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In the frenzy of next generation genetic sequencing and proteomics, single-cell level analysis has begun to find its place in the crux of personalized medicine and cancer research. Single live cell 3D imaging technology is one of the most useful ways of providing spatial and morphological details inside living single cells. It provides a window to uncover the mysteries of protein structure and folding, as well as genetic expression over time, which will tremendously improve the state of the fields of biophysics and biomedical research. This thesis project specifically demonstrates a method for live single cell rotation required to image them in the single live cell CT imaging platform. The method of rotation proposed in this thesis uses dynamic optical traps generated by a phase-only spatial light modulator (SLM) to exert torque on a single mammalian cell. Laser patterns carrying the holographic information of the traps are delivered from the SLM through a transformation telescope into the objective lens and onto its focal plane to produce the desired optical trap "image". The phase information in the laser patterns being delivered are continuously altered by the SLM such that the structure of the wavefront produces two foci at opposite edges of the cell of interest that each moves along the circumference of the cell in opposite axial directions. Momentum generated by the motion of the foci exerts a torque on the cell, causing it to rotate. The viability of this method was demonstrated experimentally. Software was written using LabVIEW to control the display panel of the SLM.
ContributorsChan, Samantha W (Author) / Meldrum, Deridre R (Thesis advisor) / Kleim, Jeffrey A (Committee member) / Johnson, Roger H (Committee member) / Kelbauskas, Laimonas (Committee member) / Arizona State University (Publisher)
Created2013
Description
Traumatic brain injury (TBI) is a significant public health concern in the U.S., where approximately 1.7 million Americans sustain a TBI annually, an estimated 52,000 of which lead to death. Almost half (43%) of all TBI patients report experiencing long-term cognitive and/or motor dysfunction. These long-term deficits are largely due to the expansive biochemical injury that underlies the mechanical injury traditionally associated with TBI. Despite this, there are currently no clinically available therapies that directly address these underlying pathologies. Preclinical studies have looked at stem cell transplantation as a means to mitigate the effects of the biochemical injury with moderate success; however, transplants suffer very low retention and engraftment rates (2-4%). Therefore, transplants need better tools to dynamically respond to the injury microenvironment.
One approach to develop new tools for stem cell transplants may be to look towards the endogenous repair response for inspiration. Specifically, activated cell types surrounding the injury secrete the chemokine stromal cell-derived factor-1α (SDF-1α), which has been shown to play a critical role in recruiting endogenous neural progenitor/stem cells (NPSCs) to the site of injury. Therefore, it was hypothesized that improving NPSC response to SDF-1α may be a viable mechanism for improving NPSC transplant retention and migration into the surrounding host tissue. To this end, work presented here has 1. identified critical extracellular signals that mediate the NPSC response to SDF-1α, 2. incorporated these findings into the development of a transplantation platform that increases NPSC responsiveness to SDF-1α and 3. observed increased NPSC responsiveness to local exogenous SDF-1α signaling following transplantation within our novel system. Future work will include studies investigating NSPC response to endogenous, injury-induced SDF-1α and the application of this work to understanding differences between stem cell sources and their implications in cell therapies.
One approach to develop new tools for stem cell transplants may be to look towards the endogenous repair response for inspiration. Specifically, activated cell types surrounding the injury secrete the chemokine stromal cell-derived factor-1α (SDF-1α), which has been shown to play a critical role in recruiting endogenous neural progenitor/stem cells (NPSCs) to the site of injury. Therefore, it was hypothesized that improving NPSC response to SDF-1α may be a viable mechanism for improving NPSC transplant retention and migration into the surrounding host tissue. To this end, work presented here has 1. identified critical extracellular signals that mediate the NPSC response to SDF-1α, 2. incorporated these findings into the development of a transplantation platform that increases NPSC responsiveness to SDF-1α and 3. observed increased NPSC responsiveness to local exogenous SDF-1α signaling following transplantation within our novel system. Future work will include studies investigating NSPC response to endogenous, injury-induced SDF-1α and the application of this work to understanding differences between stem cell sources and their implications in cell therapies.
ContributorsAddington, Caroline (Author) / Stabenfeldt, Sarah E (Thesis advisor) / Kleim, Jeffrey A (Committee member) / Caplan, Michael R (Committee member) / Lifshitz, Jonathan (Committee member) / Massia, Stephen P (Committee member) / Arizona State University (Publisher)
Created2015