<p> The ultraviolet absorption spectrum of oxalyl chloride-fluoride has been recorded under high resolution, and has been attributed to a superposition of the spectra of the cis isomer (which appears weakly) and the trans isomer. The ultraviolet spectra of the cis isomers of oxalyl bromide, oxalyl chloride and oxalyl fluoride have also been identified. With the help of theoretical calculations, discrete absorption in the ultraviolet spectrum of trans oxalyl chloride-fluoride has been attributed to the superposition of four systems: (a) the singlet-singlet and singlet-triplet transitions which involve promotion of an electron from the highest energy non-bonding orbital (n₁) to the lowest energy antibonding orbital (π₁*) and (b) the singlet-singlet and singlet-triplet transitions which involve promotion from n₁ to the second lowest energy antibonding π orbital (π₂*). The S-S and S-T, n₁ → π₁* transitions have been analyzed in detail. </p> <p> Theoretical calculations have been carried out which indicate that α,β diketones, promotion of an electron to the lowest energy antibonding skeletal orbital (σ₁*) produces states which have a tendency towards dissociation along the C-C bond. It has been postulated that the diffuseness of the high energy absorption spectrum results from such a molecular dissociation, the Aᵤ(π₁,π₁*) state being strongly predissociated by the Aᵤ(n₁,σ₁*) state while the Aᵤ(n₁,π₁*) state is strongly predissociated by the Aᵤ(π₁,σ₁*) state. </p> <p> It has been postulated that the fluid phases of glyoxal and biacetyl consist of an equilibrium mixture of these molecules in various degrees of aggregation (e.g., monomeric, dimeric, trimeric,...). An ultraviolet band system previously assigned to a second n → π* transitions of these molecules has been reassigned to the first n → π* transition of a polymeric species. Some evidence has been assembled which supports this hypothesis. </p> / Thesis / Doctor of Philosophy (PhD)

Le mélanome est le cancer de la peau le plus mortel et l’exposition solaire est le facteur étiologique ayant la plus grande incidence sur son initiation. Cependant, l’influence des rayons UV sur la progression du mélanome primaire vers un état métastatique reste inconnue. Notre hypothèse est que les rayons UV peuvent, en plus d’initier la tumeur, stimuler la progression de la maladie vers un état métastatique. L’objectif de cette étude était donc de déterminer les conditions d’irradiation à utiliser, puis d’évaluer les effets directs et indirects des rayons UV sur la migration du mélanome. Les lignées A375, WM983a et SK-MEL-28 ont été cultivés sous forme de sphéroïdes et traitées chroniquement aux rayons UV directement ou indirectement. Puis, leur migration a été évaluée dans deux modèles 3D, soit en gel de collagène I ou en chambre de Boyd en inversée. L’exposition directe des sphéroïdes était constituée de5 minutes d’irradiation (570J/m2) au simulateur solaire tous les 12h pendant 7 jours. Aucune différence significative de migration des cellules cancéreuses n’a pu être observée dans cette condition. Pour l’exposition indirecte, les sphéroïdes ont été mis en contact avec un milieu de culture de kératinocytes immortalisés (HaCaT)ayant été préalablement irradiés de façon chronique aux UVB avec une dose de 75J/m2 tous les 12h pour un total de quinze irradiations (CLUV). Une augmentation significative de la migration des cellules cancéreuses dans le milieu CLUV a été observée pour les sphéroïdes de WM983a et SK-MEL-28. Le profilage des cytokines présentes dans le milieu CLUV a révélé un enrichissement de nombreuses cytokines tel que PDGFaa. En conclusion, le milieu CLUV augmente le potentiel de migration des trois lignées de mélanome primaire. Ainsi, l’exposition chronique aux rayons UV pourrait donc indirectement induire un plus grand pouvoir métastatique via notamment l’action de cytokines surexprimées.

