Thesis (Ph. D.)--University of Wisconsin--Madison, 1954. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 73-76).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1982. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Bibliography: leaves 115-118.

The D-domain of fibrin (ogen) was separated from the parent molecule by plasmin digestion in the presence of calcium and isolated by means of DEAE-anion exchange chromatography followed by gel-filtration in buffer containing 4 M urea. Fluorescent-D-dimer (f-D-dimer) was isolated from a plasmic digest of fibrin clotted in the presence of 2.45 mM dansyl cadaverine, a fluorescent lysine analogue. Fluorescent-D-monomer was a by-product of f-D-dimer purification, the yield being determined by the concentration of dansyl cadaverine. At 2.45 mM f-D-monomer was always present in the digest. The f-D-monomer is probably formed directly and not as a result of degradation of f-D-dimer. The molecule elutes in the fibrinogen-derived-D- monomer position on gel-filtration. A protease was isolated and partially purified from venom of the puffadder (Bitis arietans). Puffadder venom protease is characterized by its ability to cleave D-dimer into symmetrical D-monomers, smaller than plasmin-derived D-monomers from fibrinogen. This characteristic was used to detect the puffadder venom protease activity with fluorescent-D-dimer being used as the substrate. Fractions obtained were assayed for D-dimer cleavage activity and the samples analyzed by means of SDS-PAGE on 4-20% gradient gels under reducing (βME) and non-reducing conditions. The fluorescent bands were located under U.V light and photographed prior to staining with Coomassie Blue. Several methods for the purification of the protease were investigated.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1982. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 195-201).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1981. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 151-155).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1955. / Typescript. Abstracted in Dissertation abstracts, v. 16 (1956) no. 2, p. 602-603. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 149-153).

Cardiovascular diseases are the leading causes of death globally. One contributing factor that can lead to heart failure is a myocardial infarction. When an infarct occurs, an occlusion in the tissue vasculature prevents blood flow beyond this site. It results in scar tissue formation. The scar is non-contractile and reduces the working efficiency of the heart. To compensate, left ventricular remodeling will ensue resulting in enlarging of the left ventricle. This progression of events ultimately culminates in heart failure. One approach to assist patients who have suffered a heart attack is to implant a cardiac patch. Current patches are acellular and aim to retain the geometry of the left ventricle, limiting any ventricular remodeling from occurring. While these patches provide a passive support, it is hypothesized that incorporation of cells into the patches could result in functional support that could help to restore baseline function. To be effective, a cell-populated cardiac patch would need to integrate with the host tissue functionally and mechanically. In this thesis, we developed a fibrin microthread-based composite scaffold with material properties comparable to left ventricular myocardium that promotes regional cardiomyocyte alignment and physiologically relevant contractile strains. We hypothesized that a composite material could be developed where constituents of the material would complement one another to yield a mechanically reinforced scaffold that promotes cardiomyocyte function. Through manipulation of the volume fraction of the components, we manipulated the modulus of the layer without compromising contractile strain or contractile frequency of incorporated cells. Additionally, through strategic restraint of the scaffolds, we utilized cell-mediated compaction to induce a tension pattern that increased alignment of incorporated cells. This corresponded to an increase in contractile strain magnitudes, and an anisotropic contractile wave propagation through the engineered tissue. Finally, we laminated composite layers into a patch mimicking the architecture of ventricular myocardium and found that material properties of the patch were similar to properties of the target tissue. In summary, we designed a biomimetic composite patch with material properties similar to ventricular myocardium that supports cardiomyocyte alignment and contractility to promote functional and mechanical integration upon implantation.

Physiologically relevant scaffold-based tissue engineered structures have been limited in scope and viability by the diffusion limits of oxygen and other nutrients and functions provided by native vasculature in vivo. This has prevented the maintenance of healthy cell populations in scaffolds that are more than 200痠 thick. Combining concepts from microfluidics with biomaterials engineering, this project set out to engineer a perfusable fibrin-based vascular network capable of physiologically relevant flow properties as well as diffusion that supports viable cell populations. To create this system, a small artery sized (1.5 mm wide) gelatin sacrificial structure was embedded inside of a block of robust fibrin gel (4.26% w/v fibrin) then melted and rinsed out to create a perfusable vascular network. Characterization consisted of morphometric and histological analyses for channel sizes compared to the sacrificial structures, particle tracking to observe flow properties, and fluorescent dextran diffusion to measure diffusivity into the fibrin scaffold. We found that channels derived from sacrificial structures maintain their size and shape inside of the gel. Flow properties of the fluid through the channels were found to be both laminar and within expected physiological rates compared to native vessels of similar sizes. Cells on the surface of the fibrin vascular device expressed fluorescent markers that were delivered through the vascular network and perfused through the fibrin scaffold. These findings suggest that a fibrin based vascular system may provide a platform creating a functional vascular layer and for developing tissue engineered systems of increased size and complexity.

Thesis (M.A.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / 2031-01-01

Thesis (Ph. D.)--University of Wisconsin--Madison, 1951. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 106-107).