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Journal articles on the topic 'Esophageal acid exposure'

Author: Grafiati

Published: 5 June 2025

Last updated: 2 August 2025

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1

FEIN, M., K. FUCHS, G. VARGA, et al. "Ineffective esophageal motility and esophageal acid exposure." Gastroenterology 120, no. 5 (2001): A429. http://dx.doi.org/10.1016/s0016-5085(01)82127-2.

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2

Fein, Martin, Karl-Herrmann Fuchs, Gabor Varga, et al. "Ineffective esophageal motility and esophageal acid exposure." Gastroenterology 120, no. 5 (2001): A429. http://dx.doi.org/10.1016/s0016-5085(08)82127-0.

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3

Yarze, Joseph C. "Relation Between Esophageal Acid Exposure and Esophageal Peristalsis." Digestive Diseases and Sciences 53, no. 3 (2008): 861. http://dx.doi.org/10.1007/s10620-008-0205-2.

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4

Lang, Ivan M., Bidyut K. Medda, and Reza Shaker. "Effects of esophageal acidification on esophageal reflexes controlling the upper esophageal sphincter." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 1 (2019): G45—G54. http://dx.doi.org/10.1152/ajpgi.00292.2018.

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Esophageal acid exposure can alter upper esophageal sphincter (UES) function, but the mechanism is unknown. The aim of this study was to determine the effects of esophageal acid exposure on esophago-UES relaxation (EURR) and contractile (EUCR) reflexes. Cats, decrebrate ( n = 27) or chronic ( n = 4), were implanted with electromyographic electrodes on pharynx, larynx, and esophagus. The esophagus was infused with either NaCl (0.9%) or HCl (0.1 N). The EUCR was activated by balloon distension in acute cats and slow air injection in chronic cats, and the EURR was activated by rapid air injection

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5

Ossakow, Steven J., Grace Elta, Thomas Colturi, Ronald Bogdasarian, and Timothy T. Nostrant. "Esophageal Reflux and Dysmotility as the Basis for Persistent Cervical Symptoms." Annals of Otology, Rhinology & Laryngology 96, no. 4 (1987): 387–92. http://dx.doi.org/10.1177/000348948709600408.

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To examine a possible esophageal basis for cervical symptoms, we studied 63 patients with persistent cervical complaints, 36 patients with gastroesophageal reflux but no cervical symptoms, and ten normal subjects. Patients were evaluated for a history of pyrosis and regurgitation and underwent otolaryngologic examination, barium esophagram, upper endoscopy, esophageal biopsy, standard esophageal manometrics, acid reflux testing, and Bernstein examination, as well as tests of esophageal dysmotility and acid clearance time before and after bethanechol (50 μg/kg, two doses). Standard diagnostic e

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6

Ali, Rabia, Scott Kramer, Fen Wu, Yu Chen, and Abraham Khan. "Do Esophageal High-Resolution Manometry Findings Predict Esophageal Acid Exposure?" American Journal of Gastroenterology 111 (October 2016): S1247—S1248. http://dx.doi.org/10.14309/00000434-201610001-02439.

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7

Lang, Ivan M., Bidyut K. Medda, and Reza Shaker. "301 The Effect of Esophageal Acid Exposure on Esophageal Reflexes." Gastroenterology 148, no. 4 (2015): S—66. http://dx.doi.org/10.1016/s0016-5085(15)30230-4.

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8

Wilson, Janet A., Anne Pryde, Cecilia C. A. Macintyre, and R. C. Heading. "Effect of Esophageal Acid Exposure on Upper Esophageal Sphincter Pressure." Neurogastroenterology & Motility 2, no. 2 (2008): 117–20. http://dx.doi.org/10.1111/j.1365-2982.1990.tb00017.x.

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9

Chan, Walter W., and C. Prakash Gyawali. "Sa1200 Esophageal Motor Patterns in Acid-Sensitive Patients Without Abnormal Esophageal Acid Exposure." Gastroenterology 142, no. 5 (2012): S—241—S—242. http://dx.doi.org/10.1016/s0016-5085(12)60907-x.

