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From:
Roy Jamron <[log in to unmask]>
Reply To:
Roy Jamron <[log in to unmask]>
Date:
Wed, 17 Mar 2004 23:36:51 -0500
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<<Disclaimer: Verify this information before applying it to your situation.>>

There have long been reports of stress being associated with various gut
disorders such as IBS. Now a new study appearing in the current issue of
Gut reveals and examines actual physical alterations in the gut and
immunity resulting from the influence of stress early in life (at least
early in the life of rats.)  This study may be warning that stressful
events during human infancy may affect development and set the stage for
future bowel and immunity disorders in adulthood.

By the way, I recently needed a few full-text articles from the journal,
Gut, and found that Gut offers a real bargain... 30-day full unrestricted
access to all of its online articles for only $25 (and it's only $8 if you
need just one article.)  Compare that to the ripoff price of $30 for a
single article charged by Elsevier and many other medical journal
publishers.  Sitting at my home computer browsing with unrestricted access
to all the great research articles in Gut felt like being in a candy shop
with the candy free for the taking!  Since many articles appearing in these
publications are the result of research funded through public institutions
and charitable grants, why can't the other publishers follow the lead of
Gut and allow access to research at fair prices?  A publisher is entitled
to cover expenses and make a reasonable profit, but let's keep unchecked
greed out of the exchange scientific knowledge.  I, for one, will never
spend $30 for a single article.  I will first go to a university library
and copy the article for free, and the publisher won't receive a single
cent from me.  (And I often find unauthorized full-text articles posted on
the web.)  The $25 I paid Gut for unrestricted access was money well spent
and I was happy to pay it.  Kudos to Gut!  http://www.gutjnl.com

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Gut. 2004 Apr;53(4):501-6

Neonatal maternal deprivation triggers long term alterations in colonic
epithelial barrier and mucosal immunity in rats.

Barreau F, Ferrier L, Fioramonti J, Bueno L.

Neurogastroenterology and Nutrition Unit, Institut National de la Recherche
Agronomique, Toulouse, France.

BACKGROUND: Stressful events in the early period of life (for example,
maternal deprivation) have been shown to modify adult immune and
gastrointestinal tract functions. The present study aimed to establish
whether maternal deprivation affects colonic epithelial barrier and the
development of an experimental colitis in adult rats. METHODS: Male Wistar
rat pups were separated during postnatal days 2-14 or left undisturbed with
their dam. At 12 weeks of age, we assessed colonic paracellular
permeability, bacterial translocation, myeloperoxidase (MPO) activity,
mucosal mast cell density, cytokine (interleukin (IL)-1beta, IL-2, IL-4, IL-
10, and interferon gamma (IFN-gamma)) mRNA expression, and macroscopic
damage. Total gut permeability, MPO activity, and macroscopic damage were
also assessed four days after intracolonic administration of 2,4,6-
trinitrobenzenesulphonic acid (TNBS). RESULTS: Maternal deprivation
triggered a significant increase in colonic permeability associated with
bacterial translocation into the mesenteric lymph nodes, liver, and spleen.
These alterations were associated with some macroscopic damage and an
increase in colonic MPO activity, mucosal mast cell density, and cytokine
mRNA expression. Intracolonic infusion of TNBS induced a significantly
higher inflammatory reaction in separated animals, as judged by enhanced
MPO colonic levels, total gut permeability, and macroscopic lesions.
CONCLUSIONS: Maternal deprivation promotes long term alterations in the
colonic epithelial barrier associated with an exaggerated immune response
to an external immune stimulus. This suggests a role for early
psychological factors in the regulation of colonic mucosal barrier in later
life.

PMID: 15016743 [PubMed - in process]

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