Indiana University-Purdue University Indianapolis (IUPUI) / Objectives: Repair of crown margins may extend the functional life of existing crowns. However, the longevity of such treatment is unknown. This study determined the survival time of crown margin repairs (CMR) with glass-ionomer (GI) and resin-modified glass-ionomer cements. Methods: We queried axiUm (Exan Group, Coquitlam, BC, Canada) database for permanent teeth that underwent CMR in the Graduate Operative Dentistry Clinic, Indiana University School of Dentistry (IUSD), Indianapolis, Ind., USA, from January 1, 2006 through January 1, 2018. Since there is no CDT code for the CMR procedure, CDT codes for resin-composite and GI restorations (D23XX) were queried; these patients also had treatment notes that indicated CMR. The final data set included patient ID, birth date, gender, dates of treatments, CDT codes, tooth type, tooth surface and existing findings. Two examiners developed guidelines for record review and manually reviewed the clinical notes of patient records to confirm CMR. Only records that were confirmed with the presence of CMR were retained in the final dataset for survival analysis. Survival time was calculated by Kaplan-Meier statistics and a Cox Proportional Hazards model was performed to assess the influence of selected variables (p < 0.05). Results: 214 teeth (115 patients) with CMR were evaluated. Patient average age was 69.4  11.7 years old. Posterior teeth accounted for 78.5 percent (n = 168) of teeth treated. CMRs using GI had a projected 5-year survival rate of 62.9 percent (K-M Analysis) and an 8.9 percent annual failure rate. Cox Proportional Hazards Regression analysis revealed that none of the factors examined (age, gender, tooth type) affected time to failure. Conclusion: CMRs may extend the longevity of crowns with defective margins. Larger EHR studies or case control studies are needed to investigate other variables, such as the caries risk status or the severity of defects that may affect the survival rate of CMRs.

The behavior of repairable equipment is often modeled under assumptions such as perfect repair, minimal repair, or negligible repair. However the majority of equipment behavior does not fall into any of these categories. Rather, repair actions do take time and the condition of equipment following repair is not strictly "as good as new" or "as bad as it was" prior to repair. Non-homogeneous processes that reflect this type of behavior are not studied nearly as much as the minimal repair case, but they far more realistic in many situations. For this reason, the quasi-renewal process provides an appealing alternative to many existing models for describing a non-homogeneous process. A quasi-renewal process is characterized by a parameter that indicates process deterioration or improvement by falling in the interval [0,1) or (1,Infinity) respectively. This parameter is the amount by which subsequent operation or repair intervals are scaled in terms of the immediately previous operation or repair interval. Two equivalent expressions for the point availability of a system with operation intervals and repair intervals that deteriorate according to a quasi-renewal process are constructed. In addition to general expressions for the point availability, several theoretical distributions on the operation and repair intervals are considered and specific forms of the quasi-renewal and point availability functions are developed. The two point availability expressions are used to provide upper and lower bounds on the approximated point availability. Numerical results and general behavior of the point availability and quasi-renewal functions are examined. The framework provided here allows for the description and prediction of the time-dependent behavior of a non-homogeneous process without the assumption of limiting behavior, a specific cost structure, or minimal repair. / Ph. D.

No description available.

Loss of heterozygosity (LOH) is considered a causal event in the formation of many cancers, with increasing evidence suggesting that DNA double-strand breaks (DSBs) play a major role in its occurrence. Despite its prominence in cancer, however, the precise molecular mechanisms responsible for extensive LOH and how such events are suppressed in normal cells is poorly understood. To investigate the mechanisms responsible for extensive break-induced LOH in eukaryotes, this study took advantage of an assay system in which such events could be identified through screening for loss of an auxotrophic his3⁺ marker, found ~25kb distal to an HO-endonuclease cut site in a non-essential minichromosome in Schizosaccharomyces pombe. Studies using this system had previously shown that extensive break-induced LOH in wild-type background, whilst infrequent, was predominantly associated with large translocations resulting from both allelic crossovers during G2 phase and breakinduced replication (BIR). Such extensive loss of allele specific information was also found to require rhp55⁺, rhp51⁺, rhp54⁺ and mus81⁺. This study has identified an additional role for the MRN complex, Rad22 and RPA in such break-induced translocations, suggesting that both allelic crossovers and BIR require homologous recombination (HR) in fission yeast. Surprisingly, break-induced extensive LOH was still observed in HR mutants. In contrast to wild-type cells, however, such extensive LOH was found to arise predominantly through de novo telomere addition at, or near, the break-site. Interestingly, telomere addition was most frequently observed in a rad22Δ background that disrupts HR following end resection. Further analysis demonstrated that de novo telomere addition was also significantly increased in ku70Δ rhp55Δ cells. Moreover, overexpression of rhp51 in rhp55Δ cells led to a substantial reduction in break-induced de novo telomere addition. Together, these findings support a model in which HR prevents de novo telomere addition at DSBs by competing for resected ssDNA ends. In addition to providing information on break-induced LOH this study has identified a requirement for the MRN complex in efficient repair in rhp55Δ cells, which was previously found to occur via sister chromatid recombination (SCR) or a HRdependent end-joining pathway (EJ). Interestingly, deletion of MRN components also resulted in an increase in telomere addition, providing further evidence that HR competes with telomere addition for the repair of DSBs. Overall, these findings shed light on the competitive relationships between pathways of DSB repair/misrepair in S. pombe and how such mechanisms contribute to the prevention or promotion of genome instability.

