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In this study, the rapid synthesis of graphene via chemical vapor deposition (CVD) using liquefied petroleum gas (LPG), a common and low-cost carbon source majorly composed of butane and propane, as the precursor is investigated. For the synthesis of high-quality graphene, the growth conditions are optimized by controlling CVD parameters such as growth time, temperature, gas amount, and flow rate. Thus, graphene is successfully obtained from LPG in a short time. This synthesis is 10 times faster than that the conventional synthesis using methane as the carbon source. In the X-ray photoelectron spectra, the rapidly grown graphene samples obtained from LPG show small S2p signals due to the presence of few tens ppm ethanethiol in commercial LPG. In addition, graphene is synthesized using a hydrogen and LPG mixture to investigate the quality of graphene. Both samples are characterized by their peak positions and full width at half maximum values of the G and 2D peaks in the Raman spectra and Dirac points in the electrical measurements. In particular, the Dirac points of the graphene sample obtained with a growth time of 1 min sample appear around −22 VG and the sample's mobility is about 1600 cm2/V⋅s.

The number of casualties in the maritime sector is increasing consistently. To reduce the scope of search area extensions in the event of a maritime accident, maritime authorities and operation centers are currently trying to develop a quick search for survivors at sea using unmanned aerial vehicles (UAVs) in maritime search and rescue (SAR) operations. Here, we propose a two-phase method for solving the coverage path planning (CPP) problem of multiple-UAV areas in maritime SAR. In phase 1, we propose a grid-based area decomposition method that minimizes the decomposed search area to transform the search area into a graph made up of vertices and edges. In phase 2, we formulate a mixed-integer linear programming (MILP) model to derive an optimal coverage path that minimizes the completion time. To solve the model for large-scale instances, a randomized search heuristic (RSH) algorithm is developed. We conducted extensive numerical experiments to validate the performance of the algorithm. Experimental results show that the RSH yields a better solution with an approximately 0.7% optimality gap within a much shorter computation time than that of a commercial solver. In addition, our grid-based CPP algorithm outperforms those used in previous research with respect to the solution quality. Furthermore, we showed the results of real flight experiments in the marine field using the proposed algorithm.

This paper investigates the robust berth allocation problem in container terminals. To handle the uncertainties in vessel arrivals, the problem is formulated as a scenario-based two-stage stochastic programming model. Furthermore, we introduce the time buffers to the model. We then develop an algorithm for time buffer insertion, which accommodates the adaptive search procedure for the time buffer into the Particle Swarm Optimization (PSO) algorithm. Different from the traditional PSO algorithm, a core operator is designed with a modified version to take the intelligent time buffer insertion approach. The results of the numerical experiments show that the proposed method consistently provides an improved performance in terms of solution quality, compared with the previous studies and the one with a traditional operator in the PSO algorithm.

Summary Background/aims We evaluated the prognostic implication of circulating microRNA (miR)-21, miR-26a, and miR-29a in hepatocellular carcinoma (HCC) patients who underwent curative treatment. Methods The study included 120 hepatitis B virus-related HCC patients who underwent hepatic resection ( n = 63) or radiofrequency ablation ( n = 57). MiR-21, miR-26a, and miR-29a expression levels in pretreatment plasma and several clinical variables were analyzed to identify prognostic bio-markers. Results Old age, low albumin level, low platelet count, advanced tumor stage (modified Union for International Cancer Control stages III, IV), low miR-26a (hazard ratio [HR] = 1.72; 95% confidence interval [CI] = 1.04–2.83; P = 0.035), and low miR-29a (HR = 1.75; 95% CI = 1.04–2.94; P = 0.035) were identified as independent risk factors for predicting poor disease-free survival. Low miR-21, miR-26a, and miR-29a were associated with poor liver transplantation (LT)-free survival in the univariate analysis. Multivariate Cox regression analysis showed that low miR-26a (HR = 3.41; 95% CI = 1.32–8.82; P = 0.011) and low miR-29a (HR = 2.75; 95% CI = 1.10–6.85; P = 0.030), low platelet count, and advanced tumor stage were significantly associated with poor LT-free survival. Remarkable correlation was found between miR-26a and miR-29a (Spearman's rho = 0.734, P Conclusion Pretreatment levels of circulating miR-26a and miR-29a are independent prognostic markers for poor disease-free survival and LT-free survival in hepatitis B virus-related HCC patients.