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10

Krüger, Leandi, Tiffany A. Pridgen, Ellie R. Taylor, Katherine S. Garman, and Anthony T. Blikslager. "Lubiprostone protects esophageal mucosa from acid injury in porcine esophagus." American Journal of Physiology-Gastrointestinal and Liver Physiology 318, no. 4 (2020): G613—G623. http://dx.doi.org/10.1152/ajpgi.00086.2019.

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Esophageal injury from acid exposure related to gastroesophageal reflux disease is a common problem and a risk factor for development of Barrett’s esophagus and esophageal adenocarcinoma. Our previous work highlights the benefits of using porcine esophagus to study human esophageal disease because of the similarities between porcine and human esophagus. In particular, esophageal submucosal glands (ESMGs) are present in human esophagus and proximal porcine esophagus but not in rodent esophagus. Although CFTR is expressed in the ducts of ESMGs, very little is known about CFTR and alternate anion

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11

Javed, Abid, Kevin Batte, Mustafa Abdul-Hussein, and Donald Castell. "Association Between Gastric Acid Control and Esophageal Acid Exposure." American Journal of Gastroenterology 111 (October 2016): S208—S209. http://dx.doi.org/10.14309/00000434-201610001-00461.

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12

de, Gomes, Rosa da, T. Sakae, A. P. Simic, and Ricachenevsky Gurski. "Correlation between pathological distal esophageal acid exposure and ineffective esophageal motility." Acta chirurgica Iugoslavica 57, no. 2 (2010): 37–43. http://dx.doi.org/10.2298/aci1002037d.

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Aim:To assess the correlation between esophageal dysmotility, characterized as inefficient esophageal motility (IEM), and the presence of pathological acid reflux due to a structurally defective lower esophageal sphincter (LES), hiatus hernia (HH), or esophagitis in patients with suspected gastroesophageal reflux disease (GERD). Methods: 311 patients referred for GERD diagnostic procedures in a gastroesopahgeal motility laboratory were included in the study. Patients underwent an interview regarding their clinical symptoms, upper endoscopy (UE), stationary esophageal manometry, and 24-h esopha

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13

White, A., R. C. Heading, J. A. Wilson, et al. "Gastroesophageal Reflux and Posterior Laryngitis." Annals of Otology, Rhinology & Laryngology 98, no. 6 (1989): 405–10. http://dx.doi.org/10.1177/000348948909800601.

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Esophageal acid exposure was assessed by 23-hour ambulatory pH monitoring and compared with a biopsy of the posterior larynx and proximal esophagus in 97 patients with hoarseness, burning pharyngeal discomfort, or globus sensation. Patient results were compared with normal acid exposure times obtained in 54 control subjects. In 24 patients there were laryngeal abnormalities but both esophageal biopsy results and acid exposure times were normal. Laryngeal disease was found in association with prolonged acid exposure time or esophagitis in only 17 of the 97 patients (17.5%) studied. Recent repor

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14

Sondheimer, Judith M., and Gerald M. Haase. "Simultaneous pH Recordings from Multiple Esophageal Sites in Children with and without Distal Gastroesophageal Reflux." Journal of Pediatric Gastroenterology and Nutrition 7, no. 1 (1988): 46–51. http://dx.doi.org/10.1002/j.1536-4801.1988.tb09467.x.

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SummaryWe made continuous, simultaneous recordings of esophageal pH from three sites in the esophageal body, for 18–24 h, in 11 children with normal prolonged distal esophageal pH studies (Group I) and in 14 children with abnormal distal esophageal pH recordings (Group II). A flexible catheter housing four antimony microelectrodes was used, and data were stored in a portable recorder. A computer allowed for evaluation of the percent of time esophageal pH was <4.0, number of reflux episodes per hour, acid clearance time, and the duration of longest reflux episode. Recordings made while subje

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15

Kern, Mark, Krisna Chai, Adeyemi Lawal, and Reza Shaker. "Effect of esophageal acid exposure on the cortical swallowing network in healthy human subjects." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 1 (2009): G152—G158. http://dx.doi.org/10.1152/ajpgi.00062.2009.