The circumgalactic medium (CGM), loosely defined as the region between a galaxy disk and its virial radius, has long been of interest to astronomers and astrophysicists because it acts as an interface between galaxies and their surroundings. Studying it, therefore, gives us hints of how gas flows between galaxies and the intergalactic medium (IGM), fueling star formation for instance. This thesis addresses some of the current and future observation, analysis and instrumentation challenges that should be tackled for a better understanding of the CGM. Chapter 1 is an overview of science related to the CGM and of instruments that our lab works on: the Circumgalactic Hydrogen-Alpha Spectrograph (CHaS) and the Faint Intergalactic-medium Redshifted Emission Balloon (FIREBall). It sets the ground for a better understanding of the science discussed in subsequent chapters. CHaS is an IFU spectrograph installed on a 2.4 m telescope at the MDM Observatory in Arizona (Melso et al. 2022). It has high sensitivity and high spectral resolution, and it collects individual spectra from points across our targets using a microlens array, allowing us to make detailed spectral maps of observed astronomical objects. FIREBall is a balloon-born UV multi-object spectrograph, allowing us to look at yet another emission line prominent in the CGM. In this thesis, we will focus on what a future FIREBall detector might look like. Chapters 2 and 3 present data collected with CHaS in November 2021 from two very distinct objects: NGC 6946 (the Fireworks galaxy) and M76 (the Little Dumbbell nebula). Both chapters address how we process spectral data from CHaS images and the subsequent making of velocity maps. Using CHaS images, we tackle anomalous gas motion and formations in both targets. We compared the data presented in both chapters to previous literature, showing that CHaS velocity maps were more detailed and complimented previous findings. NGC 6946 is known for being a prolific star forming galaxy and also for having holes in its HI distribution, which have historically been attributed to the expansion and bursting of gas bubbles. In Chapter 2, we find that the motion around these holes is indeed consistent with expanding bubbles and galactic fountains on their edges, with velocities in the -20 km/s to 20 km/s range, consistent with what Boomsma et al. (2008) found, going up to +/-60 km/s, similar to the velocities found by Efremov et al. (2002). We also found that Long et al. (2019)'s supernova remnants candidates catalog had a clear position correlation with the boundaries of different holes in the Boomsma et al. (2008) HI hole catalog, suggesting that these holes might indeed be related to gas bubbles resulting from supernova explosions. The Little Dumbbell nebula, on the other hand, show its own set of anomalies. M76 is a butterfly planetary nebula with a central torus and two polar lobes. We find that these lobes are not completely symmetric. In fact, the wester lobe is more rounded and the eastern one is more stretched and fragmented. From our velocity maps, we propose a couple of explanations for how the ISM might interact with the nebula both in the core star's AGB phase and after the nebula is formed to give M76 its shape. Both explanations vary depending on the assumed direction of motion of the star in it its AGB phase, but both are consistent with models by Villaver, Manchado and García-Segura (2012) and Wareing et al. (2007). Moreover, we compare our data to those of other authors and find similar velocity ranges around an axis going from one lobe to another as spectral maps made by Ramos-Larios et al. (2017) and Bryce et al. (1996). Departing from observational data analysis, Chapter 4 focuses on how we can probe further into the CGM by upgrading existing instruments, turning commonplace condensed matter methods into tools for astrophysics. More specifically, Chapter 4 discusses the possibility of switching FIREBall's current UV sensitive emCCD detectors, which rely on coating to be visible-blind and on cryogenic equipment that is heavy for a balloon flight, for devices made out of hexagonal boron nitride (hBN). hBN's main energy bandgap overlaps with the emission lines that FIREBall is interested in capturing, and it can be combined with graphene (which is isomorphic to hBN) to make high quality, quantum efficient devices. While we weren't able to finish full devices, Chapter 4 discusses their fabrication in detail as well as how our Siesta SISL simulations show that even small device defects might be acceptable for a detector. The chapter ends with considerations about how one might fit individual devices as multi-pixel detectors.

The kinetics of Escherichia coli inactivation were studied using ultraviolet (UV) radiation, ozone, and UV and ozone (UVO) in combination in a batch reactor at varying pH levels (6, 7, and 8) and at a constant temperature of 25°C. The inactivation kinetics for all three treatment processes was pseudo first order, and the reaction rate constants were considered to be additive such that a combined reaction rate could be obtained by adding the kinetic rates of the processes applied and numerically small rates could be neglected in the computation of the combined rate. Statistical tests (ANOVA and student's t-test) performed on the inactivation data indicated no apparent effect of pH on the kinetics of the processes. It was found that the UVO process was the most efficient in inactivating E. coli. The increase in the inactivation rate with the UVO process is attributed to synergetic activity of UV and ozone which results in the generation of hydroxyl radicals from ozone decomposition.

Ultraviolet light (UV) and hydrogen peroxide (H2O2) decrease eggshell bacteria. However, when combined, the optimum amount of each and effects on hatchability are unknown. In Experiment 1, when compared to other concentrations of H2O2 and lengths of UV, the combination of 1.5% H2O2 and 8 minutes of UV yielded optimum results with a 3 log10 CFU/egg reduction in bacteria on the eggshell. In Experiment 2, exposing eggs to this optimum combination yielded a 1000 fold reduction in eggshell bacteria but only a numerical increase in hatch of set and hatch of fertile. In Experiment 3, eggs exposed to repetitive treatments of H2O2 and UV yielded a 4 log reduction in eggshell bacteria but no differences in hatchability or chick characteristics. In conclusion, the combination of H2O2 and UV proved to be effective for eggshell sanitization, especially when used repetitively, and did not alter hatchability.

