Investigation of the XUV Emission from the Interaction of Intense Femtosecond Laser Pulses with Solid Targets

The generation of coherent high-order harmonics from the interaction of ultra-intense femtosecond laser pulses with solid density plasmas holds the promise for table-top sources of intense extreme ultraviolet (XUV) and soft x-ray (SXR) radiation. Furthermore, they give rise to the prospect of combining the attosecond pulse duration of conventional gas-harmonic sources with the photon flux currently only available from large-scale free-electron laser or synchrotron facilities. In this thesis a series of experiments studying various aspects of harmonic generation from such a plasma source are presented and the emitted XUV-radiation is characterized spectrally, spatially and temporally. The measurements probe the dynamics of the plasma surface on a sub-laser-cycle time scale and help to increase our understanding of the harmonic generation process. It is shown that, at moderate intensities and laser contrast, the emitted harmonics are indeed phase-locked but chirped and emitted as a train of XUV-bursts of attosecond duration. Measurements with very high contrast relativistically intense driving pulses reveal the generation of harmonics up to the relativistic cutoff in a diffraction-limited beam with constant divergence observed for all wavelength. This implies that the harmonics are generated on a curved surface and travel through a focus after the target possibly opening a route towards extreme intensities in the process. In addition it is found that a target roughness on the scale of the wavelength of the highest generated harmonic does not adversely affect the harmonic beam quality implying that the generation of diffraction-limited keV-harmonic beams should be possible. In a third set of experiments the first demonstration of harmonic generation from solid targets using an 8 fs driving laser opens a route towards the generation of ultra-intense single-as pulses and gives conclusive evidence for the unequal spacing of the harmonic emission. Based on these results the development of ultra-intense sources of single as-pulses from the interaction of intense laser pulses with solid surfaces could advance at a fast pace making XUV-pump XUV-probe type investigations of nonlinear processes with attosecond time resolution feasible in the near future

Degradation Study on Solid Oxide Steam Electrolysis

Steam solid oxide electrolysis (SOE) is a method to transform electrical into chemical energy in the form of hydrogen with the prospect of very high conversion efficiencies, which could play a major role as storage capacity in future electricity systems. However, its longevity is limited by numerous degradation processes which need to be addresses before. This thesis elucidates degradation of solid oxide electrolysis cells (SOEC) by systematically investigating the influence of three key operating parameters – temperature, hydrogen gas humidity and current density – on cell deterioration. A detailed understanding of rate limiting processes governing cell performance was achieved based on experimental results as well as the application of a physico-chemical model approach. Five processes, separable by electrochemical impedance spectroscopy were identified: the ohmic resistance accounting for the conduction of ions through the electrolyte as well as contact resistances, a hydrogen electrode process representing oxygen ion conduction within the hydrogen electrodes’ YSZ backbone coupled with the charge transfer reaction, the hydrogen electrode charge transfer reaction, the oxygen electrode’s charge transfer reaction coupled with its oxygen ion transport and finally mass transport limitations. In order to study the influence of operating conditions on degradation, a series of 20 SOECs were operated for 1000 h under identical conditions, while only the investigated parameters deviated. The influence of temperature was investigated between 750 °C and 850 °C, the humidity ranged from 40 %MH to 80 %MH, while the current density varied between OCV and 1.5 A/cm2. This systematic parameter study allowed for the separation of four independent degradation processes, two of which contribute to the ohmic resistance and would be inseparable otherwise. Furthermore, it provides in-sight into the mechanism of each degradation process. One major source of degradation is caused by unidirectional transport of Ni away from the hydrogen electrode | electrolyte interface, leaving behind a porous YSZ layer virtually deprived of Ni, which effectively translates into an increase of the electrolyte’s thickness. This Ni-depletion is driven by current density and only occurs significantly at humidities of 80 %MH and temperatures of 800 °C and above. A second degradation process, also contributing to the ohmic resistance, was identified to be a partial change of the electrolyte’s crystallographic phase from cubic to tetragonal. This process shows a linear progression with the square root of time and is more pronounced at lower temperatures within the investigated range of parameters. Another important source of degradation could be linked to a change in the crystallographic structure of the oxygen electrode, which is dependent on operating temperature but largely unaffected by current density. Finally, the hydrogen electrode also exhibits degradation for most investigated conditions. While it is exposed to a series of degradation mechanisms, it is shown that the degradation mainly originates from a change of the ionic conductivity in the YSZ backbone while the charge transfer plays a minor role. Thus, observed microstructural changes resulting in a reduction of the triple phase boundary (TPB) length are not primarily responsible for hydrogen electrode degradation

Zur Kenntnis des Morphins. IX. Mitteilung. Über das Isokodeinon und über die Isomerie von Kodein, Isokodein und Pseudokodein

