Ultraviolet (UV) group III-Nitride-based light emitters have been used in various applications such as water purification, medicine, lighting and chemical detection. Despite attractive properties such as bandgap tunability in the whole UV range (UV-C to UV-A), high chemical stability and relative low cost, the low quantum efficiency hamper the full utilization. In fact, external quantum efficiencies of UV devices are below 10 % for emission wavelength shorter than 350 nm. This thesis aims to show alternative solutions to such problems by employing nanowires (NWs) structures, and target the eventual application of reliable and high power NWs-based light-emitting devices, enabling large-scale production using the established silicon foundry processes. Here, we present the improvement of injection current and optical power of AlGaN NWs LEDs by involving a metal bilayer thin film with a dual purpose: eliminate the potential barrier for carrier transport, and inhibit the formation of silicide. We then study the AlGaN/GaN UV LED design to optimize the device structure and improve the LED performance. We compared multiple devices having different active region and graded layers’ thicknesses. Improvement on the output power was achieved for larger p-AlGaN graded layer and thinner p-GaN contact layer structure due to the better hole injection and lower p-GaN absorption. The junction temperature of AlGaN-based NWs LEDs on metal bi-layer and silicon is also presented as a crucial parameter affecting the device efficiency, chromaticity and reliability. In this regard, by using the forward-voltage and peak-shift method we extracted the junction temperature values and confirmed the better heat dissipation in NWs grown on metal substrate. Finally, the origin of single and ensemble NWs current injection and injection efficiency are studied by treating the AlGaN NWs with KOH solution. Measurements based on conductive atomic force microscopy enabled a fast feedback cycle without fabricating the device. Despite the NWs technology is still at its infancy compared to the matured planar, we believe that this research effort will give important insight in advancing the AlGaN NWs devices for future industrial employment.

Autonomous firefighting platforms are being developed to support firefighters.  One aspect of this is location of a fire inside a structure.  A multi-spectral sensor platform and fire location algorithm was developed in this research to locate a fire indoors autonomously. The multi-spectral sensor platform used a long wavelength infrared (LWIR) camera and ultraviolet (UV) sensor.  The LWIR camera was chosen for its ability to see through smoke, while the UV sensor was selected for its ability to discriminate between fires and non-fire hot objects.  The fire location algorithm by radiation emission (FLARE) developed in this research used the multi-spectral sensor data to provide the robot heading angle toward the fire. The system was tested in a large-scale structural fire facility.  A series of 20 different scenarios were used to evaluate the robustness of the system including different fuel types, structural features, non-fire hot objects, and potential robot positions within the enclosure.  This demonstrated that FLARE could direct a robot towards the fire regardless of these variables. Directional fire discrimination was added to the platform by limiting the field of view of the UV sensor to that of the LWIR cameras.  Three methods were evaluated to limit the field of view of a UV sensor. These included angled plate housing, bulb cover, and slit opening housing methods. The slit opening housing method was recommended for ease of implementation and size required to limit the field of view of the sensor to the desired value. / Master of Science

This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).

This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).

<p> When chloropentafluoroacetone in the gas phase at room temperature is electronically excited in the ultraviolet region, emission is observed. This emission is assigned to a transition from the 1 (n,π*) state. Deactivation of the vibrationally excited singlet state can occur when the ketone is excited at short wavelengths. The internal heavy atom effect on both radiative and radiationless transitions from the excited singlet state is relatively small. The quenching of the chloroketone molecules in the zeroth vibrational level of the excited singlet state has been studied and the probable quenching mechanisms proposed. Intersystem crossing from the excited singlet state to the triplet state is an important process in the gas phase at room temperature. However, phosphorescence is observed only in matrices at low temperatures, e.g. 77°K. The internal heavy atom effect on radiative and radiationless transitions from the triplet state in the matrix at low temperature is small. </p> / Thesis / Doctor of Philosophy (PhD)