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No description available.

No description available.

DNA mismatch repair (MMR) recognizes and repairs bases incorrectly incorporated during DNA replication. Germ line mutations in two MMR genes, namely hMSH2 and hMLHl, account for approximately 98% of hereditary non-polyposis colorectal cancers. There is conflicting evidence for the role of hMLHl and hMSH2 in the transcription-coupled repair (TCR) pathway of nucleotide excision repair (NER). Here we have examined the role of these MMR genes in NER using two reporter gene assays. AdHCMVlacZ is a replication-deficient recombinant adenovirus that expresses the B-galactosidase reporter gene under the control of the human cytomegalovirus (HCMV) immediate-early promoter. We have reported a reduced host cell reactivation (HCR) for B-galactosidase expression of UVC-irradiated AdHCMVlacZ in TCRdeficient Cockayne syndrome (CS) fibroblasts compared with normal fibroblasts, indicating that HCR depends, at least in part, on TCR. In addition, we have reported that UVC-enhanced expression of the undamaged reporter gene is induced at lower UVC fluences to cells and at higher levels after low UVC fluences in TCR-deficient compared with normal human fibroblasts, suggesting that persistent damage in active genes triggers increased activity f~om the HCMV-driven reporter construct. We have examined HCR and UV-enhanced expression of the reporter gene in hMLHl-deficient HCT116 human colon adenocarcinoma cells and HCT116-chr3 cells (the MMR-proficient counterpart of HCT116) as well as hMSH2-deficient LoVo human colon adenocarcinoma cells and their hMSH2-proficient counterpart SW 480 cells. We show a greater UV -enhanced expression of the undamaged reporter gene after low UVC exposure in HCT116 compared with HCT 116-chr3 cells ;md in Lo Vo compared with SW 480 cells. We show also a reduced HCR in HCT 116 compared with HCT 116-chr3 cells and in Lo Vo compared with SW 480 cells. However, the reduction in HCR was less or absent when cells were pretreated with UVC. These results suggest that detection of an involvement of hMLHl and hMSH2 in TCR is dependent on UVC (254 nm) fluence to cells. We have also used these two reporter gene assays to examine the role of hMSH2 and hMLHl in the repair of oxidative DNA damage induced by UV A light (335-400 nm) and H20 2• UV A and H20 2 produce a number of oxidative lesions in DNA (such as 8hydroxyguanines and thymine glycols) that are repaired by the base excision repair (BER) pathway. \ve show a reduced HCR for B-galactosidase expression of UVAtreated AdHCMVlccZ in hMSH2-deficient LoVo human colon adenocarcinoma cells compared to their hMSH2-proficient counterpart SW480 cells, but not in hMLHl-deficient HCT116 human colon adenocarcinoma cells compared to the hMLHl-proficient HCT116-chr3 cells. We also show that pre-treatment of cells with UVA enhances reporter gene expression to higher levels and at lower UV A fluences in Lo Vo compared to SW480 cells but not in HCT116 compared to HCT116-chr3 cells. These results suggest an involvement of hMSH2 but not hMLHl in the repair of UVA-induced oxidative DNA damage. In contrast, no detectable differences were observed between SW480 and LoVo cells, as well as HCT116-chr3 compared to HCT116 cells, in both of the reporter gene assays that used H20 2 as the DNA damaging agent. Based on these results, these findings suggest that neither hMSH2 nor hMLHl play a significant role in the repair of oxidative damage induced by H202. / Thesis / Master of Science (MS)

