Thesis (Ph. D.)--University of Wisconsin--Madison, 1974. / Typescript. Vita. Description based on print version record. Includes bibliographical references (leaves 341-370).

Thesis (M.S.)--University of Wisconsin--Madison. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 39-42).

Thesis (M.S.)--University of Wisconsin--Madison, 1962. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes Bibliographical references.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1964. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves [62]-67).

Bacteroides is a genus of anaerobic bacteria that are often found in high abundance in the human colon. They have a complex relationship with their human host, conferring health benefits as members of the gut microbiota but also acting as opportunistic pathogens. Though many of the virulence factors in Bacteroides have been characterized, it is currently classified as nonhemolytic. Work with Bacteroides isolates led to the observation, by happenstance, of unexpected hemolytic activity in multiple species. After incubation on blood agar plates, we observed that some isolates were clearly hemolytic, but only when plated in close proximity to certain, ‘activating’ isolates. We performed a systematic screen for hemolytic activity on a library of 94 Bacteroides isolates and identified one which was able to activate hemolysis in 30% of the collection. Using timelapse photography, we show this zone of hemolysis begins between the two colonies and proceeds in a retrograde fashion towards the ‘activated’ colony. The asymmetrical patterns of hemolysis are unlike any bacterial synergy reported to date. To investigate the mechanism behind this pattern, we combined a comparative genomics and mutagenesis approach to narrow down the genetic basis of this phenotype. Here, we characterize a unique synergistic hemolysis phenotype in Bacteroides, a genus of bacteria currently classified as nonhemolytic. This novel phenotype may provide further insight into Bacteroides as an opportunistic pathogen and may have uncovered a new mechanism by which they interact. / Thesis / Master of Science (MSc)

Cell-penetrating peptides (CPPs) mediate the delivery of macromolecules across the plasma membrane of live cells. These peptides are therefore important due to the potential of making the delivery of protein probes or therapeutics a routine procedure. However, CPP-mediated delivery is currently an inefficient process. CPP-protein conjugates are internalized into cells by endocytosis and the macromolecules remain trapped inside endosomes instead of reaching the target cellular localization. To solve this problem, we report a delivery methodology which relies on the use of a chimera of the TAT and of the Influenza HA2. TAT is a prototypical CPP that can promote macropinocytosis in live cells and HA2 is a pH-sensitive peptide that destabilizes lipid membranes upon acidification. I demonstrate that HA2-TAT can deliver a variety of macromolecular cargos into live mammalian cells by a simple co-incubation protocol. A model is described where TAT causes the endocytic uptake of cargos present in the media and that HA2 disrupts the endosomal membrane upon endosomal acidification. In addition, using red blood cells as a model system, HA2-TAT binds to membranes in a pH-dependent manner and causes the formation of pores through which macromolecules can diffuse. Additionally, the pro-apoptotic domain (PAD) peptide is also successfully delivered by HA2-TAT and shows significant apoptosis in cells through macropinocytosis.

Thesis (Ph. D.)--University of Pennsylvania, 1922. / "Reprinted from the Journal of infectious diseases, vol. 31, no. 3, September, 1922."

Inaug.-diss.-Bern. / "Diese arbeit erscheint in der Zeitschrift für hygiene und infektionskrankheiten." Lebenslauf. "Literatur": p. 24.

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