• Geomechanics and Engineering
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• v.35 no.1
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• pp.95-108
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• 2023

Soft soil ground is a crucial factor limiting the development of the construction of transportation infrastructure in coastal areas. Soft soil is characterized by low strength, low permeability and high compressibility. However, the ordinary treatment method uses Portland cement to solidify the soft soil, which has low early strength and requires a long curing time. Microbially induced carbonate precipitation (MICP) is an emerging method to address geo-environmental problems associated with geotechnical materials. In this study, a method of bio-cementitious mortars consisting of MICP and cement was proposed to stabilize the soft soil. A series of laboratory tests were conducted on MICP-treated and cement-MICP-treated (C-MICP-treated) soft soils to improve mechanical properties. Microscale observations were also undertaken to reveal the underlying mechanism of cement-soil treated by MICP. The results showed that cohesion and internal friction angles of MICP-treated soft soil were greater than those of remolded soft soil. The UCS, elastic modulus and toughness of C-MICP-treated soft soil with high moisture content (50%, 60%, 70%, 80%) were improved compared to traditional cement-soil. A remarkable difference was observed that the MICP process mainly played a role in the early curing stage (i.e., within 14 days) while cement hydration continued during the whole process. Micro-characterization revealed that the calcium carbonate filling the pores enhanced the soft soil.

• Structural Engineering and Mechanics
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• v.86 no.1
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• pp.139-156
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• 2023

The reinforced concrete lining in the hydraulic pressure tunnel tends to crack during the water-filling process. The lining will be detached from the surrounding rock due to the inner water exosmosis along concrete cracks. From the previous research achievements, the cohesive element is widely adopted to simulate the concrete crack but rarely adopted to simulate the lining-rock interface. In this study, the zero-thickness cohesive element with hydro-mechanical coupling property is not only employed to simulate the traditional concrete crack, but also innovatively introduced to simulate the lining-rock interface. Combined with the indirect-coupled method, the hydro-mechanical coupling algorithm of the reinforced concrete lining in hydraulic pressure tunnels is proposed and implemented in the finite element code ABAQUS. The calculated results reveal the cracking mechanism of the reinforced concrete lining, and match well with the observed engineering phenomenon.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.11
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• pp.6507-6512
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• 2013

The purpose of this study was to evaluate the associations of CYP1A1 genetic polymorphisms with the risk of developing esophageal cancer (EC). A case-control study was carried out in a Chinese population in which 157 hospital based EC cases and 157 population based healthy controls with 1:1 match by age and sex were included. PCR based restriction fragment length polymorphisms (PCR-RFLP) were used to detect genotypes in case and control groups. For the CYP1A1 Ile/Val polymorphism, comparing with wild genotype Ile/Ile, both the heterozygote genotype Ile/Val and the combined variant genotype Ile/Val+Val/Val increased the risk of esophageal cancer (OR: 2.05, 95%CI: 1.19-3.54, OR: 1.86, 95%CI: 1.11-3.12). No significant association was found between the CYP1A1 MspI polymorphism and EC. According to analysis of combined genotypes, the TC/AG combined genotype which contained both variant alleles of these two polymorphisms increased the risk of developing EC (OR: 2.12, 95%CI: 1.16-3.85). Our results suggested that genetic polymorphisms of CYP1A1 may increase the susceptibility to EC.

• Molecules and Cells
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• v.39 no.12
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• pp.877-887
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• 2016

Tazarotene-induced gene 1 (TIG1) is a retinoic acid-inducible protein that is considered a putative tumor suppressor. The expression of TIG1 is decreased in malignant prostate carcinoma or poorly differentiated colorectal adenocarcinoma, but TIG1 is present in benign or well-differentiated tumors. Ectopic TIG1 expression led to suppression of growth in cancer cells. However, the function of TIG1 in cell differentiation is still unknown. Using a yeast two-hybrid system, we found that transmembrane protein 192 (TMEM192) interacted with TIG1. We also found that both TIG1A and TIG1B isoforms interacted and co-localized with TMEM192 in HtTA cervical cancer cells. The expression of TIG1 induced the expression of autophagy-related proteins, including Beclin-1 and LC-3B. The silencing of TMEM192 reduced the TIG1-mediated upregulation of autophagic activity. Furthermore, silencing of either TIG1 or TMEM192 led to alleviation of the upregulation of autophagy induced by all-trans retinoic acid. Our results demonstrate that the expression of TIG1 leads to cell autophagy through TMEM192. Our study also suggests that TIG1 and TMEM192 play an important role in the all-trans retinoic acid-mediated upregulation of autophagic activity.