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Recent studies have demonstrated common cortical activity regions associated with esophageal acidification and swallowing. The effect of sensory signals imparted on these regions by esophageal acidification on swallow-related brain activity has physiological and clinical ramifications. Our aim in this study was to determine the effect of prior, unperceived esophageal acid exposure on cortical activity associated with swallowing. Functional magnetic resonance imaging (fMRI) techniques monitored brain activity associated with volitional swallowing before and after subliminal esophageal acid stim

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16

MENEGHETTI, A., P. TEDESCO, T. DAMANI, and M. PATTI. "Esophageal Mucosal Damage May Promote Dysmotility and Worsen Esophageal Acid Exposure." Journal of Gastrointestinal Surgery 9, no. 9 (2005): 1313–17. http://dx.doi.org/10.1016/j.gassur.2005.08.033.

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17

Piza-Palacios, Luis, Mercedes Cárdenas-Oña, Ximena Vásquez-Ojeda, et al. "Frequency of functional esophageal disorders in patients with refractory reflux symptoms in Lima, Peru." Revista de Gastroenterología del Perú 43, no. 3 (2023): 242–50. http://dx.doi.org/10.47892/rgp.2023.433.1498.

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Gastroesophageal reflux disease (GERD) is a clinical condition in which gastric reflux causes symptoms or damage to the esophageal mucosa. It is managed with proton pump inhibitors, however, up to 45% of patients with suspected GERD are refractory to treatment. It is necessary to establish a true GERD diagnosis by means of a digestive endoscopy, which does not show lesions in approximately 70% of patients. In this scenario, it is necessary to perform an esophageal pH-impedance measurement, a procedure that allows to determine whether exposure to gastric acid is pathological. Of this group, pat

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18

Saito, Masahiro, Tomoyuki Koike, Kenichiro Nakagawa, et al. "Strong Intra-Esophageal Reflux May Contribute to the Development of Barrett’s Adenocarcinoma and Affect the Localization." Digestion 101, no. 6 (2019): 752–60. http://dx.doi.org/10.1159/000502377.

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<b><i>Background:</i></b> There has been no study that has directly measured the esophageal reflux factors in Barrett’s adenocarcinoma (BA) using 24-h multichannel intraluminal impedance-pH monitoring (24-h MII-pH). We aimed to clarify the esophageal reflux factors in Barrett’s esophagus (BE) and BA and the factors that determine the location of BA with 24-h MII-pH. <b><i>Methods:</i></b> We performed 24-h MII-pH in 26 patients with superficial BA treated endoscopically (BA group) and 13 patients with BE (BE group) and examined the esophageal ref

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19

Cucchiara, S., A. Staiano, C. Di Lorenzo, G. De Luca, A. della Rocca, and S. Auricchio. "Pathophysiology of Gastroesophageal Reflux and Distal Esophageal Motility in Children with Gastroesophageal Reflux Disease." Journal of Pediatric Gastroenterology and Nutrition 7, no. 6 (1988): 830–36. http://dx.doi.org/10.1002/j.1536-4801.1988.tb09650.x.

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SummaryWe investigated the mechanisms of gastroesophageal reflux (GER) and esophageal motility during endogenous esophageal acid exposure in 17 patients with reflux disease alone (age range 3–20 months) (group A) and in 10 patients with reflux disease complicated by esophagitis (age range 4–19 months) (group B), by simultaneous recording distal esophageal sphincter relaxation was the predominant mechanism of reflux in both groups of subjects; however, it was more frequent in group B patients (Bpts), whereas reflux episodes due to appropriate sphincter relaxation were delected more frequently i

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20

Peters, F. T. M., E. J. Kuipers, S. Ganesh, et al. "Helicobacter pylori and esophageal acid exposure in GORD." European Journal of Gastroenterology & Hepatology 10, no. 12 (1998): A4. http://dx.doi.org/10.1097/00042737-199812000-00036.