In mice, tongue epithelial differentiation is mainly regulated by the interactions among various signalling molecules including Fgf signalling pathways. However, the subsequent signalling modulations for epithelial maturation, initiated by Fgf signalling, remain to be elucidated. Therefore, we employed an in vitro tongue organ cultivation system along with the applications of various pharmacological inhibitors against the intracellular signalling molecules of Fgf signalling pathways, including H89, LY294002, PD98059, and U0126. Following treatments with LY294002 and H89, inhibitors for PI3K and PKA, respectively, the decreased thickness of the tongue epithelium was observed along with the alteration in cell proliferative and apoptotic patterns. Meanwhile, cultivated tongues treated with MEK inhibitor U0126 or PD98059 showed significantly decreased cell proliferation in the tongue epithelium and the mesenchyme. Based on these results, we suggest that the tongue epithelium is differentiated into multiple epithelial cell layers via the PI3K and PKA pathways in tissue-specific manner during the epithelial-mesenchymal interactions.

Objective Studies of regenerative therapies have focused on the paracrine effects of mesenchymal stem cells, but little has been revealed about the humoral factors of periodontal ligament (PDL) stem cells. The aim of this study was to identify and compare the secretory factors of human permanent- and deciduous-teeth PDL cells (P-PDL and D-PDL cells, respectively) in order to understand the characteristics of these cells and their potential applications in regenerative therapies. Design Conditioned media were collected from P-PDL and D-PDL cells (P-PDL-CM and D-PDL-CM, respectively). These media were analyzed with high-performance liquid-chromatography-coupled electrospray ionization tandem mass spectrometry and a cytokine membrane assay. In addition, Western blot analysis was performed to verify the differences between the two media. Results Cytokines related to neurogenesis (NT-3 and NT-4) and angiogenesis-related cytokines (EGF and IGF-1) were identified in P-PDL-CM. The expression levels of immune-response-related cytokines (interleukins I, II, and IV) and secreted proteins related to tissue degradation and catalytic activities (matrix metallopeptidase 1 (MMP1), Proteasome subunit, alpha type, 1 (PSMA1), and cullin 7 (CUL7)) were higher in D-PDL-CM. Vasorin (VASN) was expressed more strongly in P-PDL-CM, but tudor domain containing 7 (TDRD7) was expressed more strongly in D-PDL-CM in Western blot analysis. Conclusion The cytokine expressions of the two cell types showed different patterns, especially in neurogenesis and immune responses. P-PDL cells are more suitable candidates for applications in regenerative therapies.

Objectives Wnt/β-catenin signaling has a pivotal role in the pathogenesis of hepatocellular carcinoma (HCC). The present study aimed to determine whether genetic variation in the Wnt/β-catenin signaling pathway is associated with the development and/or progression of HCC and the survival of patients with hepatitis B virus (HBV)-associated HCC. Design and methods We assessed seven single nucleotide polymorphisms (SNPs) of the AXIN1, AXIN2, CTNNB1, and WNT2 genes in 245 patients with HBV-associated HCC and 483 chronic HBV carriers without HCC. We analyzed the association of each SNP with HCC development or progression and overall survival. Results The CTNNB1 rs3864004 A allele was associated with a decreased risk of HCC development (P = 0.049). Haplotype analysis revealed a significantly higher frequency of CTNNB1 G-A/G-A haplotype at rs3864004 and rs4135385 positions in patients with HCC than in chronic HBV carriers without HCC (P = 0.042). The AXIN1 rs1805105 T > C SNP was associated with small tumor size and early tumor stage and the WNT2 rs39315 G allele was associated with advanced tumor stage in HCC. In Kaplan–Meier analysis, carriers of the AXIN1 rs214252 C allele showed longer survival than those with the TT genotype (P = 0.020). In multivariate Cox regression analysis, absence of CTNNB1 haplotype A-A at rs3864004 and rs4135385 positions and advanced tumor stage were independent poor predictors of patient survival in patients with HCC. Conclusion These findings suggest that the genetic polymorphisms in CTNNB1 gene might affect tumor development and survival in patients with HBV-associated HCC.

Although the molecular mechanisms underpinning hepatocellular carcinoma (HCC) are unknown, gene copy number and associated mRNA expression changes are frequently reported. Comparative genomic hybridization arrays spotted with 4041 bacterial artificial chromosome clones were used to assess copy number changes in 45 HCC tissues. Seventy more HCC tissues were used to validate candidate genes by using western blots and immunohistochemistry. A total of 259 clones were associated with copy number changes that significantly differed between normal liver and HCC samples. The chromosomal region 1q32.1 containing the nuclear casein kinase and cyclin-dependent kinase substrate 1 (NUCKS1) gene was associated with tumor vascular invasion. Western blot analysis demonstrated that NUCKS1 was up-regulated in 37 of 70 (52.8%) HCC tissues compared with adjacent non-tumor tissues, and over-expressed in a vast majority of HCCs (44/52, 84.6%) as determined by immunohistochemical staining. Furthermore, immunostaining of both NUCKS1 and glypican-3 improved the diagnostic prediction of HCC. Knock-down of NUCKS1 by siRNA implied the decrease in cell viability of the Hep3B cell line and reduced tumor formation in a xenograft mouse model. NUCKS1 was identified as a potential oncogene at chromosomal 1q32.1 in patients with HCC, and it might be a valuable immunodiagnostic marker for HCC.