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Bien qu’ils soient exposés tous deux aux rayons ultraviolets (UVR) solaires, cette exposition génotoxique n’entraîne pas les mêmes conséquences dans l’oeil et la peau. Le rôle des rayons UV dans l’induction et la progression des cancers cutanés est bien démontré. Ces rayons génotoxiques sont absorbés par l’ADN. Ils y induisent ainsi des changements conformationnels pouvant mener à la formation de différents dommages. On retrouve de façon prédominante la liaison de pyrimidines adjacentes en dimères cyclobutyliques de pyrimidines (CPD). Ceux-ci causent les mutations signatures responsables des cancers de la peau induits par les UVR. Cependant, aucune évidence ne démontre l’existence de cancer induit par les UVR dans la cornée. Nous avons donc tenté de découvrir les mécanismes permettant à la cornée d’éviter la transformation tumorale induite par les UVR. L’irradiation d’yeux de lapins aux rayons UVB a permis de prouver la capacité de ces rayons à induire la formation de CPD, et ce, de la cornée jusqu’au cristallin. Par la suite, l’irradiation d’yeux humains aux trois types de rayons UV (UVA, B et C) a permis d’y établir leur patron d’induction de CPD. Nous avons ainsi démontré que l’épithélium cornéen est particulièrement sensible à l’induction de CPD, tous types de rayons UV confondus. Enfin, la comparaison de la quantité de dommages présents dans des échantillons de peaux et de cornées irradiées à la même dose d’UVB a permis de démontrer que l’épithélium cornéen est 3.4 fois plus sensible à l’induction de CPD que l’épiderme. Nous avons par la suite étudié les mécanismes de réponse à ce stress. L’analyse de la viabilité cellulaire à la suite d’irradiations à différentes doses d’UVB a révélé que les cellules de la cornée et de la peau ont la même sensibilité à la mort cellulaire induite par les UVR. Nous avons alors analysé la vitesse de réparation des dommages induits par les UVR. Nos résultats démontrent que les CPD sont réparés 4 fois plus rapidement dans les cellules de la cornée que de la peau. L’analyse des protéines de reconnaissance des dommages a révélé que les cellules de la cornée possèdent plus de protéines DDB2 que les cellules de la peau, et ce, surtout liées à la chromatine. Nous avons alors tenté d’identifier la cause de cette accumulation. Nos analyses révèlent que la cornée possède une moins grande quantité d’ARNm DDB2, mais que la demi-vie de la protéine y est plus longue. Enfin, nos résultats suggèrent que l’accumulation de DDB2 dans les cellules de la cornée est entre autres due à une demi-vie plus longue de la protéine. Cette forte présence de DDB2 dans les cellules de la cornée permettrait un meilleur balayage de l’ADN, faciliterait de ce fait la détection de CPD ainsi que leur réparation et contribuerait donc à la capacité de la cornée à éviter la transformation tumorale induite par les UVR. / Even though they are both exposed to ultraviolet (UV) light, eye and skin do not share the same consequences following this genotoxic exposure. The role of UV rays in the induction and progression of skin cancer is well documented. These genotoxic wavelengths are absorbed by DNA, inducing conformational changes and thus leading to the formation of different forms of damage. The preeminent UV-induced DNA damage is formed by the covalent bond of adjacent pyrimidines to form cyclobutane pyrimidine dimers (CPD), which are responsible for the signature UV mutations found in UV-induced skin cancer. However, no evidence has shown the existence of UV-induced cancer in the cornea. We have thus undertaken to study the UV stress response mechanisms to understand how the cornea avoid UV-induced transformation. Irradiation of rabbit eyes with UVB wavelengths allowed us to prove the capacity of UV light to induce CPD formation, even more so, CPD were found from the cornea up to the lens. Thereafter, irradiation of human eyes with the three UV types (UVA, B and C) allowed us to establish their CPD induction pattern. We thus confirmed the fact that the corneal epithelium is particularly sensitive to the induction of CPD from all UV types. The analysis of DNA damage in samples of skin and cornea irradiated to the same UVB dose showed that corneal epithelium is 3.4 times more sensitive to CPD induction than epidermis. We then investigated the stress response mechanisms. The analysis of cellular viability following irradiation of cells to different UVB doses, revealed cells from the corneal epithelium and the epidermis were equally sensitive to UV-induced cell death. We then analysed the efficiency of UV-induced DNA damage repair. Our results show that CPD repair is 4 times more efficient in corneal cells than in skin cells. Analysis of recognition proteins revealed a strong presence of DDB2 in corneal cells and more particularly bound to their chromatin. We thus attempted to understand the reason of this accumulation. Our results reveal a lesser quantity of DDB2 mRNA in corneal cells, but a longer half-life of the DDB2 protein. Taken together, our results suggest the accumulation of DDB2 in corneal cells is due to a longer half-life of the protein, which compensates for a lesser mRNA quantity. This strong presence of DDB2 would allow a better scavenging of DNA in corneal cells and thus facilitate damage detection, enhance CPD repair and contribute to capacity of the cornea to avoid tumour transformation.

The problem was to study the behavior of several hydrocarbons when they were subjected to ultraviolet light of 2536 Å in the presence of mercury vapor.

