Possible cause of colitis found

Yes, I do think there is genetic component to U.C. because our immune systems don't respond to germs in our guts like with people who have "normal" immune systems.

To call one faulty gene a cause is a bit over the top though, I would say it is likely more of a contributing factor to being susceptible to the disease. Even so, any possible treatments from this discovery would probably be more than a decade away.

www.healthcanal.com/genetics-birth-defects/19333-Largest-Canadian-IBD-study-uncovers-gene-associated-with-ulcerative-colitis.html

Here's a better article I found about the study.

So what do we do to suppress the expression of RAC1 gene ?

This gene plays a role in endothelial permeability and cancer

www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2011000500015

The Rho family of small guanosine triphosphatases (GTPases) is a subgroup of the Ras superfamily of
GTPases. In this family, Rac1, one of the most extensively studied members, was initially discovered as Ras-related C3 botulinum toxin substrate 1 in 1989 (2). The small GTPase Rac1 is a critical mediator of various aspects of endothelial cell functions (4). Rac1 signaling can affect cell growth through a variety of mechanisms. In addition to its effects on gene expression, Rac1 regulates the production of reactive oxygen species, endothelial permeability and cell adhesion, all of which have been implicated in the deterioration of neurovascular integrity in neurological diseases (3). Recent studies have implicated aberrant Rac1 activity not only in tumorigenesis, but also in neurodegenerative disorders, mental retardation syndromes, cirrhosis of the liver, and cardio-remodeling/hypertension. Rac1 expression levels have been found to be higher than normal in CCs as well as in stomach, breast, and lung cancers (3).

Here is it shown to be necessary for healing of oral wounds

www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0010503

Conclusions/Significance
Together, these observations support that while the normal development and homeostasis of the interfollicular skin and oral mucosa do not require Rac1 function, the interfollicular and oral epithelial stem cells may require a Rac1-dependent program to orchestrate the tissue response to injury and ultimate for wound closure. Ultimately, these findings may enable the molecular characterization of the acute tissue regenerative response of these stem cell populations, thus facilitating the identification of novel molecular-targeted strategies aimed at accelerating wound closure.

Post Edited (aguywithuc) : 8/3/2011 4:31:00 PM (GMT-6)

Just remember that the UC itself has to be triggered. It's what remains after the initial assault. It also has a particular pattern...so in truth, it doesn't really matter what caused it. It reacted because of something, so the tendency was most likely there anyway.

As well...extended family can be pretty big and many never talked about poo issues. I suspect my mom had it, I can't believe all the bleeding issues and urgency was from her "piles". Plus, she was a smoker..many realise it suppresses some of the symptoms, but obviously not the disease itself.

I have no idea of who else in my "family" has/had IBD issues. Unless I did a or asked a million questions to people I couldn't care less about, I'll never know.

q

Wtih crohn's and identical twins, a study done by Dr. Kevin Rioux from a university in Canada, he states that if one twin has CD there is a 40-60% chance the other twin will also develop the disease.

My mom had UC and I have crohn's...I'm the youngest of 6 kids (that mom had) and I have a different father than the rest of my siblings (technically I'm an "only child" from my parents)...my dad had no bowel issues, and so far none of my older siblings have either IBD, but 2 do have IBS issues (as do I, on top of my crohn's)....The genetic link for either IBD is becomming stronger (IMO) based on the uprise of "pediactric IBD that has been noted (at least across Canada).