Information Outlook, March 1999

Volume 3, Issue 3https://scholarworks.sjsu.edu/sla_io_1999/1002/thumbnail.jp

Can marks and report cards be abolished in the Elementary schools?

Thesis (M.A.)--Boston University This item was digitized by the Internet Archive

Central Florida Future, April 22, 1998

Reception held to get to know the dean; he garage comes tumbling down; Earth Day Blowout to honor Mother Nature; Deal\u27s achievements deserving of an alumnus award.https://stars.library.ucf.edu/centralfloridafuture/2457/thumbnail.jp

Annual report of the town officers of the town of Stratford, New Hampshire, including report of the school district, for the year ending December 31, 2002. Happy 230th, Stratford!

This is an annual report containing vital statistics for a town/city in the state of New Hampshire

Records Management System: Pilot Projects Functional Report, 1998

The Iowa Department of Transportation began preparation for the acquisition of an electronic document management system in 1996. The first phase was development of a strategic plan. The plan provided guidelines for defining the acquisition and implementation of a document management system to automate document handling and distribution. Phase 2 involved developing draft standards (document, indexing and technology) for planning and implementation of a document management system. These standards were to identify existing industry standards and determine which standards would best support the specific requirements of the Iowa Department of Transportation. During development of these standards, the decision was made to enlarge the scope of this effort from a document management system to a records management system (RMS). Phase .3 identified business processes that were to be further developed as pilot projects of a much larger agency-wide records management system

Scrapbooks

Spanning from the beginning of his career to the dawn of the internet, the scrapbook covers the years 1967 to 1997 and showcase flyers, newspaper articles, critic reviews, programs, promotional materials, newsletters and photographs highlighting his work.https://digitalcommons.colum.edu/lofstromcollection/1002/thumbnail.jp

CHRONIC COLONIZATION OF CLOSTRIDIOIDES DIFFICILE FROM HUMAN COLON CANCER-ASSOCIATED BIOFILMS INDUCES COLON TUMORIGENESIS IN APCMIN/+ MICE

Despite extensive studies on the pathogenesis of acute Clostridioides difficile (C. difficile) infection (CDI), CDI has never been associated with colorectal cancer (CRC). Analyzing microbial species sequences from our previous study, we identified C. difficile DNA in the subsets of biofilm-positive (BF+) human colonic mucosal homogenates that promoted colon tumorigenesis after inoculation into germ-free (GF) ApcMin∆850/+;Il10-/- and ApcMin∆850/+ mice or specific-pathogen-free (SPF) ApcMin∆716/+ mice. These results raised an unexpected question of whether persistent mucosal colonization of C. difficile contributes to human colon tumor development. To address this question, we developed a chronic C. difficile infection mouse model in this study that allows sustained and non-lethal C. difficile colonization for 12 weeks in SPF ApcMin∆716/+ mice. Our results show that toxin-producing C. difficile strains, especially our human CRC-associated isolate CIm_2663, enhance colon tumor formation in SPF ApcMin∆716/+ mice. In addition, we evaluated the spatial localization of C. difficile strains in the infected mouse colons. We detected most of C. difficile in the colon lumen with sparse mucus invasion, but C. difficile did not aggregate to assemble biofilms in either GF wild-type mice or SPF ApcMin∆716/+ mice. The persistent in vivo production of C. difficile toxins, particularly toxin B, correlates with mouse colon tumor counts, suggesting that a toxin-dependent mechanism contributes to C. difficile-induced colon tumorigenesis. Of note, the colonization of toxigenic C. difficile strains induces low-grade chronic inflammation, displaying predominant infiltration of macrophages over time in colonic mucosa. Although pro-oncogenic cytokine IL-17A is similarly upregulated in all tumors regardless of C. difficile infection, toxigenic C. difficile strains suppress potential anti-tumorigenic cytokines IFN-γ and IL-25 in tumors, suggesting C. difficile infection may modify tumor microenvironment, at least partly, by shaping inflammatory signatures. Our results support that chronic C. difficile toxin exposure predisposes normal colonic epithelial cells to a pro-inflammatory, pro-tumorigenic environment that fosters persistent epithelial hyperplasia and sequential tumor progression. In summary, toxigenic C. difficile chronic colonization enhances colon tumorigenesis in ApcMin∆716/+ mice involving a mechanism dependent on persistent toxin B production and host immune responses