No description available.

In this thesis we have used temperature and high pressure to investigate the loss mechanisms present in visible, near infrared and infrared strained and unstrained semiconductor lasers. We find that tensile strained lasers show pressure dependent loss mechanisms similar in magnitude to those of unstrained and compressively strained devices. We present for the first time measurements of the temperature sensitivity of long wavelength lasers as a function of high pressure. Unstrained lasers show a pressure dependent temperature sensitivity whilst tensile strained lasers do not, over the range 150K to 300K. This leads us to conclude that phonon assisted Auger may be more significant than band to band Auger in tensile strained devices. We also demonstrate a possible mechanism for the decrease of Auger for these quantum well structures by estimating the effect of pressure on the gain - carrier density relation. High pressure measurements on 800nm GaAs quantum well lasers with superlattice barriers show the effect of changing the relative positions of the superlattice barrier IF and X minima. We find that the threshold current increases rapidly when the barrier is made indirect and conclude that this effect is due to repopulation of the barrier X minima with electrons from the active quantum well. For visible lasers we find that above lOkbar the effect of pressure on the threshold current is an increase which is attributable to losses from the active region to the X minima in the barrier. For a Philips bulk visible laser the threshold current remains relatively constant with pressure below lOkbar, whereas a Philips compressively strained device shows a decrease in Iý of about 25% up to 6kbar, a behaviour never seen before in short wavelength lasers. For the Philips 1% compressively strained laser the increase in Ith above 6kbar is also attributed to losses to the X minima. Measurements of a 1% compressively strained IBM laser showed immediate increases of threshold current with pressure, which is again attributed to the X minima in the barriers.

No description available.

Thesis (M.S.)--University of Delaware, 2007. / Principal faculty advisor: Kalmia Kniel, Dept. of Animal & Food Sciences. Includes bibliographical references.

Thesis (Ph. D.)--University of Texas at Austin, 2004. / Supervisor: Ben R. Hodges. Vita. Includes bibliographical references.

Glaucoma is characterized by retinal ganglion cell apoptosis leading to a corresponding loss of the visual field. Elevated intraocular pressure is the principal clinical association of this disease and its reduction remains the mainstay of current therapy. This research established an in-vitro glaucoma model and investigated the direct effects of increased hydrostatic pressure on retinal ganglion cell survival as well as the cellular response to changes in pressure. In the first part of this thesis (chapter 3) the direct effects of pressure on retinal ganglion cell survival was established. The differentiated RGC5 cell line was subjected to elevated pressure 100 mmHg for a period of two hours in a pressure chamber. Cell apoptosis was then detected by TdT-mediated dITP Nick-End Labelling (TUNEL). Quantitative analysis of the percentage of apoptotic cells between the control and pressure groups by Laser Scanning Cytometry (LSC) revealed that pressure alone induced significant apoptosis. Furthermore, caspase-3 cleavage was detected in the pressure treated cells by Western blot analysis. The next three chapters investigated how the applied pressure may be mediated through cellular mechno-sensitive structures. TWIK Related Arachiodonic Acid stimulated K+ channel (TRAAK) is a mechano-gated neuronal potassium channel, which can be opened by pressure and arachidonic acid. In chapter 4, TRAAK was identified as expressed on the rat RGC5 cell line. This was determined by both immunostaining and RT-PCR. Opening this channel by arachidonic acid induced significant apoptosis in RGC5 neurons; elevated extracellular K+ concentration and blockage of TRAAK by gadolinium inhibited both arachidonic acid and pressure-induced apoptosis. These results indicated that elevated pressure resulted in opening of the outward potassium channel-TRAAK and consequently potassium ion efflux and apoptotic volume decrease (AVD). Data from chapter 5 revealed that pressure also caused actin reorganization with both F- and G-actin shifts. At the early stage (following 2 hours pressure treatment), actin polymerization led to G-actin pool decrease and disinhibition of DNase1 in the cytoplasm. This has been suggested to lead to DNase1 nuclear translocation and contribution to DNA fragmentation associated with apoptosis. The preliminary microarray results of chapter 6 revealed pressure effects on gene expression Included in the many up- and down-regulated genes was; down-regulation of antiapoptotic gene- BcL-x and up- regulation of Damage-Induced Neuronal Endopeptidase (DINE) after pressure treatment. This study showed that elevated pressure induced RGC5 apoptosis and affected multi cellular mechanosnesitive structures. These results may indicate new mechanisms of RGC neuron apoptosis and further therapeutic strategies.

Thesis (Ph. D.)--Washington State University. / Includes bibliographical references.

No description available.

No description available.

Glaucoma is characterized by retinal ganglion cell apoptosis leading to a corresponding loss of the visual field. Elevated intraocular pressure is the principal clinical association of this disease and its reduction remains the mainstay of current therapy. This research established an in-vitro glaucoma model and investigated the direct effects of increased hydrostatic pressure on retinal ganglion cell survival as well as the cellular response to changes in pressure. In the first part of this thesis (chapter 3) the direct effects of pressure on retinal ganglion cell survival was established. The differentiated RGC5 cell line was subjected to elevated pressure 100 mmHg for a period of two hours in a pressure chamber. Cell apoptosis was then detected by TdT-mediated dITP Nick-End Labelling (TUNEL). Quantitative analysis of the percentage of apoptotic cells between the control and pressure groups by Laser Scanning Cytometry (LSC) revealed that pressure alone induced significant apoptosis. Furthermore, caspase-3 cleavage was detected in the pressure treated cells by Western blot analysis. The next three chapters investigated how the applied pressure may be mediated through cellular mechno-sensitive structures. TWIK Related Arachiodonic Acid stimulated K+ channel (TRAAK) is a mechano-gated neuronal potassium channel, which can be opened by pressure and arachidonic acid. In chapter 4, TRAAK was identified as expressed on the rat RGC5 cell line. This was determined by both immunostaining and RT-PCR. Opening this channel by arachidonic acid induced significant apoptosis in RGC5 neurons; elevated extracellular K+ concentration and blockage of TRAAK by gadolinium inhibited both arachidonic acid and pressure-induced apoptosis. These results indicated that elevated pressure resulted in opening of the outward potassium channel-TRAAK and consequently potassium ion efflux and apoptotic volume decrease (AVD). Data from chapter 5 revealed that pressure also caused actin reorganization with both F- and G-actin shifts. At the early stage (following 2 hours pressure treatment), actin polymerization led to G-actin pool decrease and disinhibition of DNase1 in the cytoplasm. This has been suggested to lead to DNase1 nuclear translocation and contribution to DNA fragmentation associated with apoptosis. The preliminary microarray results of chapter 6 revealed pressure effects on gene expression Included in the many up- and down-regulated genes was; down-regulation of antiapoptotic gene- BcL-x and up- regulation of Damage-Induced Neuronal Endopeptidase (DINE) after pressure treatment. This study showed that elevated pressure induced RGC5 apoptosis and affected multi cellular mechanosnesitive structures. These results may indicate new mechanisms of RGC neuron apoptosis and further therapeutic strategies.