• Journal of the Optical Society of Korea
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• v.17 no.3
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• pp.231-236
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• 2013

We present both theoretically and experimentally the thermo-optic characteristics of micro-structured optical fiber (MOF) filled with mixed liquid. The performance of MOF depends on the efficient interaction between the fundamental mode of the transmitted light wave and the tunable thermo-optic materials in the cladding. The numerical simulation indicates that the confinement loss of MOF presents higher temperature dependence with higher air-filling ratios $d/{\Lambda}$, longer incident wavelength and fewer air holes in the cladding. For the 4cm liquid-filled grapefruit MOF, we demonstrate from experiments that different proportions of solutions lead to tunable temperature sensitive ranges. The insertion loss and the extinction ratio are 3~4 dB and approximate 20 dB, respectively. The proposed liquid-filling MOF will be developed as thermo-optic sensor, attenuator or optical switch with the advantages of simple structure, compact configuration and easy fabrication.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.1
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• pp.23-29
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• 2015

Background: Current cancer therapy mainly focuses on identifying novel targets crucial for tumorigenesis. The FoxM1 is of preference as an anticancer target, due to its significance in execution of mitosis, cell cycle progression, as well as other signal pathways leading to tumorigenesis. FoxM1 is partially regulated by oncoproteins or tumor suppressors, which are often mutated, lost, or overexpressed in human cancer. Since sustaining proliferating signaling is an important hallmark of cancer, FoxM1 is overexpressed in a series of human malignancies. Alarge-scale gene expression analysis also identified FoxM1 as a differentially-expressed gene in most solid tumors. Furthermore, overexpressed FoxM1 is correlated with the prognosis of cancer patients, as verified in a series of malignancies by Cox regression analysis. Thus, extensive studies have been conducted to explore the roles of FoxM1 in tumorigenesis, making it an attractive target for anticancer therapy. Several antitumor drugs have been reported to target or inhibit FoxM1 expression in different cancers, and down-regulation of FoxM1 also abrogates drug resistance in some cancer cell lines, highlighting a promising future for FoxM1 application in the clinic.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.7
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• pp.3465-3469
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• 2012

Aim: Platinum agents have shown to be effective in the treatment of colorectal cancer. We assessed whether single nucleotide polymorphisms (SNPs) in GSTP1, ERCC1 Asn118Asn and ERCC2 Lys751Gln might predict the overall survival in patients receiving oxaliplatin-based chemotherapy in a Chinese population. Methods: SNPs of GSTP1, ERCC1 Asn118Asn and ERCC2 Lys751Gln in 335 colorectal cancer patients were assessed using TaqMan nuclease assays. Results: At the time of final analysis on Nov. 2011, the median follow-up period was 37.7 months (range from 1 to 60 months). A total of 229 patients died during follow-up. Our study showed GSTP1 Val/Val (HR=0.44, 95% CI=0.18-0.98), ERCC1 C/C (HR=0.20, 95% CI=0.10-0.79) and ERCC2 G/G (HR=0.48, 95% CI=0.19-0.97) to be significantly associated with better survival of colorectal cancer. GSTP1 Val/Val, ERCC1 C/C and ERCC2 G/G were also related to longer survival among patients with colon cancer, with HRs (95% CIs) of 0.41 (0.16-0.91), 0.16 (0.09-0.74) and 0.34 (0.16-0.91), respectively. Conclusion: GSTP1, GSTP1, ERCC1 Asn118Asn and ERCC2 Lys751Gln genotyping might facilitate tailored oxaliplatin-based chemotherapy for colorectal cancer patients.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.13
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• pp.5201-5205
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• 2014

Emodin, a natural anthraquinone isolated from the traditional Chinese medicine Radix rhizoma Rhei, can induce apoptosis in many kinds of cancer cells. This study demonstrated that emodin induces apoptosis in human colon cancer HCT116 cells by provoking oxidative stress, which subsequently triggers a p53-mitochondrial apoptotic pathway. Emodin induced mitochondrial transmembrane potential loss, increase in Bax and decrease in Bcl-2 expression and mitochondrial translocation and release of cytochrome c to cytosol in HCT116 cells. In response to emodin-treatment, ROS increased rapidly, and subsequently p53 was overexpressed. Pretreatment with the antioxidant NAC diminished apoptosis and p53 overexpression induced by emodin. Transfecting p53 siRNA also attenuated apoptosis induced by emodin, Bax expression and mitochondrial translocation being reduced compared to treatment with emodin alone. Taken together, these results indicate that ROS is a trigger of emodin-induced apoptosis in HCT116 cells, and p53 expression increases under oxidative stress, leading to Bax-mediated mitochondrial apoptosis.