A recent genome-wide association study (GWAS) for hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) identified two loci (rs7574865 in STAT4 and rs9275319 in HLA-DQ) in a Chinese population. We attempted to replicate the associations between the two SNP loci and the risk of HCC in a Korean population. The rs7574865 in STAT4 and rs9275319 in HLA-DQ were genotyped in a total of 3838 Korean subjects composed of 287 HBV-related hepatocellular carcinoma patients, 671 chronic hepatitis B virus (CHB) patients, and 2880 population controls using TaqMan genotyping assay. Gene expression was measured by microarray. A logistic regression analysis revealed that rs7574865 in STAT4 and rs9275319 in HLA-DQ were associated with the risk of CHB (OR = 1.25, P = 0.0002 and OR = 1.57, P= 1.44 × 10(-10), respectively). However, these loci were no association with the risk of HBV-related HCC among CHB patients. In the gene expression analyses, although no significant differences in mRNA expression of nearby genes according to genotypes were detected, a significantly decreased mRNA expression in HCC subjects was observed in STAT4, HLA-DQA1, and HLA-DQB1. Although the genetic effects of two HCC susceptibility loci were not replicated, the two loci were found to exert susceptibility effects on the risk of CHB in a Korean population. In addition, the decreased mRNA expression of STAT4, HLA-DQA1, and HLA-DQB1 in HCC tissue might provide a clue to understanding their role in the progression to HCC.

We aimed to investigate the use of novel serum biomarkers for predicting the recurrence and survival of patients with hepatitis B virus (HBV)-related early hepatocellular carcinoma (HCC) after hepatic resection or radiofrequency ablation (RFA).One hundred and five patients with HBV-related HCC, who fulfilled the Milan criteria without vascular invasion and underwent hepatic resection or RFA, were followed-up for a median duration of 52months. Pretreatment serum concentrations of 16 cytokines including interleukin-6 (IL-6) were measured by using a Luminex 200 system. The measured serum cytokines and several clinical factors were analyzed retrospectively.Univariate analysis showed that patients with lower pretreatment serum levels of IL-10, IL-6, monocyte chemoattractant protein-1, and tumor necrosis factor-α had significantly shorter disease-free survival (DFS) than those with higher levels. Multivariate analysis revealed that a low serum IL-6 level (⩽33.00pg/mL; hazard ratio [HR]=5.39; 95% confidence interval [CI]=1.27-22.93; P=0.022), low platelet count (100×10(9)/L; HR=2.23; 95% CI=1.28-3.89; P=0.005), and low serum albumin level (⩽3.5g/L; HR=2.26; 95% CI=1.28-3.97; P=0.005) had a negative prognostic impact on DFS. In the analysis for overall survival, a low serum platelet level (100×10(9)/L; HR=2.80; 95% CI=1.31-5.99; P=0.008) and multiple tumor (⩾2; HR=4.05; 95% CI=1.56-10.48; P=0.004) showed a negative prognostic impact on the overall survival.A low serum IL-6 level is, in addition to low platelet count and low serum albumin level, an independent prognostic factor for DFS in patients with HBV-related early HCC who underwent hepatic resection or RFA with curative intention.

Background In some patients with severe tricuspid regurgitation (TR) who undergo tricuspid annuloplasty (TAP), significant remnant TR is detected early after TAP but diminishes after long-term follow-up. We sought to investigate the outcome of significant residual TR early after TAP and the predictors for late improvement of TR. Methods A total of 58 consecutive patients presenting with moderate to severe TR early (5.7 ± 2.0 days) after TAP and before discharge were enrolled in this study. Echocardiography was repeated for 32.3 ± 28.6 months after TAP, and improvements in TR were defined as mild or less TR. Clinical data and echocardiographic studies were retrospectively analyzed. Results Twenty-nine (50%) patients showed late improvement in TR during follow-up. Multivariate Cox regression analysis revealed that tricuspid valve (TV) tenting height measured early after TAP ( P = 0.020) and execution of the Maze procedure with TAP ( P = 0.049) were independent predictors for late improvement of significant early remnant TR. The rates of late TR improvement were higher in patients with an early postoperative TV tenting height ≥ 9.1 mm ( P = 0.026) and in patients who underwent a Maze procedure ( P = 0.033) than in other groups of patients. Conclusions Half of patients with significant remnant TR early after TAP show late improvement in TR. Evaluation of a combined Maze procedure and TV tenting height early after TAP will help identify patients for whom repeated TV surgery may be deferred.

