 0.09; MOI=50, mRNA=1.12±0.09, protein=1.01±0.18; MOI=100, mRNA=1.50±0.08, protein= 1.80±0.15; P<0.05). The proliferation of PANC-1 cells was suppressed significantly when transfected by Ad- PUMA in a dose-dependent manner(r=-0.98655), which was more significant combined with radiation (r= -0.971 26, P<0.05). Meanwhile, the apoptotic rate was increased in the same manner [for pre- and post- irradiation, which was (45.4±5.26)% and (73.2±6.62)%, respectively, P<0.05]. From 7 to 35 d after PUMA gene transfection and radiotherapy, the tumor growth was significantly slower than those of irradiation group, transfection group and control group [35 d after therapy, the volume of tumor was (19.82±6.45)mm³, (39.5±9.23)mm³, (33.6±10.3)mm³ and (52.0±11.43)mm³, respectively, P<0.05]. And the apoptotic index was increased in the same manner (AI=0.43±0.05, 0.29±0.10, 0.24±0.05 and 0.00±0.00, respectively, P<0.05). Conclusions: Recombinant adenoviral-mediated PUMA gene combined with irradiation could increase the cell-killing effect on pancreatic carcinoma. It is better than that of either one kind of therapy. (authors)

[en] Objective: To investigate the expression of hypoxia-inducible factor 2α (HIF-2α) and its relationships with vascular endothelial growth factor (VEGF) and microvessel density(MVD) in angiogenesis, and the relationship to the clinicopathologic features of human pancreatic carcinoma. Methods: The expressions of HIF-2α and VEGF as well as the value of MVD were detected by immunohistochemical method of SP in 60 cases of resected specimen of pancreatic carcinoma and their corresponding normal pancreatic tissue served as the control group. The correlations among them, and their relationships to the clinicopathologic characteristics of human pancreatic carcinoma were analyzed. Results: The positive expressions of HIF-2α and VEGF in pancreatic carcinoma were significantly higher than that in the control group (P<0.05).The value of MVD was also significantly higher than that in the control group(P<0.05). The expression of HIF-2α was positively correlated with the expression of VEGF and the value of MVD closely(P<0.05). The positivity rates of HIF-2α and VEGF were closely related with TNM staging and tumor size of human pancreatic carcinoma respectively. Conclusion: HIF-2α is overexpressed in pancreatic carcinoma, and its expression is closely correlated with the expression of VEGF and the value of MVD. It may be involved in the angiogenesis of human pancreatic carcinoma by upregulating the expression of VEGF, and play an important role in the carcinogenesis and aggression of pancreatic carcinoma. (authors)

[en] We theoretically investigate the generation of five-partite continuous-variable (CV) entanglement through injection-seeded non-degenerate optical parametric amplification cascaded two sum-frequency processes in only one optical superlattice without optical cavities. The idle can be generated by optical parametric amplification of pump and signal. Then, one beam will be generated by the cascaded sum-frequency process of pump and idle, and another beam will be produced by the cascaded sum-frequency process of pump and signal in the same optical superlattice. The phase-mismatching in the cascaded nonlinear processes can be compensated by three reciprocals of the optical superlattice by a quasi-phase-matching technique. The conversion dynamics among the cascaded nonlinear processes is analyzed by using a quantum stochastic method. The five-partite entanglement among pump, signal, idle, and two sum-frequency beams are discussed by applying a sufficient inseparability criteria for the five-partite CV entanglement proposed by Van Loock and Furusawa. This scheme of five-partite entanglement generation with different frequencies has potential applications in quantum communication and computation networks. (letter)

[en] Resistance to Fas Ligand (FasL) mediated apoptosis plays an important role in tumorigenesis. Decoy receptor 3 (DcR3) is reported to interact with FasL and is overexpressed in some malignant tumors. We sought to investigate the role of DcR3 in resistance to FasL in pancreatic cancer. We compared expression of apoptosis related genes between FasL-resistant SW1990 and FasL-sensitive Patu8988 pancreatic cell lines by microarray analysis. We explored the impact of siRNA knockdown of, or exogenous supplementation with, DcR3 on FasL-induced cell growth inhibition in pancreatic cancer cell lines and expression of proteins involved in apoptotic signaling. We assessed the level of DcR3 protein and ERK1/2 phosphorylation in tumor and non-tumor tissue samples of 66 patients with pancreatic carcinoma. RNAi knockdown of DcR3 expression in SW1990 cells reduced resistance to FasL-induced apoptosis, and supplementation of Patu8988 with rDcR3 had the opposite effect. RNAi knockdown of DcR3 in SW1990 cells elevated expression of caspase 3, 8 and 9, and reduced ERK1/2 phosphorylation (P < 0.05), but did not alter phosphorylated-Akt expression. 47 tumor tissue specimens, but only 15 matched non-tumor specimens stained for DcR3 (χ"2 = 31.1447, P < 0.001). The proliferation index of DcR3 positive specimens (14.26  ±  2.67%) was significantly higher than that of DcR3 negative specimens (43.58  ±  7.88%, P < 0.01). DcR3 expression positively correlated with p-ERK1/2 expression in pancreatic cancer tissues (r = 0.607, P < 0.001). DcR3 enhances ERK1/2 phosphorylation and opposes FasL signaling in pancreatic cancer cells. - Highlights: • We investigated the role of DcR3 in FasL resistance in pancreatic cancer. • Knockdown of DcR3 in SW1990 cells reduced resistance to FasL-induced apoptosis. • DcR3 knockdown also elevated caspase expression, and reduced ERK1/2 phosphorylation. • Tumor and non-tumor tissues were collected from 66 pancreatic carcinoma patients. • 47 tumor tissue specimens, but only 15 matched non-tumor specimens contained DcR3