No description available.

No description available.

No description available.

Three studies regarding Escherichia coli O157:H7 in apple cider were conducted. The objectives were: to evaluate the effectiveness of wash and sanitizers for removing E. coli O157:H7 from apples; to survey cider producer practices; and to determine the efficacy of ultraviolet light for reducing E. coli O157:H7 in cider. Apples with a five-strain acid resistant mixture of E. coli O157:H7 were treated with 200 ppm hypochlorite, a phosphoric acid-based fruit wash, 5% acetic acid, 5% acetic acid followed by 3% hydrogen peroxide, a peroxyacetic acid-based solution, and distilled water. The water wash caused insignificant reductions. All other treatments caused significant reductions. Acetic acid and peroxyacetic acid were the most effective with reductions of 3.1 and 2.6 logs, respectively. The survey determined that most producers are small, seasonal operations. Most use sound orchard management practices, clean and sanitize daily, sort and wash apples, use refrigeration, and try to prevent contamination. However, some use drop and damaged apples. Few use chemical sanitizers on apples, preservatives, pasteurize cider, or have HACCP programs. Cider inoculated with the same mixture of E. coli O157:H7 was processed using a thin- film ultraviolet disinfection unit operating at 254 nm. Dosages ranged from 9,402 to 61,005 æW- sec/cm2. Treatment significantly reduced E. coli O157:H7 (pó 0.0001) with a mean reduction of 3.81 log CFU/ml. Reduction was also affected by the level of background microflora in cider. Results indicate that ultraviolet light can reduce this pathogen in cider. However, additional reduction measures are necessary to achieve the required 5 log reduction. / Master of Science

No description available.

We developed an extreme ultraviolet (EUV) polarimeter, which employs laser-generated high-order harmonics as the light source. This relatively high-flux directional EUV source has available wavelengths between 8 nm and 62 nm and easily rotatable linear polarization. The polarimeter will aid researchers at BYU in characterizing EUV thin films and improving their understanding of materials for use in EUV optics. This first-time workhorse application of laser high harmonics enables polarization-sensitive reflection measurements not previously available in the EUV. We have constructed a versatile positioning system that places harmonics on the microchannel plate detector with an accuracy of 0.3 mm, which allows a spectral resolution of about 180. We have demonstrated that reflectance as low as 0.2% can be measured at EUV wavelengths and that this data is repeatable to within the error of our source stability (~7% fluctuation). We have compared reflectance data with that taken from the same sample at Beamline 6.3.2 at the Advanced Light Source. This data agrees well from 5 degrees to 30 degrees and the angular locations of the interference fringes also agree.