We investigated flexible amorphous InGaZnO ( a -IGZO) thin film transistors (TFTs) on a polyimide (PI) substrate by using organic/inorganic hybrid gate dielectrics of poly-4vinyl phenol (PVP) and ultrathin Al 2 O 3 . IGZO TFTs were fabricated with hybrid PVP/Al 2 O 3 gate dielectrics having Al 2 O 3 layers of different nanoscale thicknesses, which were deposited by atomic layer deposition (ALD). The electrical characteristics of the TFTs with the organic/inorganic hybrid gate dielectrics were measured after cyclic bending up to 1,00,000 cycles at the bending radius of 10 mm. The ultrathin Al 2 O 3 layer in the hybrid gate dielectrics improved the mechanical flexibility and protected the organic gate dielectric against damage during the sputter deposition of the IGZO layer. Finite elements method (FEM) simulations along with the structural characterization of the cyclically bent device showed the importance of optimizing the thickness of the Al 2 O 3 layer in the hybrid gate dielectrics to obtain mechanically stable and flexible a -IGZO TFTs.

Ameloblastoma is the most frequent odontogenic epithelial tumor in the jaw. Though ameloblastoma belongs to benign odontogenic tumors, it exhibits a locally aggressive behavior with high recurrence rate. However, molecular markers predicting the recurrence have not been reported yet. The aim of this study was to find the prognostic markers in ameloblastoma. To detect apoptosis-related genes showing difference of expression level between ameloblastomas and normal oral tissues, the public database was analyzed. As results, OPG and Bcl-2 were identified as 2 most upregulated genes in ameloblastomas. To confirm public database analysis, in vitro study was conducted by use of AM-1 cell line. AM-1 cells expressed higher level of OPG and Bcl-2, compared with normal human epidermal keratinocytes (HEK). Exposing AM-1 cells to various environmental factors during culture in the 3-dimensional collagen gels were increased level of OPG and Bcl-2 than monoculture. To evaluate tumor-forming properties of AM-1 cells, subrenal capsule assay was conducted using AM-1 cells with hTERT-hNOF. As results, tumor formation were observed in 3 weeks, in which OPG and Bcl-2 expression was identified. To evaluate whether OPG and Bcl-2 regulates cell viability and apoptosis in AM-1 cells, siRNA transfection was conducted. As results, the knockdown of OPG and Bcl-2 reduced the cell viability and promoted the apoptosis of AM-1 cells. Knockdown of OPG and Bcl-2 decreased tumorigenesis. Eighty-nine cases of ameloblastomas were used for this study. Recurrence rate was 20.2%. Then, to validate whether these genes are associated to recurrence in ameloblastomas, immuno-histochemistry were performed. Each positivity classified 2 group by appropriate scoring system, low and high expression. The OPG and Bcl-2 expression was significantly associated with recurrence in conservative treatment group. These studies indicate that OPG and Bcl-2 status were independent predictive factors for recurrence.

Objectives The accuracies of biomarkers checked in the hepatic vein (HV) and peripheral vein (PV) were compared in the prediction of advanced fibrosis (AF) of liver. Methods Patients with chronic viral hepatitis (n = 101) who underwent hepatic venous pressure gradient, liver biopsy, and paired HV–PV samples (6 biomarkers: hyaluronic acid [HA], haptoglobin, matrix metalloproteinase-2 [MMP2], tissue inhibitor of metalloproteinases-1 [TIMP1], procollagen III N-terminal peptide [PIIINP], and apolipoprotein-A1 [Apo-A1]) were enrolled. Results Differences were displayed between the HV and PV in the predictive logit-models for predicting AF (− 3.13 + 0.017 × MMP2 − 0.019 × haptoglobin and − 0.270 + 0.007 × HA − 0.018 × haptoglobin, respectively). In the area under the receiver operating characteristic curves, PIIINP (0.74/0.68, p = 0.03), MMP2 (0.72/0.63, p = 0.04), HA (0.79/0.76, p = 0.94), Apo-A1 (0.56/0.48, p = 0.73), and predictive logit-model (0.81/0.78, p = 0.68) showed higher diagnostic value in the HV sample. Conclusions While most biomarkers were correlated better with hepatic fibrosis in HV than in PV, individually and in predictive logit-models, they were inadequate to determine the degree of advanced fibrosis.

