AN OCCUPATIONAL INJURY MANAGEMENT INFORMATION SYSTEM FOR THE UNIVERSITY OF TEXAS HEALTH SCIENCE CENTER AT HOUSTON

The purpose of this research and development project was to develop a method, a design, and a prototype for gathering, managing, and presenting data about occupational injuries.^ State-of-the-art systems analysis and design methodologies were applied to the long standing problem in the field of occupational safety and health of processing workplace injuries data into information for safety and health program management as well as preliminary research about accident etiologies. The top-down planning and bottom-up implementation approach was utilized to design an occupational injury management information system. A description of a managerial control system and a comprehensive system to integrate safety and health program management was provided.^ The project showed that current management information systems (MIS) theory and methods could be applied successfully to the problems of employee injury surveillance and control program performance evaluation. The model developed in the first section was applied at The University of Texas Health Science Center at Houston (UTHSCH).^ The system in current use at the UTHSCH was described and evaluated, and a prototype was developed for the UTHSCH. The prototype incorporated procedures for collecting, storing, and retrieving records of injuries and the procedures necessary to prepare reports, analyses, and graphics for management in the Health Science Center. Examples of reports, analyses, and graphics presenting UTHSCH and computer generated data were included.^ It was concluded that a pilot test of this MIS should be implemented and evaluated at the UTHSCH and other settings. Further research and development efforts for the total safety and health management information systems, control systems, component systems, and variable selection should be pursued. Finally, integration of the safety and health program MIS into the comprehensive or executive MIS was recommended. ^

Clinical Impact of Couch Top and Rails on IMRT and Arc Therapy

Purpose: To evaluate the clinical impact of the Varian Exact Couch on dose and volume coverage to targets and critical structures and tumor control probability (TCP) for 6-MV IMRT and Arc Therapy. Methods: Five clinical prostate patients were planned with both, 6-MV 8-field IMRT and 6-MV 2-field RapidArc using the Eclipse treatment planning system (TPS). These plans neglected treatment couch attenuation, as is standard clinical practice. Dose distributions were then recalculated in Eclipse with the inclusion of the Varian Exact Couch (imaging couch top) and the rails in varying configurations. The changes in dose and coverage were evaluated using the DVHs from each plan iteration. We used a tumor control probability (TCP) model to calculate losses in tumor control resulting from not accounting for the couch top and rails. We also verified dose measurements in a phantom. Results: Failure to account for the treatment couch and rails resulted in clinically unacceptable dose and volume coverage losses to the target for both IMRT and RapidArc. The couch caused average dose losses (relative to plans that ignored the couch) to the prostate of 4.2% and 2.0% for IMRT with the rails out and in, respectively, and 3.2% and 2.9% for RapidArc with the rails out and in, respectively. On average, the percentage of the target covered by the prescribed dose dropped to 35% and 84% for IMRT (rails out and in, respectively) and to 18% and 17% for RapidArc (rails out and in, respectively). The TCP was also reduced by as much as 10.5% (6.3% on average). Dose and volume coverage losses for IMRT plans were primarily due to the rails, while the imaging couch top contributed most to losses for RapidArc. Both the couch top and rails contribute to dose and coverage losses that can render plans clinically unacceptable. A follow-up study we performed found that the less attenuating unipanel mesh couch top available with the Varian Exact couch does not cause a clinically impactful loss of dose or coverage for IMRT but still causes an unacceptable loss for RapidArc. Conclusions: Both the imaging couch top and rails contribute to dose and coverage loss to a degree that, if included, would prevent the plan from meeting clinical planning criteria. Therefore, the imaging and mesh couch tops and rails should be accounted for in Arc Therapy and the imaging couch and rails only in IMRT treatment planning.

Control of {\it recA\/} expression in {\it Escherichia coli}

The recA gene is essential for SOS response induction, for inducible DNA repair and for homologous recombination in E. coli. The level of recA expression is significant for these functions. A basal level of about 1000 molecules of RecA protein is sufficient for homologous recombination of the cell and is essential for the induction of the SOS response. Based on previous observations, two models regarding the origin of the basal RecA protein were postulated. One was that it comes from the leaky expression of the LexA repressed promoter. The other was that it is from another weak but constitutive promoter. The first part of this thesis is to study these possibilities. An $\Omega$ cartridge containing the transcription terminator of gene 32 of T4 phage was exploited to define a second promoter for recA expression. Insertion of this $\Omega$ cartridge downstream of the known promoter gave rise to only minor expression. Purification and N-terminus sequencing of the RecA protein from the insertion mutant did not support the existence of a second promoter. To determine whether the basal RecA is due to the leaky expression of the known LexA repressed promoter, recA expression of a SOS induction minus strain (basal level expression of recA) was compared with that of a recA promoter down mutation recA1270. The result demonstrated that there is leaky expression from the LexA repressed promoter. All the evidence supports the conclusion that there is only one promoter for both basal and induced expression levels of recA.^ Several translation enhancer sequences which are complementary to different regions of the 16S rRNA were found to exist in recA mRNA. The leader sequence of recA mRNA is highly complementary to a region of the 16S rRNA. Thus it appeared that recA expression could be regulated at post-transcriptional levels. The second part of this thesis is focused on the study of the post-transcriptional control of recA expression. Deletions of the complementary regions were created to examine their effect on recA expression. The results indicated that all of the complementary regions were important for the normal expression of recA and their effects were post-transcriptional. RNA secondary structures of wild type recA mRNA was inspected and a stem-loop structure was revealed. The expression down mutations at codon 10 and 11 were found to stabilize this structure. The conclusions of the second part of this thesis are that there is post-transcriptional control for recA expression and the leader sequence of recA mRNA plays more than one role in the control of recA expression. ^