Comparison of in vivo and in vitro models to evaluate pulp temperature rise during exposure to a Polywave® LED light curing unit

Objectives: To measure and compare in vivo and in vitro pulp temperature (PT) increase (ΔTEMP) over baseline, physiologic temperature using the same intact upper premolars exposed to the same Polywave® LED curing light. Methodology: After local Ethics Committee approval (#255,945), local anesthesia, rubber dam isolation, small occlusal preparations/minute pulp exposure (n=15) were performed in teeth requiring extraction for orthodontic reasons. A sterile probe of a temperature measurement system (Temperature Data Acquisition, Physitemp) was placed within the pulp chamber and the buccal surface was sequentially exposed to a LED LCU (Bluephase 20i, Ivoclar Vivadent) using the following exposure modes: 10-s low or high, 5-s Turbo, and 60-s high. Afterwards, the teeth were extracted and K-type thermocouples were placed within the pulp chamber through the original access. The teeth were attached to an assembly simulating the in vivo environment, being similarly exposed while real-time temperature (°C) was recorded. ΔTEMP values and time for temperature to reach maximum (ΔTIME) were subjected to two-way ANOVA and Bonferroni's post-hoc tests (pre-set alpha 0.05). Results: Higher ΔTEMP was observed in vitro than in vivo. No significant difference in ΔTIME was observed between test conditions. A significant, positive relationship was observed between radiant exposure and ΔTEMP for both conditions (in vivo: r2=0.917; p<0.001; in vitro: r2=0.919; p<0.001). Conclusion: Although the in vitro model overestimated in vivo PT increase, in vitro PT rise was close to in vivo values for clinically relevant exposure modes

Designing simulation-based learning activities: A systematic approach

Containing examples of innovations from around the world, the book offers opportunities to make clear connections between the underlying rationale for the use of simulation, and what this looks like in practice

Analysis of stress induced retinoblastoma protein activation using an SiRNA screen

Activation of the retinoblastoma protein (RB), by stresses such as ionizing radiation (IR) or hypoxia, causes a cell cycle arrest and has been suggested to convey therapeutic resistance to cancer cells. To investigate the cell signaling networks mediating RB activation, with the aim of uncovering potential targets for sensitisation of cancer cells, I developed and carried out a high-throughput RNA interference screen of the Dharmacon kinome-covering small interfering (si)RNA library. This identified seven siRNA gene targets required for RB activation in response to ionizing radiation; PRPK, PRKACG, STK4, DYRK1A, HK1, CDK4 and p21-cip1/waf1. Silencing of these genes effectively reduced the percentage of cells exhibiting G1-like characteristics after IR treatment. Two of these seven targeted genes, PRPK and STK4, appear to be involved in IR-induced p21-cip1/waf1 upregulation and silencing of these two genes sensitised colon carcinoma cells to radiation treatment. Biochemical characterisation of cells with PRPK knockdown revealed that its expression is required for p53 upregulation and activation in response to IR. The work presented here provides first time evidence of a role for PRPK in the radiation response and implicates this gene product and the gene product of STK4 as targets to sensitise cells to radiation. The work further identifies other gene products necessary for RB activation and G1/S checkpoint activation, yet ablation of these did not confer loss of p21-cip1/waf1 induction or sensitisation to irradiation, indicating wiring of these gene products into mechanisms that promote radiation survival in the absence of RB activity and G1/S checkpoint control.EThOS - Electronic Theses Online ServiceGBUnited Kingdo