Photodynamic therapy (PDT) is a form of cancer treatment involving light, a photosensitizer and oxygen, whereby the photosensitizer is preferentially taken up by tumour cells, excited when exposed to light of the appropriate wavelength, and generates cytotoxic excited singlet oxygen that damages and destroys cells. Photofrin is the only approved photosensitizer for clinical use in treating esophageal and early and late lung cancers in the U.S., Canada and several other countries. Despite its effectiveness in treating some tumour types, Photofrin use has some limitations and thus photosensitizers are continuously being studied to find more efficient ways of killing tumour cells. Previous reports have described the isolation of photodynamic therapy resistant human colon carcinoma HT29 cells. HT29/P14, HT29/All and HT29/N8 were isolated by repeated in vitro PDT treatment to the 1-10% survival level followed by regrowth of single surviving colonies using the photosensitizers Photofrin, Aluminium Phthalocyanine Tetrasulphonate (AlPcS4) and Nile Blue A respectively. These PDT resistant HT29 variants all display increased levels of BNip3, Bcl-2 and the heat shock protein 27 (Hsp 27), but decreased levels of Bax and the mutant HT29 p53 protein. Since mutant p53 and increased expression of Hsp27 and Bcl-2 and have been associated with resistance to various chemotherapeutic agents in some tumour cells, whereas Bax and BNip3 are potent inducers of apoptosis, it was considered of interest to examine the sensitivity of these PDT resistant HT29 variants to other cytotoxic agents. Cell sensitivity to ultraviolet (UV) A radiation (UV A), a mixture of UV A and UVB (UV AlB), UVC, or cisplatin was determined by a comparison of the D37 values for clonogenic survival in the variants compared to that in parental HT29 cells. The HT29 PDT resistant variants were not cross-resistant to cisplatin or UVC. In contrast, HT29/P14, HT29/All and HT29/N8 all showed a significant increase in cisplatin sensitivity, while HT29/All cells also showed a significant increase in UVC sensitivity. HT29/N8, and HT29/P14 both showed a significant increase in UVA resistance compared to HT29 cells whereas HT29/All did not. HT29/P14 was the only POT-resistant cell line significantly cross-resistant to UVA/B relative to HT29. While HT29/P14 and HT29/All both showed a slight increase in resistance to Photofrinmediated PDT compared to HT29/Parental, this increase was only significant for HT29/All. However, HT29/N8 was significantly more sensitive to Photofrin-mediated PDT than HT29/Parental. To complicate matters, clonogenic variability was observed amongst the two HT29 sources examined, since one of the original HT29 cell lines showed a significantly higher resistance to Photofrin-mediated PDT compared to the other parental HT29 cells that were used to derive the PDT -resistant cell lines. To examine if the differences in sensitivity of the PDT-resistant cell lines compared to parental HT29 cells in response to cisplatin and UV radiation were due to differences in DNA repair, host cell reactivation (HCR) experiments were performed with a UVC damaged B-galactosidase reporter gene from the adenovirus Ad5HCMVSp1LacZ. HCR ofthe UV-damaged reporter gene was reduced in HT29/All (the cell line most sensitive to UVC) compared to the parental HT29 cells at high multiplicities of infection of the virus. This suggests the possibility of a decreased DNA repair capacity for HT29/ A 11 cells. However, due to differences in cellular morphology between HT29 and HT29/All cells, as well as possible differences in expression of the reporter gene, it was inconclusive that the difference in HCR reflects a true difference in DNA repair between HT29 and HT29/All cells. Hsp27 over expression alone was not responsible for the increased cisplatin sensitivity of the HT29 PDT resistant variants since there was no correlation of Hsp27 protein expression levels to l/D37 (used as a measure of sensitivity), for the cisplatin colony survival assays. In addition, Hsp27 protein expression levels did not correlate with UVC, cisplatin or UV A sensitivity suggesting that Hsp27 may be uniquely involved in making cells more resistant to PDT. p53 but not BNip3 protein levels correlated with sensitivity of cells to UV A, whereas no correlation was observed between p53 or Hsp27 protein expression levels and UVC sensitivity. p53 and p21 protein levels were not altered in either parental HT29 or the HT29/P14 POT-resistant variant following UVC and cisplatin exposure, respectively. In addition, introduction of wild-type p53 (using infection of a replication deficient adenovirus vector encoding the wild-type p53 gene), into parental HT29 or the PDT -resistant HT29/P 14 variant, had no effect on cisplatin sensitivity compared to cells infected with a control adenovirus vector expressing the LacZ gene. Taken together, these results suggest that the increased sensitivity of the PDT resistant variants to cisplatin did not result from differences in p53-dependent cisplatininduced cell cycle arrest. A strong correlation of cellular cisplatin sensitivity to the ratio of BNip3 to p53 protein levels, suggests that alterations in the expression of several different genes, including a reduced expression of the mutant HT29 p53 protein and an increased expression of BNip3, contribute to the increased cisplatin sensitivity of the HT29 PDT resistant variants. It has been reported previously that apoptosis induced by BNip3 is significantly inhibited by both wild type and mutated p53. Since pro-apoptotic BNip3 is over expressed in all three PDT-resistant HT29 cell lines, and BNip3/p53 protein expression levels were correlated to cisplatin sensitivity, this suggests that cisplatin kills HT29 cells through a BNip3-mediated apoptotic pathway. / Thesis / Master of Science (MS)