Les rayons ultraviolets (UVR) font partie du spectre solaire et sont classés selon leur longueur d'onde en UVA (315 nm-400 nm), UVB (280 nm-315 nm) et UVC (100 nm-280 nm). Les UVA et une portion des UVB traversent la couche d'ozone et atteignent la surface terrestre, affectant la peau et les yeux. La peau se compose de l'épiderme, du derme et de l'hypoderme. Les UVR peuvent causer des dommages cellulaires et des dommages directs à l'ADN sous forme de dimères de pyrimidines (CPD et 6-4PP). Les dommages à l'ADN peuvent mener à la formation de mutations impliquées dans l'initiation et la progression des cancers de peau. La réparation des dommages à l'ADN couplée à l'arrêt du cycle cellulaire, ainsi que la mort cellulaire programmée sont des mécanismes de protection contre la transformation tumorale. En effet, la mort cellulaire régulée (RCD), permet de supprimer les cellules endommagées. Il existe de nombreuses voies de RCD, parmi lesquelles se trouve l'apoptose, la nécroptose, la ferroptose et la parthanatos. L'apoptose est connue pour être activée par les UVR, tandis que peu d'études examinent les voies non-apoptotiques initiées par les UVR. Cette thèse s'intéresse à l'étude des voies de RCD activées par les UVB dans les fibroblastes de derme humain (NHDF). En premier lieu, l'activation potentielle des voies non-apoptotiques de nécroptose, ferroptose et parthanatos par les UVB, a été étudiée, en plus de l'apoptose. L'investigation de ces voies a été réalisée à l'aide d'inhibiteurs pharmacologiques de la nécroptose, ferroptose, parthanatose et de l'apoptose, suite à une irradiation létale d'UVB. Nos résultats démontrent que seule l'apoptose est mesurable dans les NHDF exposés aux UVB, tandis que la nécroptose, ferroptose et parthanatos ne sont pas activées par les UVB, et ce, même suite à l'inhibition de l'apoptose. Ainsi, l'apoptose est la réponse principale des NHDF à une exposition létale d'UVB. En parallèle de la mort cellulaire, une déplétion du pool de NAD+ est observée dans les NHDF, dû en partie à l'activation de la protéine de parylation PARP1. Par la suite, la participation des protéines RIPK3 et MLKL dans la mort UV-induite a été étudiée. En effet, une précédente étude a mis en évidence une augmentation de la transcription de RIPK3 à la suite d'irradiations chroniques d'UVB, faisant de RIPK3 une protéine d'intérêt. RIPK3, sous forme phosphorylée, est connue pour être impliquée dans la nécroptose au côté de la protéine MLKL. Dans cette partie, la contribution de RIPK3 et de MLKL dans la mort UVB-induite des NHDF a été mise en évidence par déplétion partielle des protéines cibles. L'utilisation d'inhibiteurs de la nécroptose et l'étude des niveaux de phosphorylation de RIPK3 et MLKL démontre que cette implication est indépendante de leur activité nécroptotique. RIPK3 protège les NHDF de la mort UV-induite par un mécanisme indirect à l'apoptose, tandis que MLKL sensibilise les cellules à l'apoptose UV-induite. Enfin, le régime d'irradiation, soit l'exposition des cellules à une irradiation unique ou à des irradiations chroniques d'UVB, peut influencer la réponse cellulaire. En effet, la réparation des dommages à l'ADN des NHDF a été étudiée au sein du laboratoire et est modifiée selon le régime d'irradiation. Le rôle du régime d'irradiation, unique et chronique, sur la mort cellulaire induite par les rayons UVB dans les NHDF a donc aussi été étudiée. Pour ce faire, les cellules ont été prétraitées ou non par de faibles irradiations chroniques d'UVB (CLUV) puis ont été exposées à une dose létale d'UVB. Les résultats montrent que le régime d'irradiation chronique ne modifie pas la voie de mort activée par les UVB, qui reste apoptotique, et n'entraine pas de changement dans la proportion de cellules en voie de mort. Ainsi, la réponse de mort cellulaire des NHDF n'est pas modifiée par le régime d'irradiation UVB, contrairement à la réparation de l'ADN. Cette thèse établie que l'exposition des NHDF à une dose létale d'UVB induit l'activation de l'apoptose, sans activation des voies non-apoptotiques (nécroptose, ferroptose, parthanatos), et ce même suite à un régime d'irradiation CLUV. De plus, cette étude révèle deux nouveaux acteurs de la mort UV-induite des NHDF : RIPK3 et MLKL. Cette thèse présente des éléments nouveaux qui s'ajoutent à l'ensemble des connaissances et permettent une compréhension plus complète de la réponse cellulaire au stress génotoxique UVB. / Ultraviolet radiation (UVR) is part of the solar spectra. UVR are composed of UVA (315 nm-400 nm), UVB (280 nm-315 nm) and UVC (100 nm-280 nm). UVA and part of UVB reach the earth and affect our skin and eyes. Skin comprises epidermis, dermis and hypodermis layers. UVA and UVB lead to both cellular damage and direct DNA damage, mainly dipyrimidine dimers (CPD and 6-4PP). UV-induced DNA damage can be converted into skin cancer-driver mutations. DNA damage repair mechanisms and regulated cell death (RCD) are two mechanisms protecting cells from tumoral transformation. RCD, such as apoptosis, necroptosis, ferroptosis and parthanatos, remove damaged cells. UVR can induce apoptosis in skin cells, while little is known about non-apoptotic cell death following UVR. This thesis focuses on RCD pathways induced by UVB in normal human dermal fibroblasts (NHDF). First, possible activation of necroptosis, ferroptosis and parthanatos by UVB was investigated, as well as apoptosis, by use of pharmacologic inhibitors. Our results show that only apoptosis can be measured after UVB irradiation in NHDF, while no necroptosis, ferroptosis or parthanatos could be measured, with or without apoptosis inhibition. Apoptosis is thus a key response in NHDF exposed to a lethal UVB dose. Simultaneously with cell death, a drastic decrease in NAD+ was observed in irradiated NHDF, partly due to the activation of PARP1 polymerase. Secondly, the involvement of RIPK3 and MLKL proteins in UV-induced death was investigated. A previous study demonstrated an increase in RIPK3 transcription following chronic UVB irradiations, showing a potential involvement of RIPK3 in UV-induced cell response. Phosphorylated RIPK3 is known to be involved in necroptosis alongside phosphorylated MLKL. Using RIPK3 and MLKL knockdown, our results demonstrate RIPK3 and MLKL involvement in UVB-induced cell death. Use of necroptosis inhibitors plus the study of RIPK3 and MLKL phosphorylation confirmed that their roles are independent of their necroptotic activities. In fact, RIPK3 protects NHDF from UVB-induced cell death by a non-apoptotic mechanism, while MLKL sensitizes cells to UVB-induced apoptosis. Finally, irradiation regime, i.e. chronic irradiations versus unique irradiation, can influence the cellular response. Indeed, DNA damage repair has been studied in the laboratory and is modified by the irradiation regime in NHDF. Thus, we investigated the effect of chronic irradiations on UVB-induced cell death in NHDF. Cells were pre-treated or not with low chronic UVB doses (CLUV) and then exposed to a lethal UVB dose. The results show that with or without CLUV pre-treatment, UVB induced apoptosis with the same proportion of dying cells. Thus, NHDF cell death response is not altered by chronic expositions to UVB, unlike DNA repair. This thesis establishes that NHDF exposure to a lethal UVB dose induces the activation of apoptosis, without activation of non-apoptotic cell death pathways (necroptosis, ferroptosis, parthanatos), even after chronic irradiations (CLUV). In addition, two new actors of UVB-induced cell death, namely RIPK3 and MLKL, are presented here. This thesis presents new elements that help better understand the global cellular response to UVB genotoxic stress.