L'exposition aux rayons ultraviolets (UV) est essentielle à la vie et bénéfique pour la santé humaine. Cependant, la surexposition aux UV solaires, en particulier aux UVB, rayons les plus énergétiques atteignant la surface terrestre, peut entrainer des cancers de la peau chez l'être-humain comme les cancers de la peau de type non-mélanome (NMSC). La capacité des UVB à initier des NMSC provient principalement de leurs habilités à causer des dommages directs à l'ADN, tels que les dimères cyclobutyliques de pyrimidine (CPD) et les produits pyrimidine-pyrimidone (6-4PP), qui sont pris en charge par le mécanisme de réparation par excision de nucléotide (NER). L'incidence croissante de NMSC chez les patients déficients pour l'une des protéines de la NER souligne l'importance d'un processus fonctionnel. Par conséquent, une meilleure compréhension des mécanismes moléculaires de la NER permettrait de mettre en évidence de nouvelles cibles thérapeutiques pour la prévention ou le traitement des cancers de la peau. L'une des premières réponses cellulaires aux dommages CPD/6-4PP induits par UVB dans la peau des mammifères est l'activation de l'enzyme nucléaire poly(ADP-ribose) polymérase-1 (PARP1) qui catalyse la formation de polymères d'ADP-ribose. Les précédents travaux de notre laboratoire et d'autres équipes ont démontré que PARP1 et son activité enzymatique facilitent la NER en collaboration avec la protéine UV-damaged DNA binding protein 2 (DDB2), qui va aussi s'accumuler rapidement aux sites CPD/6-4PP pendant la phase de reconnaissance des dommages à l'ADN de la NER. Cependant, plusieurs aspects des interactions de PARP1 avec DDB2 et avec les dommages directs à l'ADN sont inconnus. Ainsi, le premier objectif de mon projet de doctorat a été de caractériser précisément la nature de la liaison de PARP1 aux dommages CPD/6-4PP induits par UV vis-à-vis la protéine DDB2. Mes recherches ont mis en évidence l'empreinte asymétrique formée par PARP1 de -12 à +9 nucléotides de chaque côté des dommages CPD/6-4PP en présence ou en absence de DDB2. Nous avons également démontré que PARP1 augmente l'affinité de DDB2 pour les dommages CPD/6-4PP. De plus, les résultats de notre étude indiquent un rôle de PARP1 indépendant de DDB2 pendant la phase de reconnaissance des dommages à l'ADN. Cibler PARP1 et son rôle dans les voies de réparation des dommages à l'ADN est l'une des stratégies les plus efficaces développées ces dernières années pour le traitement des cancers des ovaires et du sein. L'application translationnelle de mon projet de doctorat a alors été de comprendre le rôle de PARP1 dans la NER dans le contexte des NMSC. À cet égard, nous avons développé un modèle PARP1-KO dans la lignée de souris SKH-1, qui est un modèle largement adopté pour étudier les NMSC induits par UVB. Puisque les souris SKH-1 développent principalement des carcinomes spinocellulaires (CSC) cutanés après une exposition chronique aux UVB, notre étude rapporte le rôle de PARP1 dans le développement des CSC. En utilisant les souris nouvellement créées SKH-1 PARP1-KO et les souris SKH-1 PARP1-WT avec ou sans application topique d'inhibiteurs de PARP, nous avons mis en évidence que l'absence de PARP1 ou de son activité dans la peau des souris SKH-1 mâles et femelles réduit significativement le fardeau tumoral des CSC et prolonge la période de latence du développement tumoral. L'étude hebdomadaire de l'apparition et de la croissance de tumeurs tout au long du protocole révèlent aussi que cibler PARP1 est très efficace pour ralentir, à l'étape pré-maligne, le développement de CSC. Nos résultats sont surprenants à la lumière des propriétés onco-suppressives rapportées de PARP1 et de son activité catalytique dans des cas de cancérogenèse induits par des dommages à l'ADN causés par des agents alkylants, ainsi que de la susceptibilité croissante des souris knock-out pour d'autres protéines de la NER à développer des CSC induits par UVB. Le rôle de PARP1 dans les mécanismes cellulaires induits par UVB autres que la NER, comme la mort cellulaire et les modulations immunes, pourrait expliquer nos observations. Alors que d'autres analyses sont nécessaires pour comprendre le rôle de PARP1 dans ces mécanismes, notre étude met en avant l'utilisation potentielle d'inhibiteurs de PARP comme nouvel agent chimiopréventif contre les CSC induits par UVB. / The exposure to solar ultraviolet radiation (UV) is essential to life and beneficial to human health. However, an overexposure to terrestrial solar UV, especially its most energetic component UVB, can cause skin cancers including the non-melanoma skin cancers (NMSC) in humans. The NMSC initiating properties of UVB arise predominantly from their ability to cause direct DNA damage such as cyclobutane pyrimidine dimers (CPD) and 6-4photoproducts (6-4PP), which are repaired via nucleotide excision repair (NER) pathway. The increased incidence of NMSC in patients with hereditary defects in NER pathway proteins underscores the importance of efficient NER in humans. Therefore, detailed understanding of the molecular operation of NER pathway can provide novel therapeutic targets for the prevention or treatment of skin cancers. One of the earliest responses of the mammalian skin cells to UVB-induced CPD or 6-4PP is the activation of the nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP1), which catalyzes the formation of polymers of ADP-ribose (PAR). The previous work from other teams and our laboratory have shown that PARP1 and its enzymatic activity facilitate NER in collaboration with UV-damaged DNA binding protein 2 (DDB2), which also rapidly accumulates at the CPD/6-4PP site during the DNA damage recognition stage of NER. However, many aspects of interaction of PARP1 with DDB2 and direct DNA damage are not understood. Therefore, the first aim of my doctoral project was to characterize the precise nature of binding of PARP1 vis-à-vis DDB2 at UV-induced CPD/6-4PP. My doctoral research demonstrates that PARP1 casts asymmetric footprint from −12 to +9 nucleotides on either side of the CPD/6-4PP in presence or absence of DDB2. We also demonstrated that PARP1 facilitates the binding of DDB2 to CPD/6-4PP. Moreover, our study reports DDB2-independent role of PARP1 during the DNA damage recognition phase in NER. Targeting the role of PARP1 in DNA strand break repair pathways has emerged as one of the successful strategies for the treatment of ovarian and breast cancers in last decade. Consequently, the ultimate translational goal of my doctoral project was to understand the implication of NER facilitating role of PARP1 in NMSC. In this regard, we first developed a PARP1-KO model in the albino hairless SKH-1 mouse strain, which is a widely adopted mouse model to study UVB-induced NMSC. Since SKH-1 mice mainly develop cutaneous squamous cell carcinoma (SCC) upon chronic UVB-exposure, our present study reports the role of PARP1 in development of SCC. Using the newly developed PARP1-KO and PARP1-WT SKH-1 mice with or without topical application of PARP inhibitor, we report that the absence of PARP1 or its activity in skin of both male and female SKH-1 mice significantly reduces the SCC tumor burden and prolongs the tumor latency period. The analyses of appearance and growth of individual tumors on a weekly basis during this protocol also revealed that targeting of PARP1 was most effective in suppressing the premalignant stage of the SCC development. Our results are surprising in light of the reported onco-suppressive property of PARP1 and its catalytic activity in alkylating DNA damage-induced tumorigenesis and the increased susceptibility of other NER protein knock-out mice to UVB-induced SCC. We reason that the roles of PARP1 in UVB-induced cellular processes other than NER, such as cell death and immune modulations, can account for our observation. While further studies are required to understand these roles of PARP1 in UVB-induced cellular processes, our study underscores the potential for use of PARP inhibitors as a novel chemopreventive agents against UVB-induced SCC.

