Thesis (M. Hous. M.)--University of Hong Kong, 1997. / Includes bibliographical references (leaf 147-150).

Thesis (M. Hous. M.)--University of Hong Kong, 1995. / "1995"--Cover. Includes bibliographical references.

Zugl.: Karlsruhe, Univ., Diss., 2009

Thesis (M.Hous.M.)--University of Hong Kong, 1995. / "1995"--Cover. Includes bibliographical references. Also available in print.

Thesis (M.Hous.M.)--University of Hong Kong, 1997. / Includes bibliographical references (leaves 147-150). Also available in print.

Thesis (M.Hous.M.)--University of Hong Kong, 1999. / Includes bibliographical references (leaves ii-xv). Also available in print.

Universiẗat, Diss., 1999--Bochum.

Thesis (Ph.D.)--University of Delaware, 2006. / Principal faculty advisor: Jack R. Vinson, Dept. of Mechanical Engineering. Includes bibliographical references.

No description available.

Lyme borreliosis (LB) is caused by spirocheter of Borrelia burgdorferi sensu lato. There are different types of borrelia species and some differ in their ability to survive in the presence of the complement system. B. afzelii is complementresistant while B. garinii is complementsensitive. This is based on the ability to recruit immune regulators, such as factor H to the bacterial surface and prevent activation of the complement system. Some individuals may show anti-Borrelia antibodies without having developed clinical symptoms. This may indicate a more effective immune response against spirochetes. The aim of this study was to investigate differences in complement activation by measuring C3a and sC5b-9 with sandwich ELISA between two previously Borrelia-exposed groups; individuals with previous subclinical Lyme borreliosis (SB) and patients previously diagnosed with neuroborreliosis (NB), and a control group without signs of LB exposure. Samples analyzed in this study consisted of controls (Ctrl, n = 8st), SB (n = 60st) and NB (n = 22st). Plasma from the groups were activated with ACA1 and Lu59. To compare the relative increase between the groups, complement factor C3a and the soluble terminal complement complex, sC5b-9, were analyzed using sandwich-ELISA.The analysis of C3a and sC5b-9 showed higher activation with Lu59 than ACA1, which is consistent with previous studies. According to C3a-analysis, no significant differences were observed between the groups for neither ACA1 nor Lu59. According to sC5b-9-analysis, a significant difference between SB and Ctrl (p= 0,0081) for Lu59 was observed. Conclusion of the studie was that further studies are required to interpret how this complement activation affects LB from a clinical prespective.