gastroesophageal reflux/protease

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Gastroesophageal reflux disease does not lead to changes in the secretory leukocyte protease inhibitor expression in esophageal mucosa.

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Prijava / prijava

OBJECTIVE Secretory leukocyte protease inhibitor (SLPI) serves as a 'defense shield' against serine proteases in inflammation. Gastroesophageal reflux disease (GERD) is associated with chronic inflammation and histomorphological alterations of the gastroesophageal junction and esophageal mucosa.

Mucosal Two-Step Pathogenesis in Gastroesophageal Reflux Disease: Repeated Weakly Acidic Stimulation and Activation of Protease-Activated Receptor-2 on Mucosal Interleukin-8 Secretion.

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Prijava / prijava

BACKGROUND Activation of protease-activated receptor-2 (PAR2) is involved in the mucosal immune pathogenesis of gastroesophageal reflux disease (GERD) that is characterized by proinflammatory cytokines such as interleukin-8 (IL-8). PAR2 activation on epithelial cells induces epithelial IL-8

Sputum proteomic signature of gastro-oesophageal reflux in patients with severe asthma.

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Prijava / prijava

Gastro-oesophageal reflux disease (GORD) has long been associated with poor asthma control without an established cause-effect relationship. 610 asthmatics (421 severe/88 mild-moderate) and 101 healthy controls were assessed clinically and a subset of 154 severe asthmatics underwent proteomic

Inflammation and oxidative stress in gastroesophageal reflux disease.

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Prijava / prijava

The etiology of esophageal mucosal injury is complex, since it may involve the reflux of gastric acid, bile acid, and pancreatic juice, external factors such as drugs and alcohol, or functional factors such as esophagogastric motility. The mechanism of esophageal mucosal injury has gradually been

[Gastroesophageal reflux in patients with chronic nonspecific lung diseases].

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Prijava / prijava

The author examined 30 patients with clinical symptoms of gastroesophageal reflux. The patients suffered of bronchial asthma (19) and chronic obstructive bronchitis (11). Intraesophageal and intragastric proteolysis with subsequent digestion of the protein substrate in solutions with different

Essential role of pepsin in pathogenesis of acid reflux esophagitis in rats.

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Prijava / prijava

Pepsin, a protease activated by gastric acid, is a component of the refluxate, yet the role of pepsin in the pathogenesis of reflux esophagitis has not been well studied. In the present study, we examined the effect of pepstatin, a specific inhibitor of pepsin, on acid reflux esophagitis. Acid

Gastroesophageal reflux disease--from reflux episodes to mucosal inflammation.

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Prijava / prijava

Gastroesophageal reflux disease (GERD) affects 20-30% of the population in Western countries, and is one of the most common clinical problems in daily practice. GERD-associated functional and structural abnormalities are caused by recurrent exposure of the esophagus to acidic and nonacidic refluxate

Proteinase-activated receptor-2 in the pathogenesis of gastroesophageal reflux disease.

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Prijava / prijava

OBJECTIVE The proteinase-activated receptor-2 (PAR-2) is activated by serine proteases and has been demonstrated to induce proinflammatory and neuroinflammatory effects. It is considered to alter transepithelial resistance and mediates visceral hypersensitivity. This study aimed to evaluate the

Chronic stress augments esophageal inflammation, and alters the expression of transient receptor potential vanilloid 1 and protease‑activated receptor 2 in a murine model.

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Prijava / prijava

Stress is a pivotal factor for inflammation, reactive oxygen species (ROS) production and formation of visceral hypersensitivity (VH) in the process of gastroesophageal reflux disease (GERD). In the present study, the effects of stress on esophageal inflammation, oxidative stress and VH were

Protease-Activated Receptor-2 Up-Regulates Transient Receptor Potential Vanilloid 4 Function in Mouse Esophageal Keratinocyte.

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Prijava / prijava

BACKGROUND The reflux of pancreatic-duodenal fluids is implicated in the pathophysiology of proton-pump inhibitor-resistant gastroesophageal reflux disease (GERD). Protease-activated receptor-2 (PAR-2) is activated by proteases, the pancreatic enzyme, trypsin, and the activated PAR-2 enhances

Expression of protease-activated-receptor 2 (PAR-2) in human esophageal mucosa.

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Prijava / prijava

OBJECTIVE The role of duodenal reflux in gastroesophageal reflux disease (GERD) containing bile salts and pancreatic enzymes (with special attention to trypsin) is still under discussion. Proteinase-activated receptors (PARs) are a novel family and PAR-2 is a unique member of this family because it

Desensitization to pancreatic enzyme intolerance in a child with cystic fibrosis.

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Prijava / prijava

OBJECTIVE Pancreatic enzyme is essential in the treatment of cystic fibrosis (CF), but intolerance to it occasionally occurs. We encountered a child who was intolerant to multiple commercially available preparations of pancreatic enzymes and, hence, desensitization was attempted, with

Comparison of extraction methods for quantitation of methionine and selenomethionine in yeast by species specific isotope dilution gas chromatography-mass spectrometry.

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Prijava / prijava

Fourteen extraction methods commonly cited in the literature were evaluated for the quantitation of methionine (Met) and selenomethionine (SeMet) in a yeast candidate certified reference material (CRM). Species specific isotope dilution (ID) gas chromatography-mass spectrometry (GC-MS) was utilized

Molecular, genetic, and cellular bases for treating eosinophilic esophagitis.

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Prijava / prijava

Eosinophilic esophagitis (EoE) was historically distinguished from gastroesophageal reflux disease on the basis of histology and lack of responsiveness to acid suppressive therapy, but it is now appreciated that esophageal eosinophilia can respond to proton pump inhibitors. Genetic and environmental

[Cytokine expression in GERD].

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Prijava / prijava

The mechanism of esophageal mucosal injury has gradually been understood at the microbiological level. It is particularly important that pro-inflammatory factors, such as inflammatory cytokines, leukocytes and oxidative stress, have been demonstrated to be involved in the development of

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