Oncogenic CagA Promotes Gastric Cancer Risk via Activating ERK Signaling Pathways: A Nested Case-Control Study

Background: CagA cellular interaction via activation of the ERK signaling pathway may be a starting point in the development of gastric cancer. This study aimed to evaluate whether genes involved in ERK downstream signaling pathways activated by CagA are susceptible genetic markers for gastric cancer. Methods: In the discovery phase, a total of 580 SNPs within +/-5 kbp of 30 candidate genes were genotyped to examine an association with gastric cancer risk in the Korean Multi-center Cancer Cohort (100 incident gastric cancer case-control sets). The most significant SNPs (raw or permutated p value??0.02) identified in the discovery analysis were re-evaluated in the extension phase using unconditional logistic regression model (400 gastric cancer case-control sets). Combined analyses including pooled-and meta-analysis were conducted to summarize all the results. Results: 24 SNPs in eight genes (ERK, Dock180, C3G, Rap1, Src, CrkL, Mek and Crk) were significantly associated with gastric cancer risk in the individual SNP analyses in the discovery phase (p??0.05). In the extension analyses, ERK rs5999749, Dock180 rs4635002 and C3G rs7853122 showed marginally significant gene-dose effects for gastric cancer. Consistently, final combined analysis presented the SNPs as significantly associated with gastric cancer risk (OR = 1.56, [95% CI: 1.19-2.06], OR = 0.61, [95% CI: 0.43-0.87], OR = 0.59, [95% CI: 0.54-0.76], respectively). Conclusions: Our findings suggest that ERK rs5999749, Dock180 rs4635002 and C3G rs7853122 are genetic determinants in gastric carcinogenesis

Genetic Susceptibility on CagA-Interacting Molecules and Gene-Environment Interaction with Phytoestrogens: A Putative Risk Factor for Gastric Cancer

OBJECTIVES: To evaluate whether genes that encode CagA-interacting molecules (SRC, PTPN11, CRK, CRKL, CSK, c-MET and GRB2) are associated with gastric cancer risk and whether an interaction between these genes and phytoestrogens modify gastric cancer risk. METHODS: In the discovery phase, 137 candidate SNPs in seven genes were analyzed in 76 incident gastric cancer cases and 322 matched controls from the Korean Multi-Center Cancer Cohort. Five significant SNPs in three genes (SRC, c-MET and CRK) were re-evaluated in 386 cases and 348 controls in the extension phase. Odds ratios (ORs) for gastric cancer risk were estimated adjusted for age, smoking, H. pylori seropositivity and CagA strain positivity. Summarized ORs in the total study population (462 cases and 670 controls) were presented using pooled- and meta-analysis. Plasma concentrations of phytoestrogens (genistein, daidzein, equol and enterolactone) were measured using the time-resolved fluoroimmunoassay. RESULTS: SRC rs6122566, rs6124914, c-MET rs41739, and CRK rs7208768 showed significant genetic effects for gastric cancer in both the pooled and meta-analysis without heterogeneity (pooled OR = 3.96 [95% CI 2.05-7.65], 1.24 [95% CI = 1.01-1.53], 1.19 [95% CI = 1.01-1.41], and 1.37 [95% CI = 1.15-1.62], respectively; meta OR = 4.59 [95% CI 2.74-7.70], 1.36 [95% CI = 1.09-1.70], 1.20 [95% CI = 1.00-1.44], and 1.32 [95% CI = 1.10-1.57], respectively). Risk allele of CRK rs7208768 had a significantly increased risk for gastric cancer at low phytoestrogen levels (p interaction<0.05). CONCLUSIONS: Our findings suggest that SRC, c-MET and CRK play a key role in gastric carcinogenesis by modulating CagA signal transductions and interaction between CRK gene and phytoestrogens modify gastric cancer risk

Effect of fluoroethylene carbonate additive on interfacial properties of silicon thin-film electrode

A silicon thin-film electrode (thickness= 200nm) is prepared by E-beam evaporation and deposition on copper foil. The electrochemical performance of a lithium/silicon thin-film cell is investigated in ethylene carbonate/diethyl carbonate/1.3 M LiPF6 with and without 3 wt.% fluoroethylene carbonate (FEC). The addition of FEC remarkably improves discharge capacity retention and coulombic efficiency. The surface morphology and chemical composition of the solid electrolyte interphase (SEI) formed on the surface of the silicon thin-film electrode after cycling are studied through scanning electron microscopy and X-ray photoelectron spectroscopy analysis. A smoother and more stable SEI layer structure is generated by the introduction of the FEC additive to the electrolyte.close16913

Association between Urine Creatinine Excretion and Arterial Stiffness in Chronic Kidney Disease: Data from the KNOW-CKD Study

Background/Aims: Previous studies have shown that low muscle mass is associated with arterial stiffness, as measured by pulse wave velocity (PWV), in a population without chronic kidney disease (CKD). This link between low muscle mass and arterial stiffness may explain why patients with CKD have poor cardiovascular outcomes. However, the association between muscle mass and arterial stiffness in CKD patients is not well known. Methods: Between 2011 and 2013, 1,529 CKD patients were enrolled in the prospective Korean Cohort Study for Outcome in Patients With Chronic Kidney Disease (KNOW-CKD). We analyzed 888 participants from this cohort who underwent measurements of 24-hr urinary creatinine excretion (UCr) and brachial-ankle PWV (baPWV) at baseline examination. The mean of the right and left baPWV (mPWV) was used as a marker of arterial stiffness. Results: The baPWV values varied according to the UCr quartile (1,630±412, 1,544±387, 1,527±282 and 1,406±246 for the 1st to 4th quartiles of UCr, respectively, PConclusion: Low muscle mass estimated by low UCr was associated high baPWV in pre-dialysis CKD patients in Korea. Further studies are needed to confirm the causal relationship between UCR and baPWV, and the role of muscle mass in the development of cardiovascular disease in CKD