Diabetes mellitus is a major risk factor for coronary artery disease (CAD) and for diffuse and progressive atherosclerosis. We evaluated the outcomes of drug-eluting stent (DES) placement and coronary artery bypass grafting (CABG) in 891 diabetic patients (489 for DES implantation and 402 for CABG) and 2,151 nondiabetic patients (1,058 for DES implantation and 1,093 for CABG) with multivessel CAD treated from January 2003 through December 2005 and followed up for a median 5.6 years. Outcomes of interest included death; the composite outcome of death, myocardial infarction (MI), or stroke; and repeat revascularization. In diabetic patients, after adjusting for baseline covariates, 5-year risk of death (hazard ratio 1.01, 95% confidence interval 0.77 to 1.33, p = 0.96) and the composite of death, MI, or stroke (hazard ratio 1.03, 95% confidence interval 0.80 to 1.31, p = 0.91) were similar in patients undergoing DES or CABG. However, rate of repeat revascularization was significantly higher in the DES group (hazard ratio 3.69, 95% confidence interval 2.64 to 5.17, p

Objectives The aims of this study were to determine the changes in serum histologic surrogate markers and to identify the serum markers predicting treatment response in patients with chronic hepatitis B (CHB) during entecavir treatment. Design and methods Sixty CHB patients who received entecavir for 12 months were included. We assessed serum markers of liver fibrosis and/or inflammation at baseline and after 12 months of entecavir treatment. Results The procollagen III N-terminal peptide (PIIINP) and TIMP1, MMP2, hyaluronic acid and cytokeratin 18 fragment levels were significantly decreased and the haptoglobin level was significantly increased from baseline after entecavir treatment. Multivariate analysis identified PIIINP (P = 0.028) and the initial virologic response (P = 0.019) as independent predictors of HBeAg loss. Conclusion During entecavir treatment, most serum markers of liver fibrosis and inflammation improved in patients with CHB. The PIIINP level at baseline and the initial virologic response are independent predictors of HBeAg loss.

The runt-domain transcription factor Runx3 plays crucial roles during development such as regulating gene expression. It has been shown that Runx3 is involved in neurogenesis, thymopoiesis and functions like a tumor suppressor. Runx3 null mouse die soon after birth as a result of multiple organ defects. Runx3 null mouse lung shows an abnormal phenotype and loss of Runx3 induced remodeling in the lung. Interestingly, lung adenocarcinoma is observed in Runx3 heterozygous mice at 18 months of age. During lung development various cellular and molecular events occur such as cell proliferation, cell death, differentiation and epithelial-mesenchymal transition (EMT). To understand the specific lethal events in Runx3 null mice, we examined cellular and molecular networks involved in EMT, and EMT inducers were quantified by RT-qPCR during lung development. Excessive EMT was observed in lungs at PN1 day in Runx3 null mice and PN18 months in Runx3 heterozygous mice. Pharmacologic inhibition of EMT was used to curb tumor progression. In this study, U0126 was injected to pregnant mouse for inhibition of pERK signaling. After U0126 treatment, life spans of newborn mice were increased and lung hyperplasia was partially rescued by down-regulated cell proliferation and EMT. Our data suggest that Runx3 is involved in crucial regulation of alveolar differentiation and tumor suppression in developing mouse lung.

Objectives The goal of the study was to clarify whether new biomarkers independently contribute to the diagnosis of cirrhosis. Design and methods A total of 142 consecutive patients with HBeAg positive chronic hepatitis who underwent liver biopsy were recruited. The Cirrhosis Score (CS)-1 was derived from routine laboratory data only. The CS-2 was calculated using all correlates obtained from both routine laboratory data and 7 new biomarkers. Results A comparison of the area under the receiver operating characteristic (ROC) curve between CS-1 [0.84 (95% CI, 0.74 to 0.94)] and CS-2 [0.86 (0.78 to 0.95)] showed no superior diagnostic accuracy of CS-2 over CS-1 ( p = 0.24). Conclusions None of the new biomarkers had value in addition to readily available laboratory data for differentiating cirrhosis from HBeAg positive chronic hepatitis B.

We evaluate the rate of decay for solutions to second order parabolic equations, which vanish on the boundary, while the right-hand side is allowed to be unbounded. Our approach is based on a special growth lemma, and it works for both divergence and non-divergence equations, in domains satisfying a general “exterior measure condition” (A). The result for elliptic case is published in Cho and Safonov (2007) [2] .

Genetic variants of the human branched chain alpha-keto acid dehydrogenase, E1-beta subunit (BCKDHB) gene were identified and they have been associated with premature ovarian failure (POF). Reconstructed haplotype from these variants was also associated with POF.