• Smart Structures and Systems
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• v.21 no.5
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• pp.695-703
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• 2018

Based on monitoring data collected from the Nanjing Dashengguan Bridge over the last five years, this paper systematically investigates the effects of temperature field and train loadings on the structural responses of this long-span high-speed railway bridge, and establishes the early warning thresholds for various structural responses. Then, some lessons drawn from the structural health monitoring system of this bridge are summarized. The main context includes: (1) Polynomial regression models are established for monitoring temperature effects on modal frequencies of the main girder and hangers, longitudinal displacements of the bearings, and static strains of the truss members; (2) The correlation between structural vibration accelerations and train speeds is investigated, focusing on the resonance characteristics of the bridge at the specific train speeds; (3) With regard to various static and dynamic responses of the bridge, early warning thresholds are established by using mean control chart analysis and probabilistic analysis; (4) Two lessons are drawn from the experiences in the bridge operation, which involves the lacks of the health monitoring for telescopic devices on the beam-end and bolt fractures in key members of the main truss.

• Geomechanics and Engineering
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• v.20 no.5
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• pp.461-474
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• 2020

Analysing the incompatible deformation and damage evolution around the tunnels in mixed strata is significant for evaluating the tunnel stability, as well as the interaction between the support system and the surrounding rock mass. To investigate this issue, confined compression tests were conducted on upper-soft and lower-hard strata specimens containing a circular hole using a rock testing system, the physical mechanical properties were then investigated. Then, the incompatible deformation and failure modes of the specimens were analysed based on the digital speckle correlation method (DSCM) and Acoustic Emission (AE) data. Finally, numerical simulations were conducted to explore the damage evolution of the mixed strata. The results indicate that at low inclination angles, the deformation and v-shaped notches inside the hole are controlled by the structure plane. Progressive spalling failure occurs at the sidewalls along the structure plane in soft rock. But the transmission of the loading force between the soft rock and hard rock are different in local. At high inclination angles, v-shaped notches are approximately perpendicular to the structure plane, and the soft and hard rock bear common loads. Incompatible deformation between the soft rock and hard rock controls the failure process. At inclination angles of 0°, 30° and 90°, incompatible deformations are closely related to rock damage. At 60°, incompatible deformations and rock damage are discordant due that the soft rock and hard rock alternately bears the major loads during the failure process. The failure trend and modes of the numerical results agree very well with those observed in the experimental results. As the inclination angles increase, the proportion of the shear or tensile damage exhibits a nonlinear increase or decrease, suggesting that the inclination angle of mixed strata may promote shear damage and restrain tensile damage.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.4
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• pp.1993-1998
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• 2016

The effects of carbon-ion irradiation on cancer cell telomere function have not been comprehensively studied. In our previous report cancer cells with telomere dysfunction were more sensitive to carbon-ion irradiation, but the underlying mechanisms remained unclear. Here we found that telomerase activity was suppressed by carbon-ion irradiation via hTERT down-regulation. Inhibition of telomere activity by MST-312 further increased cancer cell radiosensitivity to carbon-ion radiation. hTERT suppression caused by either carbon-ion irradiation or MST-312 impaired mitochondrial function, as indicated by decreased membrane potential, mtDNA copy number, mitochondrial mass, total ATP levels and elevated reactive oxygen species (ROS). PGC-$1{\alpha}$ expression was repressed after carbion-ion irradiation, and hTERT inhibition by MST-312 could further exacerbate this effect. Lowering the mitochondrial ROS level by MitoTEMPO could partially counteract the induction of cellular senescence induced by carbon-ion radiation and MST-312 incubation. Taken together, the current data suggest that telomere-mitochondrion links play a role in the induction of senescence in MCF-7 cells after carbon-ion irradiation.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.10
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• pp.5007-5010
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• 2012

