Efforts to expand access to cochlear implants may be impeded by financial incentives. Facilitating access for Medicare and Medicaid patients could require changes in payment policies.
A simple rat model of chronic intestinal inflammation was adapted to mice in order to ascertain whether mast cells play an essential role in its induction or perpetuation. Colitis was induced in C57BL mice by intrarectal administration of trinitrobenzene sulfonic acid in 50% ethanol. Higher doses of trinitrobenzene sulfonic acid per gram of body weight were required in mice than rats, with a narrower effective dose range (the upper dose limited by unacceptable mortality and the lower by decreased inflammation). Colons of treated mice were macroscopically inflamed, with transmural damage, adhesions to adjacent structures, and ulcerations. Inflammation was scored subjectively and by tissue weight and myeloperoxidase content; each index was increased dose-dependently by trinitrobenzene sulfonic acid doses of 0.3-10 mg. Six milligrams of trinitrobenzene sulfonic acid induced reproducible inflammation for up to four weeks. Trinitrobenzene sulfonic acid could induce inflammation in both mast-cell-deficient W/Wv mice and their normal +/+ littermates in a similar fashion. Thus it is possible to induce chronic colitis in the mouse. Mast cells are not essential participants in this process.
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