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.

Slides:



Advertisements
Similar presentations
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Advertisements

Figure 3 Low-grade inflammation in FGID
Figure 2 Enteroids can model transport physiology
Figure 4 The gut microbiota directly influences T-cell differentiation
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 2 The three most commonly performed bariatric surgical procedures Figure 2 | The three most commonly performed bariatric surgical procedures. a.
Figure 3 The fat–intestine–kidney axis
Figure 1 Gut microorganisms at the intersection of several diseases
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 1 Worldwide incidence of CCA
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 The microbiome–gut–brain axis
Figure 1 Organs involved in coeliac-disease-associated autoimmunity
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
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
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 1 Schematic outlining the results of Buffington et al.
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.
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.
Figure 2 Switching of biologic agents and biosimilars
Figure 2 Brain networks contributing to IBS symptoms
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 5 Intestinal lymph draining pattern and contents
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 1 An overview of the TIMER microbiota–host
to the liver and promote patient-derived xenograft tumour growth
Figure 7 Example colonic high-resolution manometry
Figure 1 Environmental factors contributing to IBD pathogenesis
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 13C-octanoic acid gastric emptying breath test
in the UK (1961–2012), France (1961–2014) and Italy (1961–2010)
Figure 2 Key brain–immune–gut interactions
Figure 4 Diverse molecular mechanisms of long non-coding RNAs
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Cross-sectional integrated brain–gut model of IBS pathophysiology
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 Pro-inflammatory and anti-inflammatory effects of the gut microbiota Figure 2 | Pro-inflammatory and anti-inflammatory effects of the gut microbiota.
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 Logistical requirements for autologous
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 6 Assessment of colonic transit time with radiopaque markers
Figure 2 New therapeutic approaches in IBD with their specific targets
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
Figure 1 Colonic inflammation in IBD and link to the gut microbiota
Figure 4 4D printing schemes and time-evolving structure geometries
Figure 2 Classifications and appearance of CCAs
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 Enhanced imaging techniques and autofluorescence endoscopy for Barrett oesophagus Figure 2 | Enhanced imaging techniques and autofluorescence.
Increase in proliferation and activation of immune cells in peripheral blood after NKTR-214 treatment. Increase in proliferation and activation of immune.
Presentation transcript:

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 environment. The model includes both peripheral and central components, which are in bidirectional interactions. Bottom-up influences are shown on the right side, top-down influences on the left side of the graph. Abbreviations: ENS, enteric nervous system; HPA, hypothalamic–pituitary–adrenal; PBMC, peripheral blood mononuclear cell; SNS, sympathetic nervous system. Modified with permission from Nature Publishing Group © Irwin, M.R. & Cole, S.W. Nat. Rev. Immunol. 11, 625–632 (2011).103 Modified with permission from Nature Publishing Group © Irwin, M.R. & Cole, S.W. Nat. Rev. Immunol. 11, 625–632 (2011)103 Mayer, E. A. et al. (2015) Towards a systems view of IBS Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2015.121