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21

Kessing, Boudewijn F., Albert J. Bredenoord, Pim W. Weijenborg, Gerrit J. M. Hemmink, Clara M. Loots, and A. J. P. M. Smout. "Esophageal Acid Exposure Decreases Intraluminal Baseline Impedance Levels." American Journal of Gastroenterology 106, no. 12 (2011): 2093–97. http://dx.doi.org/10.1038/ajg.2011.276.

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22

Carpizo, Darren R., Andrea J. H. Reaka, W. Reid Glaws, et al. "Acute acid exposure increases rabbit esophageal cell proliferation." Journal of Laboratory and Clinical Medicine 131, no. 2 (1998): 157–62. http://dx.doi.org/10.1016/s0022-2143(98)90158-5.

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23

DiBaise, John K., John Lof, and Eamonn M. M. Quigley. "Can symptoms predict esophageal acid exposure in GERD?" Gastroenterology 114 (April 1998): A102. http://dx.doi.org/10.1016/s0016-5085(98)80415-0.

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24

Peters, FTM, EJ Kuipers, S. Ganesh, et al. "Helicobacter pylori and esophageal acid exposure in GERD." Gastroenterology 114 (April 1998): A257. http://dx.doi.org/10.1016/s0016-5085(98)81048-2.

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25

Akimoto, Shunsuke, Saurabh Singhal, Takahiro Masuda, Se Ryung Yamamoto, Wendy Jo Svetanoff, and Sumeet K. Mittal. "Esophagogastric Junction Morphology and Distal Esophageal Acid Exposure." Digestive Diseases and Sciences 61, no. 12 (2016): 3537–44. http://dx.doi.org/10.1007/s10620-016-4331-y.

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26

Korsten, Mark A., Alan S. Rosman, Susan Fishbein, Robert D. Shlein, Heidi E. Goldberg, and Alexander Biener. "Chronic xerostomia increases esophageal acid exposure and is associated with esophageal injury." American Journal of Medicine 90, no. 6 (1991): 701–6. http://dx.doi.org/10.1016/s0002-9343(05)80058-0.

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27

Korsten, Mark A., Alan S. Rosman, Susan Fishbein, Robert D. Shlein, Heidi E. Goldberg, and Alexander Biener. "Chronic xerostomia increases esophageal acid exposure and is associated with esophageal injury." American Journal of Medicine 90, no. 1 (1991): 701–6. http://dx.doi.org/10.1016/0002-9343(91)90665-k.

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28

Achem, A. Cristina, Sami R. Achem, Mark E. Stark, and Kenneth R. DeVault. "Failure of esophageal peristalsis in older patients: association with esophageal acid exposure." American Journal of Gastroenterology 98, no. 1 (2003): 35–39. http://dx.doi.org/10.1111/j.1572-0241.2003.07188.x.

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29

Gentile, Nicole, Benjamin Bick, Felicity Enders, et al. "Predictors of Abnormal Esophageal Acid Exposure in Patients with Eosinophilic Esophageal Infiltration." American Journal of Gastroenterology 108 (October 2013): S20—S21. http://dx.doi.org/10.14309/00000434-201310001-00060.

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30

Ours, Tina M., W. Keith Fackler, Joel E. Richter, and Michael F. Vaezi. "Nocturnal Acid Breakthrough: Clinical Significance and Correlation With Esophageal Acid Exposure." American Journal of Gastroenterology 98, no. 3 (2003): 545–50. http://dx.doi.org/10.1111/j.1572-0241.2003.07304.x.

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31

Rafiee, Parvaneh, Monica E. Theriot, Victoria M. Nelson, et al. "Human esophageal microvascular endothelial cells respond to acidic pH stress by PI3K/AKT and p38 MAPK-regulated induction of Hsp70 and Hsp27." American Journal of Physiology-Cell Physiology 291, no. 5 (2006): C931—C945. http://dx.doi.org/10.1152/ajpcell.00474.2005.

