Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

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Gastroesophageal Reflux Disease (GERD). * Definition: inflammation of the lower part of the esophagus due to abnormal reflux of gastric contents into.
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Edward N. Janoff, Phillip D. Smith  Gastroenterology 
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 Exosome composition
promotes the oncogenic activity of CagA
Figure 5 Dendritic cells in liver inflammation
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 7 Treatment algorithm for perianal fistulizing disease
Figure 6 Injection of mesenchymal stem cells in perianal fistulas
Figure 2 A stage-based approach to the treatment of NAFLD
Figure 1 Gut microorganisms at the intersection of several diseases
Figure 5 Lipid droplet consumption
Figure 1 Suppression of SLC22A3 and A-to-I editing
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 3 The T-cell cytokine tree in IBD
Figure 1 Organs involved in coeliac-disease-associated autoimmunity
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 1 Biosimilar development process
Figure 3 The 'leaky gut' hypothesis
Figure 2 Effect of PPIs on gastric physiology
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 4 Tumour-induced neutrophil extracellular trap
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 1 HCV life cycle and site of action of DAAs
Figure 6 Combination therapy for HCC
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 4 Proinflammatory immune cells and their crosstalk in patients with IBD Figure 4 | Proinflammatory immune cells and their crosstalk in patients.
Volume 137, Issue 5, Pages (November 2009)
Figure 1 Definition and concept of ACLF
Figure 2 Switching of biologic agents and biosimilars
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 7 Example colonic high-resolution manometry
Figure 1 Environmental factors contributing to IBD pathogenesis
Figure 4 Examples of reflux episodes on pH and pH-impedance monitoring
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 13C-octanoic acid gastric emptying breath test
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Figure 3 Mechanisms of NS5B-mediated RNA synthesis
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 Three distinct paracellular epithelial
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 Schematic of normal and abnormal liver regeneration
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 3 Strategies to improve liver regeneration
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 New therapeutic approaches in IBD with their specific targets
Figure 5 Systems biological model of IBS
Figure 4 Role of exosomes in the pathogenesis of alcoholic hepatitis
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 Lifelong influences on the gut microbiome from
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Edward N. Janoff, Phillip D. Smith  Gastroenterology 
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Figure 1 The spread of colorectal cancer metastases
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Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2016.106 Figure 1 Macroscopic and microscopic changes during gastroesophageal reflux Figure 1 | Macroscopic and microscopic changes during gastroesophageal reflux. Schematic representation of the macroscopic (erosion) and microscopic changes (hyperplasia of basal layer, elongation of papillae and widened intercellular spaces) in the oesophageal epithelium that are associated with gastroesophageal reflux. a | Traditional concept, in which the acid-induced death of the surface epithelia from refluxed gastric juice is the initiating event, resulting in inflammation progressing into the lamina propria. b | New concept, as proposed by Dunbar and colleagues1, in which refluxed gastric juice initiates a cytokine-mediated influx of T cells that cause microscopic changes and, ultimately, erosions. Smout, A. J. P. M. & Bredenoord, A. J. (2016) A challenge to our view of reflux oesophagitis pathogenesis Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2016.106