Tooth development is regulated by reciprocal interactions between epithelial and mesenchymal cells. Several morphological studies suggest that growth factors secreted from these cells regulate tooth development. These growth factors induce undifferentiated cells in the tooth germ to differentiate into tooth-forming cells. Many growth factors are reportedly expressed in the developing tooth, but the key molecule underlying tooth root development is still unknown. There is a considerable amount of data on the expression and function of bone morphogenetic proteins (BMPs) during tooth development, but the relationship between BMPs and tooth root development has not been analyzed extensively. This prompted us to examine the expression patterns of BMP4 and BMP receptors (BMPRs) at the apical region of the tooth germ during mouse tooth root development. We found that BMP4 was strictly expressed in the apical mesenchyme, and that BMPRs were localized in Hertwig's epithelial root sheath (HERS). We also investigated the possible roles of BMP4 in HERS during the early stage of tooth root development. Our organ-culture results indicated that BMP4 regulates HERS formation via harmonious interactions with its own antagonist, noggin, by preventing elongation and maintaining cell proliferation. BMP4 may therefore be useful in various tissue-engineering applications as a regulator of tooth root formation.

Background Insertion of self-expandable metallic stents (SEMS) can provide rapid relief of malignant colorectal obstruction and can be used as a palliative treatment or as a bridge to surgery. A SEMS can be classified as an uncovered or covered stent. Both types of stents have their own merits and demerits. Objective The objectives of this study were to compare success rates, durability, and complication rates of uncovered and covered stent groups of malignant colorectal obstruction. Designs and Setting A nonrandomized prospective, single-center study. Methods We studied 80 patients with malignant colorectal obstruction: colon cancer in 70 patients, metastatic lesion of advanced gastric cancer in 8 patients, and cervix cancer in 2 patients. Insertion of uncovered stents was attempted in 39 patients (before surgery in 20, palliative in 19), and covered stents were used in 41 (before surgery in 23, palliative in 18). Intervention The stent was inserted into the obstructive sites for preoperative or palliative purposes by using the through-the-scope method. After stent insertion, the patients had regular follow-ups, either as clinical checkups or telephone interviews. Main Outcome Measurement Insertion success rate, durability, and complication rate according to stent type. Results Technical and clinical success rates of uncovered and covered stents were not different (100%; 95.1%, P > .05, 100%; 97.4%, P > .05). The early stent migration rate was not different in both groups. The late stent migration was more common in the covered stent group than the uncovered stent group (0% vs 40%, respectively, P = .005). Loss of stent function during the long-term follow-up period was more frequent in the covered stent group than in the uncovered stent group (18.8% vs 60%, respectively, P = .018). Limitation This was a small-sized, nonrandomized, prospective, single-center study. Confirmation of large-scale, multicenter, randomized, prospective outcome is required. Conclusions Insertion of either an uncovered or covered stent is similarly an effective treatment modality of malignant colorectal obstruction for preoperative purposes. However, there are no advantages of covered stents over uncovered stents during the follow-up period in the palliative purpose.

The enamel knot (EK), which is located in the center of bud and cap stage tooth germs, is a transitory cluster of non-dividing epithelial cells. The EK acts as a signaling center that provides positional information for tooth morphogenesis and regulates the growth of tooth cusps by inducing secondary EKs. The morphological, cellular, and molecular events leading to the relationship between the primary and secondary EKs have not been described clearly. This study investigated the relationship between the primary and secondary EKs in the maxillary and mandibular first molars of mice. The location of the primary EK and secondary EKs was investigated by chasing Fgf4 expression patterns in tooth germ at some intervals of in vitro culture, and the relationship between the primary EK and secondary EK was examined by tracing the primary EK cells in the E13.5 tooth germs which were frontally half sliced to expose the primary EK. After 48 hr, the primary EK cells in the sliced tooth germs were located on the buccal secondary EKs, which correspond to the future paracone in maxilla and protoconid in mandible. The Bmp4 expression in buccal part of the dental mesenchyme might be related with the lower growth in buccal epithelium than in lingual epithelium, and the Msx2 expressing area in epithelium was overlapped with the enamel cord (or septum) and cell dense area. The enamel cord might connect the primary EK with enamel navel to fix the location of the primary EK in the buccal side during the cap to bell stages. Overall, these results suggest that primary EK cells strictly contribute to form the paracone or protoconid, which are the main cusps of the tooth in the maxilla or mandible.

Mice and rats, two species of rodents, show some dental similarities such as tooth number and cusp number, and differences such as tooth size and cusp size. In this study, the tooth size, tooth number, cusp size and cusp number, which are four major factors of the tooth patterning, were investigated by the heterospecific recombinations of tissues from the molar tooth germs of mice and rats. Our results suggest that the dental epithelium and mesenchyme determine the cusp size and tooth size respectively and the cusp number is co-regulated by the tooth size and cusp size. It is also suggested that the mesenchymal cell number regulates not the tooth size but the tooth number. The relationships among these factors in tooth patterning including micropatterning (cusp size and cusp number) and macropatterning (tooth size and tooth number) were analyzed in a reaction diffusion mechanism. Key molecules determining the patterning of teeth remains to be elucidated for controlling the tooth size and cusp size of bioengineered tooth.

