HUMAN VISCERAL PAIN

"The anatomical, physiological, and molecular basis of chronic visceral pain in humans"

 Coordinatore QUEEN MARY UNIVERSITY OF LONDON 

 Organization address address: 327 MILE END ROAD
city: LONDON
postcode: E1 4NS

contact info
Titolo: Ms.
Nome: Tanya
Cognome: Szendeffy
Email: send email
Telefono: +44 20 7882 7266

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 281˙680 €
 EC contributo 281˙680 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2010-IIF
 Funding Scheme MC-IIF
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-05-10   -   2014-05-09

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    QUEEN MARY UNIVERSITY OF LONDON

 Organization address address: 327 MILE END ROAD
city: LONDON
postcode: E1 4NS

contact info
Titolo: Ms.
Nome: Tanya
Cognome: Szendeffy
Email: send email
Telefono: +44 20 7882 7266

UK (LONDON) coordinator 281˙680.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

pain    sensory    function    health    functional    colon    mechanisms    disease    visceral    cvp    animal    tissue    structure    nerves    human    molecular    subtypes    hypersensitivity   

 Obiettivo del progetto (Objective)

'Chronic visceral pain (CVP) is one of the most frequent reasons for seeking health care. Pain can arise from inflammatory disease, but 50% of patients with visceral pain have no diagnostic abnormalities, and are classed as “functional”. Both types of CVP are poorly understood, but animal studies show that they involve hypersensitivity of visceral sensory nerves, and some of the molecular mechanisms of hypersensitivity are emerging. We now need a translational program which identifies molecular targets and how they change in human disease. My work has investigated structure and function of visceral sensory nerves and identified mechanisms of hypersensitivity in animal models. Now I shall test these concepts in human tissue, and thus strengthen the basic-clinical interface in the biology of visceral pain. Major questions to be addressed are: 1. What functional and anatomical subtypes of sensory nerves innervate the human colon? 2. Which molecular targets exist in human sensory nerves that can be modulated pharmacologically? 3. How is the structure, function and pharmacology of human sensory nerves altered in disease? I shall optimise methods for working with human tissue. This involves recording of sensory nerves in vitro from surgical resections of uninflamed, inflamed or hypersensitive human colon. This will show the different subtypes and modalities of sensory nerves in the human bowel, and their specialization for specific functions in pain vs other processes. It will also test the concept I generated from animal work, that certain channels and receptors are enriched in pain sensing nerves. This work will provide insight into how pain develops in human disease. Along with functional recordings, the expression of candidate molecules on sensory endings and their structure will be studied, to provide a complete picture in health and disease. An insight into ways to combat CVP will emerge from these studies. It also has ramifications for other pain pathologies.'

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