Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1999. / Copies of author's previously published articles in plastic pocket inside back end-paper. Errata is pasted onto front end-papers. Bibliography: leaves 181-208.

Thesis (doctoral)--Lund University, 1995. / Added t.p. with thesis statement inserted.

Thesis (doctoral)--Lund University, 1995. / Added t.p. with thesis statement inserted.

No description available.

Copies of author's previously published articles in plastic pocket inside back end-paper. / Errata is pasted onto front end-papers. / Bibliography: leaves 181-208. / xi, 208, [161] leaves, [28] leaves of plates : ill. (chiefly col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Demonstrates that resistance to primary N. brasiliensis occurs within the first twenty-four hours of a primary infection in Interleukin-5 (IL-5) transgenic mice. Reduced parasite fecundity within the small intestines of this host appears to result from a culmination of early attrition at the inoculation site and lungs, in addition to adverse events in the local intestinal environment. Implies that eosinophils and not some other indirect consequence of over-expression of IL-5 are responsible for this resistance. / Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1999

Copies of author's previously published articles in plastic pocket inside back end-paper. / Errata is pasted onto front end-papers. / Bibliography: leaves 181-208. / xi, 208, [161] leaves, [28] leaves of plates : ill. (chiefly col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Demonstrates that resistance to primary N. brasiliensis occurs within the first twenty-four hours of a primary infection in Interleukin-5 (IL-5) transgenic mice. Reduced parasite fecundity within the small intestines of this host appears to result from a culmination of early attrition at the inoculation site and lungs, in addition to adverse events in the local intestinal environment. Implies that eosinophils and not some other indirect consequence of over-expression of IL-5 are responsible for this resistance. / Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1999

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1984. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographies.

The phospholipase B activity was assayed in the small intestines, spleen and liver/bile duct of nonsensitized and sensitized mice infected with Fasciola hepatica. The primary infection resulted in a significant increase in phospholipase B activity in the small intestine, spleen and liver/bile duct over that of uninfected control animals. The response to the challenge infection was characterized by an earlier increase in enzyme activity with values significantly above those found for the primary infection in the same tissues. These data demonstrate that one response of mice to infection with F. hepatica is characterized by an increased phospholipase B activity. Thus, the enzyme response is not unique to cestode and nematode infections, but also is part of or associated with the inflammatory mechanisms against trematode infections. In addition, phospholipase B was demonstrated in leukocytes using electron microscopic histochemical techniques. Leukocytes were harvested from peritoneal exudates of mice. Cells were fixed in 4% calcium-forol fixative for 30 minutes at roan temperature for electron microscopy, after which they were incubated at 370C in medium at pH 6.6 containing 2 aM lysolecithin and Cal2 . The fatty acids released during the hydrolytic reaction were trapped as a calcium precipitate and were converted to a lead precipitate for electron microscopy by treatment with lead nitrate. The reaction products were observed to be present in eosinophils and absent in neutrophils, lymphocytes and macrophages. It is concluded that the eosinophilic leukocyte is the carrier cell for phospholipase B in inflanmatory reactions.

No description available.