The enamel knot (EK), which is a transient signaling center in the tooth germ, regulates both the differential growth of the dental epithelium and the tooth shape. In this study, the regeneration of the EK was evaluated. The EK regions were removed from the E14 and E16 dental epithelia, and the remaining epithelia were recombined with their original dental mesenchymes. All these tooth germs could develop into calcified teeth after being transplanted into the kidney capsule for 3 weeks. One primary EK was regenerated earlier, and two or three secondary EKs were regenerated later in culture. When simply recombined without removing the EK, the tooth germ, which had four secondary EKs and four cuspal areas of the dental papilla, generated one primary EK first and subsequent secondary EKs. These results indicate that the patterning of the EK in all tooth germs always starts from a primary EK independent of the direct epithelial or mesenchymal control. This suggests that neither the dental epithelium nor the dental mesenchyme can dictate the pattern or number of the EK formation, but the interaction between the dental epithelium and the dental mesenchyme is essential for the regeneration and patterning of the EKs.

Few data are available on the long-term clinical outcome of patients with acute myocardial infarction (AMI) complicated by propound cardiogenic shock or cardiac arrest who receive extracorporeal membrane oxygenation (ECMO) assisted primary percutaneous coronary intervention (PCI). This study

Objective: To quantify mitochondrial DNA using real-time PCR in women with premature ovarian failure (POF) and a control group. Design: Prospective study. Setting: Genome Research Center for Reproductive Medicine and Infertility, Korea Ministry of Health & Welfare. Patient(s): Thrity patients with POF and 30 control individuals. Intervention(s): The mitochondrial DNA content was quantified using real-time PCR. The effectiveness of the assay was determined by relative quantification using the comparative threshold cycle (C T ) method. Main Outcome Measure(s): Relative quantification of mitochondrial DNA content. Result(s): The mitochondrial DNA content was significantly lower in the POF group than in the control group (0.58 ± 0.38 vs. 1.15 ± 0.67; P

Despite evidence that Helicobacter pylori (H. pylori) infection is closely associated with stress in gastric ulcer patients, the underlying mechanism why ulcer recurrence after stress is augmented especially in patients with H. pylori remains unknown. In this study, we found that oxidative stress played a critical role in the augmented mucosal damage provoked by water immersion restraint stress (WIRS) in H. pylori infection and that an antioxidant, alpha-tocopherol, could ameliorate the aggravation of stress-associated gastric mucosal damage. Two hundred forty SD rats were divided into two groups according to H. pylori inoculation, and after 24 weeks of H. pylori infection, the water immersion restraint stress was imposed for 30, 120, or 480 min, respectively. To evaluate the therapeutic effects of an antioxidant, alpha-tocopherol was administrated 40 mg/kg daily prior to imposing WIRS. Remarkably increased hemorrhagic lesions and bleeding indexes were noted in the H. pylori-infected group with statistical significance (P < 0.05) compared to the noninfected group at the same duration of WIRS. Significantly higher oxidative stress documented by iNOS, lipid peroxides, and GSH level was detected in gastric homogenates of the H. pylori-infected group. Proteomic analysis using 2-dimensional electrophoresis showed a decrease of HSP27 and other chaperone proteins. alpha-Tocopherol pretreatment significantly prevented the gastric mucosal damage, caused by WIRS in the presence of H. pylori. alpha-Tocopherol induced HSP27 expression, which was well correlated with downregulation of iNOS mRNA. Conclusively, the presence of H. pylori caused significant deterioration of stress-induced gastric mucosal lesions through increased oxidative stress and thus antioxidant treatment such as alpha-tocopherol protected the gastric injuries.

