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Results: 1 to 10 of 82

Publication Record


Gastroesophageal Reflux Induces Protein Adducts in the Esophagus.
Caspa Gokulan R, Adcock JM, Zagol-Ikapitte I, Mernaugh R, Williams P, Washington KM, Boutaud O, Oates JA, Dikalov SI, Zaika AI
(2019) Cell Mol Gastroenterol Hepatol 7: 480-482.e7
MeSH Terms: Acetylcysteine, Animals, Benzylamines, Bile Acids and Salts, Cell Line, Cyclic N-Oxides, Esophagus, Gastroesophageal Reflux, Humans, Lipids, Mice, Spin Labels, Tumor Suppressor Protein p53
Added March 26, 2019
0 Communities
1 Members
0 Resources
13 MeSH Terms
Association Between Helicobacter pylori Exposure and Decreased Odds of Eosinophilic Esophagitis-A Systematic Review and Meta-analysis.
Shah SC, Tepler A, Peek RM, Colombel JF, Hirano I, Narula N
(2019) Clin Gastroenterol Hepatol 17: 2185-2198.e3
MeSH Terms: Eosinophilic Esophagitis, Esophagus, Helicobacter Infections, Helicobacter pylori, Humans, Immunomodulation
Show Abstract · Added March 3, 2020
BACKGROUND & AIMS - Previous or current infection with Helicobacter pylori (exposure) has been reported to protect against eosinophilic esophagitis (EoE), perhaps owing to H pylori-induced immunomodulation. However, findings vary. We performed a systematic review and meta-analysis of comparative studies to define the association between H pylori exposure and EoE more clearly.
METHODS - We searched 4 large databases to identify comparative clinical studies that included sufficient detail to determine the odds or risk of EoE (primary outcome) or esophageal eosinophilia (secondary outcome) among individuals exposed to H pylori (exposed) vs individuals who were tested and found to be unexposed. Estimates were pooled using a random-effects model. Meta-regression and sensitivity analyses were planned a priori. Studies were evaluated for quality, risk of bias, publication bias, and heterogeneity.
RESULTS - We analyzed 11 observational studies comprising data on 377,795 individuals worldwide. H pylori exposure vs nonexposure was associated with a 37% reduction in odds of EoE (odds ratio, 0.63; 95% CI, 0.51-0.78) and a 38% reduction in odds of esophageal eosinophilia (odds ratio, 0.62; 95% CI, 0.52-0.76). Fewer prospective studies found a significant association between H pylori exposure and EoE (P = .06) than retrospective studies. Effect estimates were not affected by study location, whether the studies were performed in pediatric or adult populations, time period (before vs after 2007), or prevalence of H pylori in the study population.
CONCLUSIONS - In a comprehensive meta-analysis, we found evidence for a significant association between H pylori exposure and reduced odds of EoE. Studies are needed to determine the mechanisms of this association.
Copyright © 2019 AGA Institute. Published by Elsevier Inc. All rights reserved.
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6 MeSH Terms
Trajectory optimized NUFFT: Faster non-Cartesian MRI reconstruction through prior knowledge and parallel architectures.
Smith DS, Sengupta S, Smith SA, Brian Welch E
(2019) Magn Reson Med 81: 2064-2071
MeSH Terms: Algorithms, Deglutition, Esophagus, Fourier Analysis, Humans, Hypopharynx, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Male, Mouth, Optic Nerve, Phantoms, Imaging, Programming Languages, Reproducibility of Results, Software, Whole Body Imaging
Show Abstract · Added April 10, 2019
PURPOSE - The non-uniform fast Fourier transform (NUFFT) involves interpolation of non-uniformly sampled Fourier data onto a Cartesian grid, an interpolation that is slowed by complex, non-local data access patterns. A faster NUFFT would increase the clinical relevance of the plethora of advanced non-Cartesian acquisition methods.
METHODS - Here we customize the NUFFT procedure for a radial trajectory and GPU architecture to eliminate the bottlenecks encountered when allowing for arbitrary trajectories and hardware. We call the result TRON, for TRajectory Optimized NUFFT. We benchmark the speed and accuracy TRON on a Shepp-Logan phantom and on whole-body continuous golden-angle radial MRI.
RESULTS - TRON was 6-30× faster than the closest competitor, depending on test data set, and was the most accurate code tested.
CONCLUSIONS - Specialization of the NUFFT algorithm for a particular trajectory yielded significant speed gains. TRON can be easily extended to other trajectories, such as spiral and PROPELLER. TRON can be downloaded at http://github.com/davidssmith/TRON.
