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

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

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Figure 3 Low-grade inflammation in FGID

Figure 2 Enteroids can model transport physiology

Figure 1 Imaging of a depressed intramucosal carcinoma

Figure 4 Activation of clopidogrel via cytochrome P450

Figure 5 Therapeutic paradigms for interfering with the brain–gut axis

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

Figure 6 Injection of mesenchymal stem cells in perianal fistulas

Figure 1 Patients cured of HCV infection

Figure 5 Lipid droplet consumption

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

Figure 1 Worldwide incidence of CCA

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

Figure 7 The efficacy of phosphate-binder therapy

Figure 1 Organs involved in coeliac-disease-associated autoimmunity

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

Figure 1 Biosimilar development process

Figure 3 Algorithm from working group describing

Figure 2 Effect of PPIs on gastric physiology

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

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

Figure 4 Giant lipid droplet formation

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

Figure 6 Combination therapy for HCC

Figure 2 Modelling the effect of HCV treatment on reinfection in people who inject drugs Figure 2 | Modelling the effect of HCV treatment on reinfection.

Figure 1 Definition and concept of ACLF

Figure 1 Host range of hepatitis E virus

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 3 Example wireless motility recording

to the liver and promote patient-derived xenograft tumour growth

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Figure 7 Example colonic high-resolution manometry

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

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

Figure 1 Pseudorelaxation as a consequence of

Figure 1 Environmental factors contributing to IBD pathogenesis

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

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

Figure 4 Examples of reflux episodes on pH and pH-impedance monitoring

Figure 3 Clinical algorithms in the management of NASH and diabetes mellitus Figure 3 | Clinical algorithms in the management of NASH and diabetes mellitus.

Figure 2 13C-octanoic acid gastric emptying breath test

in the UK (1961–2012), France (1961–2014) and Italy (1961–2010)

Figure 5 Representative barium defecography images

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

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

Figure 6 Possible therapeutic targets to decrease hepatic steatosis

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

Figure 5 High-resolution manometry studies performed

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 1 Brain–gut axis Brain–gut axis. Schematic of the brain–gut axis, including inputs from the gut microbiota, the ENS, the immune system and the external.

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

Figure 6 Assessment of colonic transit time with radiopaque markers

Figure 5 Systems biological model of IBS

Figure 4 Local species pools that contribute to the

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

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

Figure 2 Classifications and appearance of CCAs

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.2016.50 Figure 3 Responder rates in studies evaluating reflux inhibitors, either as monotherapy or as an add-on to acid suppressive therapy, for rGERD Figure 3 | Responder rates in studies evaluating reflux inhibitors, either as monotherapy or as an add-on to acid suppressive therapy, for rGERD. For Vakil et al.100 the left-hand yellow bars represent analysis of the entire population and the right-hand green bars represent analysis of the patients excluding those with mild or very mild symptoms. *P <0.05 compared with respective placebo group. rGERD, refractory GERD. Scarpellini, E. et al. (2016) Management of refractory typical GERD symptoms Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2016.50