Rumen fermentation and performance of Hanwoo steers fed total mixed ration with Korean rice wine residue

Abstract Background This study was conducted to evaluate the effects of adding Korean rice wine residue (RWR) in total mixed ration (TMR) on in vitro ruminal fermentation and growth performance of growing Hanwoo steers. Methods For in vitro fermentation, the experimental treatments were Control (Con: 0 % RWR + TMR), Treatment 1 (T1: 10 % RWR + TMR), and Treatment 2 (T2: 15 % RWR + TMR). The rumen fluid was collected from three Hanwoo steers and mixed with buffer solution, after which buffered rumen fluid was transferred into serum bottles containing 2 g dry matter (DM) of TMR added with or without RWR. The samples were then incubated for 0 h, 12 h, 24 h, or 48 h at 39 °C and 100 rpm. For the in vivo experiment, 27 Hanwoo steers (6 months old) with an average weight of 196 ± 8.66 kg were subjected to a 24-week feeding trial. The animals were randomly selected and equally distributed into three groups. After which the body weight, feed intake and blood characteristics of each group were investigated. Results The pH of the treatments decreased significantly relative to the control during the 12 h of incubation. Total gas production and ammonia nitrogen (NH3-N) was not affected by RWR addition. The total volatile fatty acid (VFA) was lower after 24 h of incubation but at other incubation times, the concentration was not affected by treatments. Feed cost was 8 % and 15 % lower in T1 and T2 compared to control. Blood alcohol was not detected and a significant increase in total weight gain and average daily gain were observed in Hanwoo steers fed with RWR. Conclusion Overall, the results of this study suggest that TMR amended with 15 % RWR can be used as an alternative feed resource for ruminants to reduce feed cost

Medical History and Lifestyle Factors Contributing to Epstein-Barr Virus-Associated Gastric Carcinoma and Conventional Gastric Carcinoma in Korea

Background: Epstein-Barr virus-associated gastric carcinoma (EBV-GC) has been characterized as a special gastric cancer subset. Lifestyle and other major factors that may contribute to EBV-GC and non-EBV-GC were investigated here. Materials and Methods: A total of 247 patients with gastric cancer were interviewed, clinicopathological information was retrieved, and in situ hybridization was performed for EBV-encoded small RNAs. Results: There were 18 EBV-GC (male:female=17:1) and 229 non-EBV-GC patients (male:female=161:68). A history of previous gastric ulcer was associated with EBV-GC, whereas frequent and heavy alcohol drinking was related to non-EBV-GC. Additionally, skipping breakfast was correlated with EBV-GC in male patients. Other factors, such as body mass index, history of gastritis, Helicobacter pylori infection, ABO blood type, family history of gastric cancel; education level, marital status, occupation, family status, and dietary factors, showed no significant differences between EBV-GC and non-EBV-GC. Conclusion: A history of gastric ulcer, reflecting chemical injury to the stomach mucosa, appears to contribute to development of EBV-GC. Alcohol drinking was more related to non-EBV-GC than EBV-GC.LEE JH, 2009, ANTICANCER RES, V24, P354Ladeiras-Lopes R, 2008, CANCER CAUSE CONTROL, V19, P689, DOI 10.1007/s10552-008-9132-yLiu C, 2008, NUTR REV, V66, P237, DOI 10.1111/j.1753-4887.2008.00029.xLima VP, 2008, WORLD J GASTROENTERO, V14, P884, DOI 10.3748/wjg.14.884Akiba S, 2008, CANCER SCI, V99, P195, DOI 10.1111/j.1349-7006.2007.00674.xKim HY, 2007, KOREAN J FOOD SCI AN, V27, P60Luo B, 2006, WORLD J GASTROENTERO, V12, P1842CAMPOS FI, 2006, ASIAN PAC J CANCER P, V7, P633Koriyama C, 2005, J EXP CLIN CANC RES, V24, P547Chan D, 2005, J RES PRACT INF TECH, V37, P267Sakuma K, 2005, INT J CANCER, V115, P93, DOI 10.1002/ijc.20903PLUMMER M, 2004, IARC SCI PUBL, V157, P311Chang MS, 2003, J PATHOL, V199, P447, DOI 10.1002/path.1302Chang MS, 2001, PATHOL RES PRACT, V197, P395Chang MS, 2000, HISTOPATHOLOGY, V37, P309Chang MS, 2000, PATHOL INT, V50, P486Wu MS, 2000, GASTROENTEROLOGY, V118, P1031*NAT I ALC AB ALC, 2000, 10 NAT I ALC AB ALC, P429*WHO, 2000, AS PAC PERSP RED OB, P8Carson TA, 1999, CEREAL FOOD WORLD, V44, P414Galanis DJ, 1998, INT J EPIDEMIOL, V27, P173*INT AG RES CANC, 1997, IARC MON EV CARC RIS, V70, P47Hansson LE, 1996, NEW ENGL J MED, V335, P242YAMAMOTO N, 1994, CANCER, V74, P805TOKUNAGA M, 1993, AM J PATHOL, V143, P1250BURKE AP, 1990, MODERN PATHOL, V3, P377