Photocopy of typescript. / Digitized by Kansas Correctional Industries

This thesis combines four manuscripts of which I am the first author. The first manuscript examines the phase separation process and related process parameters. This article provides detailed experimental results of the delivery and separation process. During the delivery of 40% Liquid-to-Powder-Ratio (LPR) paste, only 62[plus ou moins]3 % of the paste initially present in the 10-mL syringe could be injected. Thereafter, the remaining paste in the syringe was not amendable to injection suggesting the existence of liquid separation. The LPR of the extruded fraction of a 37% LPR paste ranged from 40.9[plus ou moins]2.0 % to 42.7[plus ou moins]2.1 %. On the other hand, a shortage of water content was measured for the paste left in the syringe. Furthermore, this shortage was gradual, ranging from 27.3[plus ou moins]1.9 % at the plunger side to 30.9[plus ou moins]1.6 % at the tip side. In addition, this article presents rheological measurements of the paste showing clearly that the limitation was not related to the viscosity of the paste but rather to the phase separation process. Specifically, the yield stresses were around 66[plus ou moins]2 Pa, 19[plus ou moins]2 Pa, and 8[plus ou moins]0 Pa for 40%, 50%, and 65% LPR suspensions, respectively. For the three studied LPRs, the viscosity rapidly dropped with an increase of shear rate to a level below 10 Pas. The second manuscript examines the possibility that fine particles migrate faster than large particles during injection, hence leading to a so-called size separation. This size separation process can be expected from the scientific literature, but had not been investigated prior to my study. In a way, the size separation is very similar to the phase separation process. An electrohydraulic system was used to control the delivery process. The result of this second study, showed no evidence of size separation. It was therefore concluded that the main mechanism underlying the limited injectability is the liquid phase filtration through the porous particles bed of the paste. The third manuscript examines the role of powder porosity ([epsilon]) and permeability. For that purpose, an electronically assisted device was used to measure the powder permeability. In this study, three powders were examined for comparison and better understanding. In addition, the powder permeability was correlated with the paste injectability. Adding 3 wt% of a fine nanosized powder to the [bêta]-TCP powder decreased the mixture permeability at a porosity of [varepsilon] = 67.5% from 6.4.10[exposant]-13 m[exposant]2 to 5.6.10[exposant]-13 m[exposant]2 and increased the injected volume fraction from 70.8[plus ou moins]1.9 % to 84.5[plus ou moins]0.9 %. The results showed clear evidence that the injectability can be improved by admixing different powders. However, permeability was not a strong predictor of the liquid separation phenomenon. The last manuscript provides a practical solution to reduce phase separation occurrence. For that purpose an ultrasonication process was suggested and applied during the delivery process to improve injectability. Specifically, sonicating the paste reduced agglomeration, decreased paste viscosity due to the shear thinning and therefore reduced phase separation. The result of the ultrasound assisted delivery was remarkably effective since it has been able to fully deliver highly concentrated paste, with minimal force exerted by hand. For instance, the injectable volume fraction of a 40% LPR paste injected with a 5-mL syringe increased significantly from 71.3[plus ou moins]0.5 % to 99.1[plus ou moins]0.9 % using 150 microns ultrasonic amplitude at a 20 kHz frequency. This chapter provides clear evidence that an electromechanical approach can be used to improve the injectability of a calcium phosphate paste. This thesis addresses an important limitation of calcium phosphate cements, namely phase separation during injection. This thesis also provides a scientific understanding and a practical solution for this problem. The electromechanical solution proposed here is one out of several possible solutions. Future work may focus on building numerical tools to help in the design of the powder and to understand the link between powder properties, rheology, syringe geometry and phase separation."--Résumé abrégé par UMI

No description available.

It is vital for the survival of an organism that it can repair damage to its DNA. Exogenous and endogenous sources of damage are dealt with by a variety of repair pathways that have evolved to repair specific types of damage. Organisms in the archaeal domain, the third domain of life, contain homologues of many of the eukaryotic repair proteins, however little is known about how damage is detected in the archaeal domain. Microarray studies in the archaeal species Sulfolobus solfataricus determined a number of genes whose expression was effected by UV radiation (work by Dr D Götz). The change in expression of nine of these genes was confirmed by RT real time PCR. The expression of these genes was then investigated after exposure to different damaging agents, Mitomycin C, Methyl methane sulfonate, Phleomycin and Hydrogen peroxide. The expression of two genes, transcription factor tfb-3 and cell division control gene cdc6-2, was up regulated in all damage conditions. There was a huge induction of the dps-like gene (sso2079) after hydrogen peroxide damage. Transcription from this genes promoter was shown to be strong in vitro (work by Dr S Paytubi) suggesting a repressor was controlling the gene in vivo. A palindromic repeat in the promoter of the dps-like gene was used to ‘fish’ for a transcriptional repressor and the Sso2273 protein, a homologue of the diphtheria toxin repressor (DtxR) from Corynebacterium diphtheria, was identified as a possible repressor. Sso2273 was expressed and purified, and its crystal structure solved, its paralogue, Sso0669, was also expressed and purified. Electrophoretic mobility shift assays showed that the Sso2273 protein does not bind DNA, and had no effect on transcription from any promoter used in in vitro transcription assays. However Sso0669 appeared to inhibit transcription, although the inhibition was not sequence specific. A knockout strain of S. solfataricus PBL2025 missing the sso2273 gene was produced and used in microarray experiments in an attempt to determine the role of Sso2273 within the cell. The absence of Sso2273 appeared to have no effect on the expression of the dps-like gene, however strong repression of an operon containing genes involved in Sulphur assimilation was observed.

published_or_final_version / Industrial Engineering / Master / Master of Science in Engineering

published_or_final_version / Industrial Engineering / Master / Master of Science in Engineering