The results from this study show how different precursors affect halonitromethane (HNM) formation as well as how different free chlorine doses can affect HNM speciation. This study shows that the low pressure ultraviolet (LPUV) and free chlorine concurrent exposure can enhance HNM formation. In addition, most previous studies in the literature showed trichloronitromethane (TCNM) forming in greater quantities followed by monochloronitromethane (MCNM) and dichloronitromethane (DCNM). However, the results of this study show that, in deionized (DI) water matrices, MCNM forms in greater quantities at chlorine to nitrogen (Cl:N) ratios less than 3, while TCNM forms in greater quantities at Cl:N ratios greater than 3. Even so, the increase in TCNM formation did not increase linearly as the Cl:N ratio increased; there was a decreased rate of return when Cl:N ratios were greater than 3. The type of nitrogenous precursors can affect the amount of HNMs formed, with glycine forming a higher amount of total HNMs compared to methylamine (MA) and dimethylamine (DMA). The source of water can also affect which HNM species is formed in greater concentrations. The limited number of real water samples showed that the river waters have higher than normal total organic carbon (TOC) and dissolved organic nitrogen (DON), which are associated with greater nitrogenous precursors and higher HNM formation. Each water source can have different nitrogenous precursors; river waters may have more algal organic matter while wastewater would have higher organic matter and synthetic chemicals. In addition, source waters can have different constituents, such as varying dissolved oxygen (DO) levels and inorganic ions, which might inhibit HNM formation or affect specification.