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The heat shock response maintains cellular homeostasis following sublethal injury. Heat shock proteins (Hsps) are induced by thermal, oxyradical, and inflammatory stress, and they chaperone denatured intracellular proteins. Hsps also chaperone signal transduction proteins, modulating signaling cascades during repeated stress. Gastroesophageal reflux disease (GERD) affects 7% of the US population, and it is linked to prolonged esophageal acid exposure. GERD is characterized by enhanced and selective leukocyte recruitment from esophageal microvasculature, implying activation of microvascular end

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32

Carlson, D. A., P. Kathpalia, J. Craft, et al. "The relationship between esophageal acid exposure and the esophageal response to volumetric distention." Neurogastroenterology & Motility 30, no. 3 (2017): e13240. http://dx.doi.org/10.1111/nmo.13240.

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33

Xenos, E. S. "The role of esophageal motility and hiatal hernia in esophageal exposure to acid." Surgical Endoscopy 16, no. 6 (2002): 914–20. http://dx.doi.org/10.1007/s00464-001-8208-5.

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34

Rogers, Benjamin, Amit Patel, Dan Wang, Basma Shahid, Gregory S. Sayuk, and C. Prakash Gyawali. "Obesity is Associated with Increased Esophageal Symptom Burden from Elevated Esophageal Acid Exposure." Gastroenterology 152, no. 5 (2017): S656—S657. http://dx.doi.org/10.1016/s0016-5085(17)32312-0.

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35

Chen, Yue-hang, Ying Jiang, Jing-Jing Wei, Wen-Ming Liu, and Ze-Hao Zhuang. "N-3 Polyunsaturated Fatty Acids Protect Esophageal Epithelial Cell From Acid Exposure." Current Developments in Nutrition 5, Supplement_2 (2021): 7. http://dx.doi.org/10.1093/cdn/nzab033_007.

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Abstract Objectives Our previous study has found that n-3 polyunsaturated fatty acids (PUFAs) inhibited inflammation in rats with esophagitis. This study was aimed to observe the protective effect of n-3 PUFAs on esophageal epithelial cells against acid damage and to explore its mechanism. Methods Human esophageal epithelial cells (Het-1A) were repeatedly treated with acidified medium (pH 5.0) and PUFAs with different ratios of n-6/n-3 (9:1, 3:1, 1:1 and 1:3, respectively), and Nrf2 agonists or inhibitors were used to assess the role of Nrf2 in mechanism of n-3 PUFAs. Western Blot and Quantita

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36

Hassan, Hamza, Reza Shaker, Elliot S. Yu, et al. "Tu1294 ACUTE ESOPHAGEAL ACID EXPOSURE SENSITIZES THE UPPER ESOPHAGEAL SPHINCTER RELAXATION RESPONSE TO ESOPHAGEAL AIR DISTENSION." Gastroenterology 164, no. 6 (2023): S—1024—S—1025. http://dx.doi.org/10.1016/s0016-5085(23)03378-4.

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37

Szczesniak, Michal M., Sergio E. Fuentealba, Anthea Burnett, and Ian J. Cook. "Differential relaxation and contractile responses of the human upper esophageal sphincter mediated by interplay of mucosal and deep mechanoreceptor activation." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 4 (2008): G982—G988. http://dx.doi.org/10.1152/ajpgi.00496.2007.

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Background and aims: the neural mechanisms of distension-induced esophagoupper esophageal sphincter (UES) reflexes have not been explored in humans. We investigated the modulation of these reflexes by mucosal anesthesia, acid exposure, and GABAB receptor activation. In 55 healthy human subjects, UES responses to rapid esophageal air insufflation and slow balloon distension were examined before and after pretreatment with 15 ml of topical esophageal lidocaine, esophageal HCl infusion, and baclofen 40 mg given orally. In response to rapid esophageal distension, UES can variably relax or contract

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38

REDINGER, N. "Intrasubject physiologic variability in 24 hour esophageal acid exposure." American Journal of Gastroenterology 98, no. 9 (2003): S20. http://dx.doi.org/10.1016/s0002-9270(03)00827-x.