© 2018 The Authors Magnetic Resonance in Medicine published by Wiley Periodicals, Inc. on behalf of International Society for Magnetic Resonance in Medicine.
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16 MeSH Terms
Activation of NADPH oxidases leads to DNA damage in esophageal cells.
Bhardwaj V, Gokulan RC, Horvat A, Yermalitskaya L, Korolkova O, Washington KM, El-Rifai W, Dikalov SI, Zaika AI
(2017) Sci Rep 7: 9956
MeSH Terms: Barrett Esophagus, Bile Acids and Salts, Cells, Cultured, DNA Damage, Epithelial Cells, Humans, NADPH Oxidase 1, NADPH Oxidase 2, Reactive Oxygen Species
Show Abstract · Added March 26, 2019
Gastroesophageal reflux disease (GERD) is the strongest known risk factor for esophageal adenocarcinoma. In the center of tumorigenic events caused by GERD is repeated damage of esophageal tissues by the refluxate. In this study, we focused on a genotoxic aspect of exposure of esophageal cells to acidic bile reflux (BA/A). Analyzing cells generated from patients with Barrett's esophagus and human esophageal specimens, we found that BA/A cause significant DNA damage that is mediated by reactive-oxygen species. ROS originate from mitochondria and NADPH oxidases. We specifically identified NOX1 and NOX2 enzymes to be responsible for ROS generation. Inhibition of NOX2 and NOX1 with siRNA or chemical inhibitors significantly suppresses ROS production and DNA damage induced by BA/A. Mechanistically, our data showed that exposure of esophageal cells to acidic bile salts induces phosphorylation of the p47 subunit of NOX2 and its translocation to the cellular membrane. This process is mediated by protein kinase C, which is activated by BA/A. Taken together, our studies suggest that inhibition of ROS induced by reflux can be a useful strategy for preventing DNA damage and decreasing the risk of tumorigenic transformation caused by GERD.
0 Communities
1 Members
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9 MeSH Terms
Prevention of DNA damage in Barrett's esophageal cells exposed to acidic bile salts.
Bhardwaj V, Horvat A, Korolkova O, Washington MK, El-Rifai W, Dikalov SI, Zaika AI
(2016) Carcinogenesis 37: 1161-1169
MeSH Terms: Acetophenones, Acids, Adenocarcinoma, Antioxidants, BRCA1 Protein, Barrett Esophagus, Bile Acids and Salts, Cell Line, Tumor, DNA Damage, DNA Repair, Esophageal Neoplasms, Gastric Acid, Gastroesophageal Reflux, Humans, Reactive Oxygen Species
Show Abstract · Added March 26, 2019
Esophageal adenocarcinoma (EA) is one of the fastest rising tumors in the USA. The major risk factor for EA is gastroesophageal reflux disease (GERD). During GERD, esophageal cells are exposed to refluxate which contains gastric acid frequently mixed with duodenal bile. This may lead to mucosal injury and Barrett's metaplasia (BE) that are important factors contributing to development of EA. In this study, we investigated DNA damage in BE cells exposed to acidic bile salts and explored for potential protective strategies. Exposure of BE cells to acidic bile salts led to significant DNA damage, which in turn, was due to generation of reactive oxygen species (ROS). We found that acidic bile salts induce a rapid increase in superoxide radicals and hydrogen peroxide, which were determined using electron paramagnetic resonance spectroscopy and Amplex Red assay. Analyzing a panel of natural antioxidants, we identified apocynin to be the most effective in protecting esophageal cells from DNA damage induced by acidic bile salts. Mechanistic analyses showed that apocynin inhibited ROS generation and increases the DNA repair capacity of BE cells. We identified BRCA1 and p73 proteins as apocynin targets. Downregulation of p73 inhibited the protective effect of apocynin. Taken together, our results suggest potential application of natural compounds such as apocynin for prevention of reflux-induced DNA damage and GERD-associated tumorigenesis.
© The Author 2016. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
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MeSH Terms
Comparative Risk Predictions of Second Cancers After Carbon-Ion Therapy Versus Proton Therapy.
