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Department of Pharmacology

 
Read more at: Food Antigen-Specific Antibodies and Mast Cell Activation in Post-Infectious Visceral Hypersensitivity

Food Antigen-Specific Antibodies and Mast Cell Activation in Post-Infectious Visceral Hypersensitivity


Read more at: Mast Cells Mediate Staphylococcal Enterotoxin B-Triggered Visceral Hypersensitivity: Potential Link Between Superantigens and Irritable Bowel Syndrome (IBS)

Mast Cells Mediate Staphylococcal Enterotoxin B-Triggered Visceral Hypersensitivity: Potential Link Between Superantigens and Irritable Bowel Syndrome (IBS)


Read more at: 772 Staphylococcal Enterotoxin B Triggers a Bystander Immune Response to Food Antigens Leading to Visceral Hypersensitivity

772 Staphylococcal Enterotoxin B Triggers a Bystander Immune Response to Food Antigens Leading to Visceral Hypersensitivity


Read more at: Evidence for TRP Channel Sensitization in IBS with Histamine 1 Receptor Antagonism as Effective Treatment

Evidence for TRP Channel Sensitization in IBS with Histamine 1 Receptor Antagonism as Effective Treatment


Read more at: GPR35 agonists inhibit TRPA1 mediated colonic nociception through suppression of Substance P release

GPR35 agonists inhibit TRPA1 mediated colonic nociception through suppression of Substance P release

Abstract


Read more at: A Conformable Organic Electronic Device for Monitoring Epithelial Integrity at the Air Liquid Interface.

A Conformable Organic Electronic Device for Monitoring Epithelial Integrity at the Air Liquid Interface.

Air liquid interfaced (ALI) epithelial barriers are essential for homeostatic functions such as nutrient transport and immunological protection. Dysfunction of such barriers are implicated in a variety of autoimmune and inflammatory disorders and, as such, sensors capable of monitoring barrier health are integral for disease modelling, diagnostics and drug screening applications.


Read more at: In Vitro Models for Investigating Intestinal Host-Pathogen Interactions.

In Vitro Models for Investigating Intestinal Host-Pathogen Interactions.

Infectious diseases are increasingly recognized as a major threat worldwide due to the rise of antimicrobial resistance and the emergence of novel pathogens. In vitro models that can adequately mimic in vivo gastrointestinal physiology are in high demand to elucidate mechanisms behind pathogen infectivity, and to aid the design of effective preventive and therapeutic interventions. There exists a trade-off between simple and high throughput models and those that are more complex and physiologically relevant.


Read more at: Stretchable device for simultaneous measurements of contractility and electrophysiology of neuromuscular tissue in the gastrointestinal tract

Stretchable device for simultaneous measurements of contractility and electrophysiology of neuromuscular tissue in the gastrointestinal tract

Devices on biological tissues can provide valuable insights into function, disease, and metabolism through electrical and mechanical signals. However, certain neuromuscular tissues, such as those in the gastrointestinal tract, undergo significant strain of up to 40% when physiologically active. Conventional inextensible devices cannot capture the dynamic responses in these tissues.


Read more at: Microbiome-driven IBS metabotypes influence response to the low FODMAP diet: insights from the faecal volatome.

Microbiome-driven IBS metabotypes influence response to the low FODMAP diet: insights from the faecal volatome.

BACKGROUND: Irritable bowel syndrome (IBS) is a common and debilitating disorder manifesting with abdominal pain and bowel dysfunction. A mainstay of treatment is dietary modification, including restriction of FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides and polyols). A greater response to a low FODMAP diet has been reported in those with a distinct IBS microbiome termed IBS-P. We investigated whether this is linked to specific changes in the metabolome in IBS-P.


Read more at: Correction to: Brf1 loss and not overexpression disrupts tissues homeostasis in the intestine, liver and pancreas.

Correction to: Brf1 loss and not overexpression disrupts tissues homeostasis in the intestine, liver and pancreas.