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39

Schoppmann, Sebastian F., and Martin F. Riegler. "Radial esophageal acid exposure and the dilated distal esophagus." Journal of Gastroenterology 47, no. 11 (2012): 1275–76. http://dx.doi.org/10.1007/s00535-012-0629-5.

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40

Redinger, Nancy A., Ali Siddiqui, Sheila Rodriguez-Stanley, and Philip B. Miner. "INTRASUBJECT PHYSIOLOGIC VARIABILITY IN 24 HOUR ESOPHAGEAL ACID EXPOSURE." American Journal of Gastroenterology 98 (September 2003): S20. http://dx.doi.org/10.1111/j.1572-0241.2003.07794.x.

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41

Soto-Pérez, Julio César, Sergio Sobrino-Cossío, Paul B. Higgins, et al. "Distal Esophageal Hypercontractility Is Related to Abnormal Acid Exposure." Archives of Medical Research 42, no. 2 (2011): 104–9. http://dx.doi.org/10.1016/j.arcmed.2011.02.003.

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42

White, Robert J., Yong Zhang, Gerald P. Morris, and William G. Paterson. "Esophagitis-related esophageal shortening in opossum is associated with longitudinal muscle hyperresponsiveness." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 3 (2001): G463—G469. http://dx.doi.org/10.1152/ajpgi.2001.280.3.g463.

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Acute intraluminal acid perfusion induces esophageal shortening in humans and opossums. Lower esophageal sphincter (LES) hypotension and peristaltic dysfunction occur in patients and animal models of reflux esophagitis. This study examined whether similar shortening and motor dysfunction occur in anesthetized opossums after repeated esophageal acid exposure and whether this is associated with longitudinal muscle (LM) hyperresponsiveness. Manometry used before and after 3 consecutive days of 45-min perfusion with 100 mmol/l HCl or normal saline measured esophageal length and motor responses to

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43

Chen, Yue-Hang, Ying Jiang, Jing-Jing Wei, et al. "N-3 polyunsaturated fatty acids protect esophageal epithelial cells from acid exposure." Food Research International 162 (December 2022): 111943. http://dx.doi.org/10.1016/j.foodres.2022.111943.

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44

Feagins, Linda A., Hui Ying Zhang, Xi Zhang, et al. "Mechanisms of oxidant production in esophageal squamous cell and Barrett's cell lines." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 2 (2008): G411—G417. http://dx.doi.org/10.1152/ajpgi.00373.2007.

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We hypothesized that differences among individuals in reflux-induced oxidant production by esophageal squamous epithelial cells might contribute to the development of Barrett's esophagus. We studied the effects of acid and bile acids on the production of reactive oxygen species (ROS) in esophageal squamous cell lines derived from gastroesophageal reflux disease patients with (NES-B3T) and without (NES-G2T) Barrett's esophagus and in a Barrett's epithelial cell line (BAR-T). Cells were incubated with an ROS-sensitive probe and exposed to acidic medium, neutral bile acid medium, or acidic bile a

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45

Lim, Gillian, Yazmin Johari, Geraldine Ooi, et al. "Diagnostic Criteria for Gastro-esophageal Reflux Following Sleeve Gastrectomy." Obesity Surgery 31, no. 4 (2021): 1464–74. http://dx.doi.org/10.1007/s11695-020-05152-5.

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Abstract Background Gastro-esophageal reflux disease (GERD) post-sleeve gastrectomy (SG) is a controversial issue and diagnostic dilemma. Strong heterogeneity exists in the assessment of reflux post-SG, and better diagnostic tools are needed to characterize symptomatic reflux. We aimed to determine the discriminant factors of symptomatic reflux and establish diagnostic thresholds for GERD following SG. Materials and Methods Patients post-SG were categorized into asymptomatic and symptomatic cohorts and completed validated symptom questionnaires. All patients underwent stationary esophageal man

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46

Domingues, Gerson Ricardo de Souza, Joaquim Prado P. Moraes-Filho, and Aline Gonçalves Leite Domingues. "Impact of prolonged 48-h wireless capsule esophageal pH monitoring on diagnosis of gastroesophageal reflux disease and evaluation of the relationship between symptoms and reflux episodes." Arquivos de Gastroenterologia 48, no. 1 (2011): 24–29. http://dx.doi.org/10.1590/s0004-28032011000100006.