Eley JG, Friedrich T, Homann KL, Howell RM, Scholz M, Durante M, Newhauser WD
(2016) Int J Radiat Oncol Biol Phys 95: 279-286
MeSH Terms: Breast, Breast Neoplasms, Carbon, Esophagus, Female, Heart, Heavy Ion Radiotherapy, Hodgkin Disease, Humans, Incidence, Linear Models, Lung, Neoplasms, Second Primary, Organs at Risk, Proton Therapy, Radiography, Radiotherapy Dosage, Radiotherapy Planning, Computer-Assisted, Relative Biological Effectiveness, Risk Assessment, Sensitivity and Specificity, Spinal Cord, Uncertainty
Show Abstract · Added March 30, 2020
PURPOSE - This work proposes a theoretical framework that enables comparative risk predictions for second cancer incidence after particle beam therapy for different ion species for individual patients, accounting for differences in relative biological effectiveness (RBE) for the competing processes of tumor initiation and cell inactivation. Our working hypothesis was that use of carbon-ion therapy instead of proton therapy would show a difference in the predicted risk of second cancer incidence in the breast for a sample of Hodgkin lymphoma (HL) patients.
METHODS AND MATERIALS - We generated biologic treatment plans and calculated relative predicted risks of second cancer in the breast by using two proposed methods: a full model derived from the linear quadratic model and a simpler linear-no-threshold model.
RESULTS - For our reference calculation, we found the predicted risk of breast cancer incidence for carbon-ion plans-to-proton plan ratio, , to be 0.75 ± 0.07 but not significantly smaller than 1 (P=.180).
CONCLUSIONS - Our findings suggest that second cancer risks are, on average, comparable between proton therapy and carbon-ion therapy.
Copyright © 2016 Elsevier Inc. All rights reserved.
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MeSH Terms
APE1-mediated DNA damage repair provides survival advantage for esophageal adenocarcinoma cells in response to acidic bile salts.
Hong J, Chen Z, Peng D, Zaika A, Revetta F, Washington MK, Belkhiri A, El-Rifai W
(2016) Oncotarget 7: 16688-702
MeSH Terms: Adenocarcinoma, Barrett Esophagus, Bile Acids and Salts, Cell Line, Tumor, Cell Survival, DNA Damage, DNA Repair, DNA-(Apurinic or Apyrimidinic Site) Lyase, Esophageal Neoplasms, Gastroesophageal Reflux, Humans
Show Abstract · Added April 8, 2016
Chronic Gastroesophageal Reflux Disease (GERD) is the main risk factor for the development of Barrett's esophagus (BE) and its progression to esophageal adenocarcinoma (EAC). Accordingly, EAC cells are subjected to high levels of oxidative stress and subsequent DNA damage. In this study, we investigated the expression and role of Apurinic/apyrimidinic endonuclease 1 (APE1) protein in promoting cancer cell survival by counteracting the lethal effects of acidic bile salts (ABS)-induced DNA damage. Immunohistochemistry analysis of human tissue samples demonstrated overexpression of APE1 in more than half of EACs (70 of 130), as compared to normal esophagus and non-dysplastic BE samples (P < 0.01). To mimic in vivo conditions, we treated in vitro cell models with a cocktail of ABS. The knockdown of endogenous APE1 in EAC FLO-1 cells significantly increased oxidative DNA damage (P < 0.01) and DNA single- and double-strand breaks (P < 0.01), whereas overexpression of APE1 in EAC OE33 cells reversed these effects. Annexin V/PI staining indicated that the APE1 expression in OE33 cells protects against ABS-induced apoptosis. In contrast, knockdown of endogenous APE1 in FLO-1 cells increased apoptosis under the same conditions. Mechanistic investigations indicated that the pro-survival function of APE1 was associated with the regulation of stress response c-Jun N-terminal protein kinase (JNK) and p38 kinases. Pharmacological inhibition of APE1 base excision repair (BER) function decreased cell survival and enhanced activation of JNK and p38 kinases by ABS. Our findings suggest that constitutive overexpression of APE1 in EAC may be an adaptive pro-survival mechanism that protects against the genotoxic lethal effects of bile reflux episodes.
0 Communities
3 Members
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11 MeSH Terms
Modifiable Risk Factors for Barrett's Esophagus and Esophageal Adenocarcinoma: Still a Shot in the Dark.
Yachimski P
(2016) Clin Gastroenterol Hepatol 14: 773-4
MeSH Terms: Adenocarcinoma, Barrett Esophagus, Humans, Risk Factors
Added May 11, 2016
0 Communities
1 Members
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4 MeSH Terms
Dietary magnesium, calcium:magnesium ratio and risk of reflux oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma: a population-based case-control study.