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Dynamics of Nanometer-Scale Foil Targets Irradiated with Relativistically Intense Laser Pulses

In this letter we report on an experimental study of high harmonic radiation generated in nanometer-scale foil targets irradiated under normal incidence. The experiments constitute the first unambiguous observation of odd-numbered relativistic harmonics generated by the $\vec{v}\times\vec{B}$ component of the Lorentz force verifying a long predicted property of solid target harmonics. Simultaneously the observed harmonic spectra allow in-situ extraction of the target density in an experimental scenario which is of utmost interest for applications such as ion acceleration by the radiation pressure of an ultraintense laser.Comment: 5 pages, 4 figure

Efficient ion acceleration by collective laser-driven electron dynamics with ultra-thin foil targets

Experiments on ion acceleration by irradiation of ultra-thin diamond-like carbon (DLC) foils, with thicknesses well below the skin depth, irradiated with laser pulses of ultra-high contrast and linear polarization, are presented. A maximum energy of 13MeV for protons and 71MeV for carbon ions is observed with a conversion efficiency of > 10%. Two-dimensional particle-in-cell (PIC) simulations reveal that the increase in ion energies can be attributed to a dominantly collective rather than thermal motion of the foil electrons, when the target becomes transparent for the incident laser pulse

Role of Chaperone Mediated Autophagy (CMA) in the Degradation of Misfolded N-CoR Protein in Non-Small Cell Lung Cancer (NSCLC) Cells

Nuclear receptor co-repressor (N-CoR) plays important role in transcriptional control mediated by several tumor suppressor proteins. Recently, we reported a role of misfolded-conformation dependent loss (MCDL) of N-CoR in the activation of oncogenic survival pathway in acute promyelocytic leukemia (APL). Since N-CoR plays important role in cellular homeostasis in various tissues, therefore, we hypothesized that an APL like MCDL of N-CoR might also be involved in other malignancy. Indeed, our initial screening of N-CoR status in various leukemia and solid tumor cells revealed an APL like MCDL of N-CoR in primary and secondary tumor cells derived from non-small cell lung cancer (NSCLC). The NSCLC cell specific N-CoR loss could be blocked by Kaletra, a clinical grade protease inhibitor and by genistein, an inhibitor of N-CoR misfolding previously characterized by us. The misfolded N-CoR presented in NSCLC cells was linked to the amplification of ER stress and was subjected to degradation by NSCLC cell specific aberrant protease activity. In NSCLC cells, misfolded N-CoR was found to be associated with Hsc70, a molecular chaperone involved in chaperone mediated autophagy (CMA). Genetic and chemical inhibition of Lamp2A, a rate limiting factor of CMA, significantly blocked the loss of N-CoR in NSCLC cells, suggesting a crucial role of CMA in N-CoR degradation. These findings identify an important role of CMA-induced degradation of misfolded N-CoR in the neutralization of ER stress and suggest a possible role of misfolded N-CoR protein in the activation of oncogenic survival pathway in NSCLC cells

Role of Misfolded N-CoR Mediated Transcriptional Deregulation of Flt3 in Acute Monocytic Leukemia (AML)-M5 Subtype

The nuclear receptor co-repressor (N-CoR) is a key component of the generic multi-protein complex involved in transcriptional control. Flt3, a key regulator of hematopoietic cell growth, is frequently deregulated in AML (acute myeloid leukemia). Here, we report that loss of N-CoR-mediated transcriptional control of Flt3 due to misfolding, contributes to malignant growth in AML of the M5 subtype (AML-M5). An analysis of hematopoietic genes in AML cells led to the identification of Flt3 as a transcriptional target of N-CoR. Flt3 level was inversely related to N-CoR status in various leukemia cells. N-CoR was associated with the Flt3 promoter in-vivo, and a reporter driven by the Flt3 promoter was effectively repressed by N-CoR. Blocking N-CoR loss with Genistein; an inhibitor of N-CoR misfolding, significantly down-regulated Flt3 levels regardless of the Flt3 receptor mutational status and promoted the differentiation of AML-M5 cells. While stimulation of the Flt3 receptor with the Flt3 ligand triggered N-CoR loss, Flt3 antibody mediated blockade of Flt3 ligand-receptor binding led to N-CoR stabilization. Genetic ablation of N-CoR potentiated Flt3 ligand induced proliferation of BA/F3 cells. These findings suggest that N-CoR-induced repression of Flt3 might be crucial for limiting the contribution of the Flt3 signaling pathway on the growth potential of leukemic cells and its deregulation due to N-CoR loss in AML-M5, could contribute to malignant growth by conferring a proliferative advantage to the leukemic blasts. Therapeutic restoration of N-CoR function could thus be a useful approach in restricting the contribution of the Flt3 signaling pathway in AML-M5 pathogenesis