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CONTEXT: Gastroesophageal reflux disease is one of the most common digestive diseases and an important cause of distress to patients. Diagnosis of this condition can require ambulatory pH monitoring. OBJECTIVES: To determine the diagnostic yield of a wireless ambulatory pH monitoring system of 48-hours, recording to diagnose daily variability of abnormal esophageal acid exposure and its symptom association. METHODS: A total of 100 consecutive patients with persistent reflux symptoms underwent wireless pH capsule placement from 2004 to 2009. The wireless pH capsule was deployed 5 cm proximal to

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47

Chen, Xin, Tadayuki Oshima, Jing Shan, Hirokazu Fukui, Jiro Watari, and Hiroto Miwa. "Bile salts disrupt human esophageal squamous epithelial barrier function by modulating tight junction proteins." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 2 (2012): G199—G208. http://dx.doi.org/10.1152/ajpgi.00454.2011.

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Reflux of acid and bile acids contributes to epithelial tissue injury in gastro-esophageal reflux disease. However, the influence of refluxed material on human esophageal stratified epithelial barrier function and tight junction (TJ) proteins has not been fully elucidated. Here, we investigated the influence of acid and bile acids on barrier function and TJ protein distribution using a newly developed air-liquid interface (ALI) in vitro culture model of stratified squamous epithelium based on primary human esophageal epithelial cells (HEECs). Under ALI conditions, HEECs formed distinct epithel

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48

Kern, Mark, Candy Hofmann, James Hyde, and Reza Shaker. "Characterization of the cerebral cortical representation of heartburn in GERD patients." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 1 (2004): G174—G181. http://dx.doi.org/10.1152/ajpgi.00184.2003.

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Although symptoms arising from the esophagus such as heartburn and pain can at times become challenging clinical problems, esophageal viscerosensation, especially with regard to chemical stimulation in humans, is incompletely understood. Our aims were 1) to characterize and ascertain the reproducibility of cerebral cortical registration of heartburn and 2) to elucidate the differences between these findings and those of esophageal subliminal acid stimulation in asymptomatic controls. We studied 11 gastroesophageal reflux disease (GERD) patients (9 males, 30–55 yr) and 15 healthy controls (8 ma

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49

Helman, Laura, Beatriz Nunes Biccas, Eponina M. O. Lemme, Paula Novais, and Viviane Fittipaldi. "Esophageal manometry findings and degree of acid exposure in short and long Barrett's esophagus." Arquivos de Gastroenterologia 49, no. 1 (2012): 64–68. http://dx.doi.org/10.1590/s0004-28032012000100011.

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CONTEXT: Barrett's esophagus (BE) is characterized by intestinal metaplasia in the distal esophagus and is classified as short-segment (<3 cm - SSBE) or long-segment (>3 cm - LSSBE). It is suggested that LSSBE is associated with more severe esophageal motor abnormalities and increased acid exposure time than SSBE. OBJECTIVE: To evaluate the prevalence of esophageal manometriy abnormalities and acid exposure times in patients with SSBE and LSSBE. METHODS: Barrett's esophagus patients identified by upper endoscopy and confirmed by histopathology were, retrospectively, reviewed and divided

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Vantrappen, G., J. Tack, G. Huyberechts, et al. "Studies on the Relationship between Esophageal Acid Exposure, Mucosal Lesions and Heartburn Using an Acid Exposure Sensor." Scandinavian Journal of Gastroenterology 37, no. 11 (2002): 1253–58. http://dx.doi.org/10.1080/003655202761020506.

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