Fundamental questions related to the locations of Cerebrospinal Spinal Fluid (CSF) absorption deficit and causes of the pressure gradients that expand the ventricles with hydrocephalus remain largely unanswered. Work in the Johnston lab over a 15 year period has demonstrated that CSF moves through the cribriform plate foramina in association with the olfactory nerves and is absorbed by a network of lymphatic vessels located within the olfactory turbinates. A kaolin-based rat model of communicating hydrocephalus was developed as a collaborative effort with Drs. McAllister, Wagshul and Li. After developing a method to quantify lymphatic CSF uptake in rats, we examined and observed that the movement of a radioactive tracer into the nasal turbinates was significantly reduced in the kaolin-injected animals compared to saline injected controls. However, it was possible that while lymphatic CSF uptake was compromised, other CSF absorption pathways may have compensated. To answer this, we measured the CSF outflow resistance (Rout) and observed it to be significantly greater in the kaolin group compared with animals receiving saline and there was a significant positive correlation between CSF Rout and ventricular volume. Nonetheless, it is not clear how impaired CSF clearance could lead to a dilation of the ventricles since the ventricular and subarachnoid compartments are in communication with one another and pressure would likely increase equally in both. At this point, we came across a theoretical paper that postulated that a drop in periventricular interstitial fluid pressure might provide an intraparenchymal pressure gradient favouring ventricular expansion. In addition, studies in non-CNS tissues indicated that a disruption of beta-1 (β1) integrin-matrix interactions could lower tissue pressure. Based on these suppositions and data, we examined if these concepts had relevance to the brain. For this, we measured pressure in the brain and observed a decline in periventricular pressures to values significantly below those monitored in the ventricular system following the injection of the anti integrin antibodies. Many of the animals developed hydrocephalus over 2 weeks post antibody injection. These data provide a novel mechanism for the generation of intraparenchymal pressure gradients that is likely contributing to ventricular expansion.

Thesis (M. Sc.)--York University, 2002. Graduate Programme in Kinesiology and Health Science. / Typescript. Includes bibliographical references (leaves 74-82). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004 & res_dat=xri:pqdiss & rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation & rft_dat=xri:pqdiss:MQ71602.

The Par6-polarity pathway regulates breast cancer metastasis, and more recently has been shown to regulate transforming growth factor β (TGFβ)-induced apoptosis. Integrins may mediate the regulation of TGFβ-induced apoptosis by Par6, as they are key regulators of cell polarity, survival and death. First, we confirmed that blocking Par6 activation significantly inhibits TGFβ-induced apoptosis in both monolayer and three-dimensional NMuMG (Normal Murine Mammary Gland) cell culture models. TGFβ altered the expression of β1 and β4 integrins in NMuMG monolayers. In addition, TGFβ significantly reduced the basal localization of α6 and β4 integrins in NMuMG three-dimensional acini-like structures (p < 0.001), which was dependent on both Par6 and TGFβ receptor I (TβRI)/SMAD activation. We went on to show that the activities of integrin pro-survival signaling mediators, NF-κB and FAK, were altered in response to TGFβ, and that blocking Par6 activation in the Par6/S345A mutant maintained polarity and basal α6 and β4 integrin expression in the presence of TGFβ in NMuMG three-dimensional structures, in addition to a significant increase in FAK activation. This suggests that TGFβ alters the expression, localization and downstream signaling of integrins, which may contribute to TGFβ-induced apoptosis

Thesis (Ph.D.) -- University of Adelaide, Dept. of Medicine, 1999. / Copy of author's previously published article in pocket on back end-paper. Includes bibliography (leaves 135-185).

Thesis (M.S.)--University of Delaware, 2007. / Principal faculty advisor: Ulhas P. Naik, Dept. of Biological Sciences. Includes bibliographical references.

Thesis (Ph. D.)--University of Nevada, Reno, 2008. / "May, 2008." Includes bibliographical references (leaves 154-169). Online version available on the World Wide Web.

Thesis (M. S.)--Biomedical Engineering, Georgia Institute of Technology, 2008. / Committee Chair: Zhu, Cheng; Committee Member: Babensee , Julia; Committee Member: Garcia, Andres; Committee Member: McIntire, Larry; Committee Member: Selvaraj, Periasamy; Committee Member: Springer, Timothy

Thesis (Ph. D.)--Biomedical Engineering, Georgia Institute of Technology, 2004. / David Collard, Committee Member ; Robert Guldberg, Committee Member ; Cheng Zhu, Committee Member ; Elliot Chaikoff, Committee Member ; Harish Radhakrishna, Committee Member ; Andres J. Garcia, Committee Chair. Includes bibliographical references.

Thesis (M. Sc.)--University of Canterbury, 2007. / Typescript (photocopy). "June 2007." Includes bibliographical references (leaves 104-110). Also available via the World Wide Web.

Thesis (Ph.D)--Mechanical Engineering, Georgia Institute of Technology, 2009. / Committee Chair: Zhu, Cheng; Committee Member: Degertekin, Levent; Committee Member: Fox, Ronald; Committee Member: Garcia, Andres; Committee Member: McIntire, Larry. Part of the SMARTech Electronic Thesis and Dissertation Collection. Non-Latin script record