Thesis (Ph. D.)--Oregon State University, 1964. / Typescript. Mounted photographs. Includes bibliographical references (leaves 143-151). Also available on the World Wide Web.

Thesis (Ph. D.)--Ohio State University, 1981. / Includes vita. Includes bibliographical references (leaves 179-184). Available online via OhioLINK's ETD Center.

Burn induces the inflammation response, and causes the intestinal barrier failure. The failure of intestinal barrier may cause organ damage. Pervious studies have shown that the increase of iNOS activity is closely related to the organ damage after burn. The expression of iNOS is regulated by the activation of NF-£eB, and that is regulated by MAPKs. The pro-inflammatory cytokines play important roles to promote the inflammation through activating a series of signal transduction cascade, via binding to their receptors on cell membrane. The signal transduction cascades are turn on, MAPKs and NF-£eB are activated and the expression of iNOS is promoted. In this study, the role of pro-inflammatory cytokine interleukin-1 receptor (IL-1R) in burn induced intestinal damage was focused on. In experiments, the animals (C57BL/6 mice) were undergone 30~35 % total body surface area (TBSA) burn. The change of intestinal permeability was examined, and intestinal mucosa was assayed for the activation of iNOS and MAPKs by immunoblotting, and the activation of NF-£eB was detected by EMSA. The results reveal that activation of NF-£eB, intestinal permeability and expression of iNOS were increased after burn in wild type mice (WT). ERK MAPK plays an important role to regulate the activation of NF-£eB and expression of iNOS. Surprisingly, the permeability had no change after burn in IL-1R knock out mice (KO). The activation of ERK, NF-£eB and the expression of iNOS were also measured in KO. The levels of p-ERK, NF-£eB activation and iNOS expression were low in KO. When WT mice were treated with U0126 (5 mg/kg i.p.) right after burn to block the activation of ERK, the activation of ERK and NF-£eB, the expression of iNOS, and the intestinal permeability were all decreased significantly. To sum up, the changes in iNOS expression, NF-£eB activation, and intestinal permeability increase are mostly related to the activation of ERK after burn. IL-1 R plays a promotion role in ERK, NF-£eB activation, and iNOS expression that lead to the increase in intestinal permeability and promote damage in intestine.

Univ., Diplomarbeit u.d.T.: Pelster, Gudrun: Vom Lächeln zum Lachen--Zugl.: Bielefeld, 2004.

Thesis (Ph. D.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 159-171). Also available online.

Thesis (M.A.) - Simon Fraser University, 2005. / Theses (Faculty of Education) / Simon Fraser University. Also issued in digital format and available on the World Wide Web.

Zugl.: Linz, Univ., Diss.

Thesis (Ed. D.)--Marshall University, 2003. / Title from document title page. Document formatted into pages; contains xiv, 221 p. Includes vita. Includes bibliographical references (p. 171-201).

Thesis (Psy. D.)--Wheaton College Graduate School, Wheaton, Ill., 2002. / Abstract. Includes bibliographical references (leaves 72-80).

Thesis (Ph. D.)--Florida State University, 2003. / Advisor: Dr. Aubrey Kent, Florida State University, College of Education, Dept. of Sport Management, Recreation Management, and Physical Education. Title and description from dissertation home page (viewed Mar. 01, 2004). Includes bibliographical references.