Objective: We conducted a prospective study to test the association between three amino acid substitution polymorphismic variants of DNA repair genes, XRCC1 (Arg194Trp), XRCC1(Arg280His) and XRCC1 (Arg399Gln), and clinical outcome of ovarian cancer patients undergoing adjuvant chemotherapy. Methods: 195 patients with primary advanced ovarian cancer and treated by adjuvant chemotherapy were included in our study. All were followed-up from Jan. 2007 to Jan. 2012. Genotyping of XRCC1 polymorphisms was conducted by TaqMan Gene Expression assays. Results: The XRCC1 194 Trp/Trp genotype conferred a significant risk of death from ovarian cancer when compared with Arg/Arg (HR=1.56, 95%CI=1.04-3.15). Similarly, those carrying the XRCC1 399 Gln/Gln genotype had a increased risk of death as compared to the XRCC1 399Arg/Arg genotype with an HR (95% CI) of 1.98 (1.09-3.93). Conclusion: This study is the first to provide evidence that XRCC1 gene polymorphisms would well be useful as surrogate markers of clinical outcome in ovarian cancer cases undergoing adjuvant chemotherapy.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.5
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• pp.2129-2132
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• 2012

Objective: To explore improved treatment by retrospectively comparing survival time of gemcitabine-based concurrent chemoradiotherapy (GemRT) versus chemotherapy (Gem) alone in patients with locally advanced pancreatic cancer (LAPC). Methods: From January 2005 to June 2010, 56 patients with LAPC from Subei People's Hospital were treated either with Gem (n=21) or GemRT (n=35). Gem consisted of 4-6 cycles gemcitabine alone (1000 mg/m2 on Days 1, 8, 15, 28-day a cycle). GemRT consisted of 50.4Gy/28F radiotherapy with concurrent 2 cycles of gemcitabine (1000 $mg/m^2$ on days of radiation 1, 8, 15, 21-day a cycle). Radiation was delivered to the gross tumor volume plus 1-1.5 cm by use of a three-dimensional conformal technique. The follow-up time was calculated from the time of diagnosis to the date of death or last contact. Kaplan-Meier methodology wes used to evaluate survival. Results: Patient characteristics were not significantly different between treatment groups. The disease control rate and the objective response rate of GemRT versus Gem was 97.1% vs 71.4%, 74.3% vs 38.1%. The overall survival (OS) was significantly better for GemRT compared to Gem (median 13 months versus 8 months; 51.4% versus 14.3% at 1 year, respectively). Conclusion: Radiation therapy at 50.4Gy with 2 concurrent cycles of gemcitabine results in favorable rates of OS. Concurrent chemoradiotherapy should be the first choice for patients with LAPC.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.3
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• pp.781-784
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• 2012

The aim of this study was to evaluate the effect of the adenovirus-mediated double suicide gene (CD/TK) for selective killing of gastric cancer cells. Gastric cancer cells SCG7901 and normal gastric epithelial cell lines were infected by adenoviruses Ad-survivin/GFP and Ad-survivin/CD/TK. GFP expression and CD-TK were detected by fluorescence microscopy and reverse transcriptase polymerase chain reaction (RT-PCR), respectively. After treatment of the infected cells with the pro-drugs ganciclovir (GCV) and/or 5-FC, the cell growth status was evaluated by methyl thiazolyl tetrazolium assay. Cell cycle changes were detected using flow cytometry. In nude mice bearing human gastric cancer, the recombinant adenovirus vector was injected directly into the tumor followed by an intraperitoneal injection of GCV and/or 5-FC. The subsequent tumor growth was then observed. The GFP gene driven by survivin could be expressed within the gastric cancer line SCG7901, but not in normal gastric epithelial cells. RT-PCR demonstrated the presence of the CD/TK gene product in the infected SCG7901 cells, but not in the infected normal gastric epithelial cells. The infected gastric cancer SCG7901, but not the gastric cells, was highly sensitive to the pro-drugs. The CD/TK fusion gene system showed significantly greater efficiency than either of the single suicide genes in killing the target cells (P<0.01). Treatment of the infected cells with the pro-drugs resulted in increased cell percentage in G0-Gl phase and decreased percentage in S phase. In nude mice bearing SCG7901 cells, treatment with the double suicide gene system significantly inhibited tumor growth, showing much stronger effects than either of the single suicide genes (P<0.01). The adenovirus-mediated CD/TK double suicide gene driven by survivin promoter combined with GCV an 5-FC treatment could be an effective therapy against experimental gastric cancer with much greater efficacy than the single suicide gene CD/TK combined with GCV or 5-FC.