The aim of this study was to investigate the effect of interferon-α (IFN-α) on the occurrence of mutations in the precore region of the hepatitis B virus (HBV). We studied 24 patients with chronic hepatitis B; 11 were non-responders to IFN therapy and 13 were untreated patients. After HBV DNA extraction from serum, nested PCR of the precore region and direct sequencing was performed. Among the baseline sera of 24 patients, three types of mutation G to A at nucleotide 1896 (A1896), 1899 (A1899), and A to T at nucleotide 1846(T1846) were found in 12 patients. The prevalence of A1896 was 45.8% (11/24), A1899 8.3% (2/24), and T1846 12.5% (3/24), respectively. A1896 was found in six out of 18 HBeAg-positive patients and in five out of six anti-HBE-positive patients. During the 1 year follow-up period, sequence changes were found in five out of 13 untreated patients: A wild-type strain was replaced by a mutant A1896 strain in two patients; mixed viral populations of wild-type strains and mutant A1896 strains were replaced by a mutant A1896 strain in one patient; and a mutant A1896 strain was replaced by a wild-type strain in two patients. In contrast, ten out of 11 non-responders had no changes in the precore region after therapy during follow-up period. A shift from predominantly wild-type strains to predominantly mutant A1896 strains was found in the remaining one non-responder. In conclusion, sequence changes in the precore region occur frequently during the course of chronic hepatitis B virus infection. IFN-α therapy may decrease the appearance of mutations in the precore region in non-responders.

In the immune system, histamine is known to suppress cytotoxic T-lymphocytes and nitrogen induced lymphocyte thymidine uptake, down-regulate some cytokines, and activate suppressor T-lymphocytes, and in the gastrointestinal system, histamine was reported to have trophic effects on gastrointestinal epithelial cells. Enhanced rates of cell proliferation by histamine are implicated in the pathogenesis. This study was designed since there is a lack of comparative data about the cell proliferations of histamine-2 receptor antagonist (H2-RA), cimetidine, ranitidine, and famotidine, in gastric cancer. KATO-III and AGS cell lines were used in this experiment. The concentrations of the histamine and cimetidine were 10(-5)-10(-8) M, respectively and those of ranitidine and famotidine were 10(-6)-10(-9)M, respectively. Cell proliferation after drug treatment was evaluated by direct cell counting, [3H]thymidine incorporation, and MTT assay. Activities of ornithine decarboxylase (ODC), a rate limiting enzyme in polyamine synthesis, were measured after each drug treatment. Protein kinase A, a cAMP-dependent protein kinase system, was assayed using [alpha-32P]ATP. Histamine showed statistically significant cell proliferating effects in a dose-dependent manner (P < 0.001), the maximal effect in 10(-5) M concentration. ODC activities were increased in accordance with the increment of cell numbers after histamine treatment. Cimetidine reversed the histamine-stimulated cell proliferation significantly, the maximal effect in 10(-5) M concentration (P < 0.01). Although ranitidine showed the tendency to attenuate the cell proliferation dose-dependently, but without statistical significance, famotidine did not show such an effect at all. cAMP-dependent protein kinase activities were significantly increased following 10(-5) M histamine treatment, also reversed significantly by cimetidine co-administration (P < 0.01). Beneficial clinical outcomes could be anticipated from cimetidine treatment in patients with gastric cancer by anti-proliferating effects against gastric cancer cells. These effects of H2-RA are likely to be mediated by specific interactions at the H2-receptor.

200 CODING MICROSATELLITE INSTABILITY AFFECTING THE GENES HT001, PTHL3, SEC63, TAF1B AND TGFBR2 IN A LYNCH-SYNDROME ASSOCIATED HEPATOCELLULAR CARCINOMA M. Casper, M. Kloor, M. von Knebel-Doeberitz, R.M. Bohle, J. Raedle, F. Lammert, V. Zimmer. Department of Medicine II, Saarland University Hospital, Homburg, Applied Tumour Biology, Institute of Pathology, University Hospital Heidelberg, Heidelberg, Institute of Pathology, Saarland University Hospital, Homburg, Department of Medicine III, Westpfalz Hospital, Kaiserslautern, Germany E-mail: markus.casper@uks.eu

P64 THE ULTRACONSERVED NON CODING RNA UC.158 IS DOWNSTREAM OF THE WNT/b-CATENIN PATHWAY IN LIVER CANCERS V. Paulus-Hock, A. Lampis, G. Ferrari, L. Boulton, R. Guest, D. Athineos, T. Jamieson, A. Veronese, R. Visone, R. Evans, G.J. Feng, T. Dale, M. Negrini, S. Forbes, T. Patel, O. Sansom, N. Valeri, C. Braconi. Institute of Cancer Sciences, University of Glasgow, Glasgow, Division of Molecular Pathology, Institute of Cancer Research, London, Scottish Centre for Regenerative Medicine, MRC Centre for Regenerative Medicine, Edinburgh, Beatson Institute for Cancer Research, Glasgow, United Kingdom; Aging Research Center, University of Chieti, Chieti, Italy; School of Biosciences, University of Cardiff, Cardiff, United Kingdom; University of Ferrara, Ferrara, Italy; Mayo Clinc, Jacksonville, FL, United States; Division of Cancer Therapeutics, Institute of Cancer Research, London, United Kingdom E-mail: chiarabraconi@gmail.com