• 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.

• Molecules and Cells
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• v.40 no.6
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• pp.393-400
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• 2017

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease characterized by lack of insulin and high glucose levels. T2DM can cause bone loss and fracture, thus leading to diabetic osteoporosis. Promoting osteogenic differentiation of osteoblasts may effectively treat diabetic osteoporosis. We previously reported that Sirtuin 1 (Sirt1), a $NAD^+$-dependent deacetylase, promotes osteogenic differentiation through downregulation of peroxisome proliferator-activated receptor (PPAR) ${\gamma}$. We also found that miR-132 regulates osteogenic differentiation by downregulating Sirt1 in a $PPAR{\beta}/{\delta}$-dependent manner. The ligand-activated transcription factor, $PPAR{\alpha}$, is another isotype of the peroxisome proliferator-activated receptor family that helps maintain bone homeostasis and promot bone formation. Whether the regulatory role of $PPAR{\alpha}$ in osteogenic differentiation is mediated via Sirt1 remains unclear. In the present study, we aimed to determine this role and the underlying mechanism by using high glucose (HG) and free fatty acids (FFA) to mimic T2DM in MC3T3-E1 cells. The results showed that HG-FFA significantly inhibited expression of $PPAR{\alpha}$, Sirt1 and osteogenic differentiation, but these effects were markedly reversed by $PPAR{\alpha}$ overexpression. Moreover, siSirt1 attenuated the positive effects of $PPAR{\alpha}$ on osteogenic differentiation, suggesting that $PPAR{\alpha}$ promotes osteogenic differentiation in a Sirt1-dependent manner. Luciferase activity assay confirmed interactions between $PPAR{\alpha}$ and Sirt1. These findings indicate that $PPAR{\alpha}$ promotes osteogenic differentiation via the Sirt1-dependent signaling pathway.

• Bulletin of the Korean Chemical Society
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• v.35 no.7
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• pp.2086-2092
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• 2014

Two novel coordination compounds $[Cu_2(pypya)_3(H_2O)_2]{\cdot}Cl{\cdot}(H_2O)_5$ (1) and $\{[Cd(pypya)(ta)_{1/2}]{\cdot}H_2O\}_n$ (2) (Hpypya=2-(3-(pyridin-2-yl)-1H-pyrazol-1-yl)acetic acid, $H_2ta$=terephthalic acid) were synthesized and characterized by single X-ray diffraction. Structure determination reveals that complex 1 and complex 2 crystallize in the triclinic system, with the P-1 space group. The asymmetric unit of 1 contains two Cu(II) ions, and their coordination modes are different. These units of complex 1 are linked together via hydrogen bonds and ${\pi}-{\pi}$ interactions, and the 3D structure of complex 1 was formed. Complex 2, a mononuclear Cd(II) coordination compound, has a 2D structure which was constructed via coordination bonds. TGA and fluorescence spectra analysis of complex 1 and complex 2 have also been studied. In addition, the geometry parameters of complex 1 have been optimized with the B3LYP method of density functional theory (DFT) to explain its coordination behavior. The electronic properties of the complex 1 and ligand Hpypya have been investigated based on the nature bond orbital (NBO) analysis at the B3LYP level of theory. The result verifies that the synergistic effect have occurred in the compound.

• 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.

• Journal of Microbiology and Biotechnology
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• v.30 no.11
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• pp.1626-1639
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• 2020

In Caenorhabditis elegans, SHN-1 is the homologue of SHANK, a scaffolding protein. In this study, we determined the molecular basis for SHN-1/SHANK in the regulation of innate immune response to fungal infection. Mutation of shn-1 increased the susceptibility to Candida albicans infection and suppressed the innate immune response. After C. albicans infection for 6, 12, or 24 h, both transcriptional expression of shn-1 and SHN-1::GFP expression were increased, implying that the activated SHN-1 may mediate a protection mechanism for C. elegans against the adverse effects from fungal infection. SHN-1 acted in both the neurons and the intestine to regulate the innate immune response to fungal infection. In the neurons, GLR-1, an AMPA ionotropic glutamate receptor, was identified as the downstream target in the regulation of innate immune response to fungal infection. GLR-1 further positively affected the function of SER-7-mediated serotonin signaling and antagonized the function of DAT-1-mediated dopamine signaling in the regulation of innate immune response to fungal infection. Our study suggests the novel function of SHN-1/SHANK in the regulation of innate immune response to fungal infection. Moreover, our results also denote the crucial role of neurotransmitter signals in mediating the function of SHN-1/SHANK in regulating innate immune response to fungal infection.

• 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.