<p>  </p> <p>Cyanobacteria are among the simplest organisms to display circadian rhythms that synchronize endogenous physiological activities with a ~12-hour-light:12-hour-dark (12L:12D) cycle of the external environment. Detected by the input pathway composed of CikA and LdpA proteins, light is transduced to the central circadian oscillator encoded by the gene cluster <em>kaiABC. </em>While KaiC phosphorylation is primarily regulated by KaiA and KaiB proteins, two key components of the output pathway, RpaA and SasA proteins, mediate between KaiC phosphorylation, genome-wide expression, and control of cell division. In this study, <em>Synechococcus elongatus </em>UTEX 2973 showed similar growth patterns when subjected to white light only and white light supplemented with ultraviolet A (UV-A) radiation under 12L:12D intervals, although UV-A radiation hindered growth during light periods. Under continuous illumination, growth rates of <em>S. elongatus </em>UTEX 2973 were reduced by UV-A radiation but reflected intrinsic circadian rhythmicity. To elucidate the critical role of the circadian clock, a mutant void of <em>kaiABC</em> was generated via the CRISPR/Cpf1 system. A dysfunctional clock severely disrupted inherent growth rhythmicity, which was exacerbated by UV-A radiation. To investigate the effects of UV-A radiation on transcription patterns in <em>S. elongatus </em>UTEX 2973, expression levels of circadian genes, specifically <em>kaiABC</em>, <em>cikA</em>, <em>lpdA</em>, <em>rpaA</em>, and <em>sasA</em>, were assessed by qPCR analysis. For the UV-A-treated wild-type strain, <em>kaiA</em> and <em>kaiB</em> expression was generally downregulated, <em>kaiC</em> expression was upregulated during the second dark period, and <em>rpaA</em> expression was either upregulated or downregulated depending on the period. For the UV-A-treated Δ<em>kaiABC </em>strain, <em>lpaA</em> expression was upregulated in darkness, whereas <em>rpaA</em> and <em>sasA</em> expression was downregulated during light periods. When Δ<em>kaiABC </em>and wild-type strains were examined in the presence and absence of UV-A radiation, expression of <em>lpaA</em>, <em>rpaA</em>, and <em>sasA</em> was universally downregulated, yet <em>cikA</em> expression was upregulated in the dark. This study was the first to evaluate the impact of UV-A radiation on cyanobacterial circadian rhythms, in which UV-A radiation negatively affected cyanobacterial growth and strongly altered gene expression patterns over time. Without the circadian clock, rhythmicity of growth and transcription was demolished, such that the consequences were aggravated for the output pathway that relayed signals downstream from the central oscillator. </p>

No description available.

The near ultraviolet absorption spectra of cyclohexanone, cyclohexanone α, α, α', α'd₄ and cyclohexanone d₁₀ have been recorded and analysed under low and high resolution. The vibrational and rotational structure accompanying the electronic singlet-singlet ṉ→π* transition have been analysed. Some complementary information has been obtained from the infrared vapour spectrum of cyclohexanones. The geometries of the ground and first excited state have been determined. In the excited state configuration, the oxygen atom was bent out of the plane of the three adjacent carbon atoms by about 30º, and the carbon oxygen bond increases by 0.08 Å between the ground state and the excited state. Some ring modes are strongly active in the electronic spectra of the three isomers. This may indicate some coupling between the carbonyl group and the ring. The results obtained by band contour analysis are consistent with those obtained by calculation of a double minimum potential function, as well as those obtained in previous work on related molecules. / Thesis / Master of Science (MSc)