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Biotech / Medical : biotech firesales -- Ignore unavailable to you. Want to Upgrade?


To: hmpa who wrote (164)12/19/2001 12:04:03 AM
From: scaram(o)uche  Respond to of 3661
 
I did a Medline for "Woods C" and insulin. Came up with something relevant, but not something on-topic (see below, interesting affiliation for the first author if not for Dr. Woods).

I was trying to see if it was HUMAN insulin administered to rats, or rat insulin.

Then I tried to determine if there were sequence differences between rat and human. I got so many hits ("amino acid sequence difference insulin rat human") that I eventually gave up searching. All of the early titles that sounded good were from the period where NLM hasn't yet put up abstracts.

So..... is the EMIS work apples to apples? They took quite a shot at ARDM, INHL et al. there.

(please note: this question is somebody else's concept.... but I can't give them credit, as I don't remember who it was that raised the potential flag originally)

J Immunol 2001 Sep 1;167(5):2950-5

Plasmid vaccination with insulin b chain prevents autoimmune diabetes in nonobese diabetic mice.

Bot A, Smith D, Bot S, Hughes A, Wolfe T, Wang L, Woods C, von Herrath M.

Department of Immunology, Alliance Pharmaceutical, San Diego, CA 92121. Departments of Immunology and Neuropharmacology, Division of Virology, The Scripps Research Institute, La Jolla, CA 92037.

The insulin B (InsB) chain bears major type 1 diabetes-associated epitopes of significance for disease in humans and nonobese diabetic (NOD) mice. Somatic expression of InsB chain initiated early in life by plasmid inoculation resulted in substantial protection of female NOD mice against disease. This was associated with a T2 shift in spleen, expansion of IL-4-producing and, to a lesser extent, of IFN-gamma-secreting T cells in pancreatic lymph nodes, as well as intermolecular Th2 epitope spreading to glutamic acid decarboxylase determinants. A critical role of IL-4 for the Ag-specific protective effect triggered by plasmid administration was revealed in female IL-4(-/-) NOD mice that developed diabetes and higher Th1 responses. Coadministration of IL-4-expressing plasmid or extension of the vaccination schedule corrected the unfavorable response of male NOD mice to DNA vaccination with InsB chain. Thus, plasmid-mediated expression of the InsB chain early in diabetes-prone mice has the potential to prevent transition to full-blown disease depending on the presence of IL-4.