Dai Q, Cantwell MM, Murray LJ, Zheng W, Anderson LA, Coleman HG, FINBAR study group
(2016) Br J Nutr 115: 342-50
MeSH Terms: Adenocarcinoma, Aged, Alcohol Drinking, Barrett Esophagus, Body Mass Index, Calcium, Dietary, Case-Control Studies, Diet, Diet Records, Educational Status, Esophageal Neoplasms, Esophagitis, Peptic, Humans, Ireland, Magnesium, Middle Aged, Northern Ireland, Odds Ratio, Risk Factors, Smoking
Show Abstract · Added May 6, 2016
Evidence suggests a role of Mg and the ratio of Ca:Mg intakes in the prevention of colonic carcinogenesis. The association between these nutrients and oesophageal adenocarcinoma - a tumour with increasing incidence in developed countries and poor survival rates - has yet to be explored. The aim of this investigation was to explore the association between Mg intake and related nutrients and risk of oesophageal adenocarcinoma and its precursor conditions, Barrett's oesophagus and reflux oesophagitis. This analysis included cases of oesophageal adenocarcinoma (n 218), Barrett's oesophagus (n 212), reflux oesophagitis (n 208) and population-based controls (n 252) recruited between 2002 and 2005 throughout the island of Ireland. All the subjects completed a 101-item FFQ. Unconditional logistic regression analysis was applied to determine odds of disease according to dietary intakes of Mg, Ca and Ca:Mg ratio. After adjustment for potential confounders, individuals consuming the highest amounts of Mg from foods had significant reductions in the odds of reflux oesophagitis (OR 0·31; 95 % CI 0·11, 0·87) and Barrett's oesophagus (OR 0·29; 95 % CI 0·12, 0·71) compared with individuals consuming the lowest amounts of Mg. The protective effect of Mg was more apparent in the context of a low Ca:Mg intake ratio. No significant associations were observed for Mg intake and oesophageal adenocarcinoma risk (OR 0·77; 95 % CI 0·30, 1·99 comparing the highest and the lowest tertiles of consumption). In conclusion, dietary Mg intakes were inversely associated with reflux oesophagitis and Barrett's oesophagus risk in this Irish population.
0 Communities
1 Members
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20 MeSH Terms
Phase Ib Randomized, Double-Blinded, Placebo-Controlled, Dose Escalation Study of Polyphenon E in Patients with Barrett's Esophagus.
Joe AK, Schnoll-Sussman F, Bresalier RS, Abrams JA, Hibshoosh H, Cheung K, Friedman RA, Yang CS, Milne GL, Liu DD, Lee JJ, Abdul K, Bigg M, Foreman J, Su T, Wang X, Ahmed A, Neugut AI, Akpa E, Lippman SM, Perloff M, Brown PH, Lightdale CJ
(2015) Cancer Prev Res (Phila) 8: 1131-7
MeSH Terms: Aged, Aged, 80 and over, Barrett Esophagus, Biopsy, Catechin, Chromatography, High Pressure Liquid, Dose-Response Relationship, Drug, Double-Blind Method, Esophagoscopy, Female, Humans, Male, Middle Aged, Phytotherapy
Show Abstract · Added March 10, 2016
This study was conducted to determine the safety and efficacy of the green tea-derived Polyphenon E (Poly E) in patients with Barrett's Esophagus (BE). Subjects were randomized to a 6-month, twice daily (BID) oral treatment of placebo or Poly E (200, 400, or 600 mg). Endoscopic evaluation, including biopsies, was performed before and after treatment. The primary objective was to demonstrate safety; secondary objectives investigated catechin accumulation and effects in clinical specimens. Of the 44 enrolled subjects, 11 received placebo, and 33 received Poly E. No dose-limiting toxicities were encountered, and a maximum tolerated dose (MTD) was not reached. The recommended phase II dose was 600 mg twice daily. The most common treatment-related adverse events (AE) in Poly E-treated subjects were grade I and II nausea, grade I belching, and grade I lactate dehydrogenase (LDH) elevation. No treatment-related AEs were reported in placebo-treated subjects, aside from grade I laboratory abnormalities. Pill counts and subject diaries were not consistently collected, and compliance was difficult to determine. However, on the basis of an intention-to-treat analysis, there was a significant relationship between Poly E dose and esophageal EGCG level--mean changes (pmol/g) of 0.79 (placebo), 6.06 (200 mg), 35.67 (400 mg), and 34.95 (600 mg); P = 0.005. There was a possible relationship between Poly E dose and urine PGE-M concentration. In conclusion, Poly E was well-tolerated, and treatment with Poly E (400 and 600 mg) but not Poly E (200 mg) or placebo resulted in clinically relevant and detectable EGCG accumulation in the target organ, esophageal mucosa.
©2015 American Association for Cancer Research.
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14 MeSH Terms