Objective: To investigate the association between hospital investment in human resources variables and patient safety, specifically after surgery adverse events in Florida hospitals. We performed the analysis to identify the association of after surgery complication rates with full time equivalent employees (FTEs) per admission and per patient day, expenses per admission and per patient day and, the percent of total operating expense accounted for by payroll expenses. Design: A cross sectional analysis using inpatient hospital discharge data and financial data from seventy short-term general hospitals, both for-profit and not-for-profit. Methods: Discharge data from year 2000 was obtained from Agency for Health Care Administration (AHCA). This data was used to calculate Agency for Healthcare Research and Quality (AHRQ) Patient Safety Indicators (PSIs) related to after surgery complications in 840,945 hospital discharge records from 70 short-term general hospitals across the state of Florida. The predictor variables include: payroll expenditures per admission, payroll expenditures per patient day, personnel (FTE) per admission, personnel (FTE) per patient day and payroll expense as a percent of total operating expenses. Main outcome measures: Nine patient safety indicators defined by AHQR and specific to after surgery complications: complications of anesthesia, foreign body left during procedure, postoperative hemorrhage or hematoma, postoperative physiologic and metabolic derangement, postoperative pulmonary embolism or deep vein thrombosis, postoperative respiratory failure, postoperative sepsis, postoperative wound dehiscence. Results: Patient safety indicator rate showed an inverse relationship with the percent of total operating expense represented by payroll, Personnel per patient day and personnel per admission. The patient safety indicators showing significant relationship with hospital human resource characteristics are postoperative hemorrhage or hematoma (p=0.0002), postoperative hip fracture (p<0.0001), and postoperative sepsis (p=0.0371). Conclusion: Human resource investment is positively related to favorable outcomes, although the effect varies across the type of outcomes.

"April 1999." Includes bibliographical references (leaves 46-51). Aims to collect information about the numbers of dental workers who are sensitive or allergic to nickel and to help identify signs which might predict those people who are most likely to be sensitive to nickel. Uses a standard patch test to identify sensitive subjects.

Gestational diabetes (GDM) is a potentially serious disorder requiring timely diagnosis and management to prevent adverse maternal and fetal outcomes. Of increasing concern today, when treating the woman with GDM, is the need to provide every woman with an intensive management plan to optimise the likelihood of favourable pregnancy outcomes. Early identification of those women with GDM who require insulin therapy in addition to diet therapy would be beneficial in the planning and standardisation of clinical management protocols, to enhance pregnancy outcomes and increase cost benefits with improved allocation of resources. The aim of this study was to evaluate the ability of the fasting plasma glucose level (FPG) at diagnosis to predict an increased risk to the fetus and the need for insulin therapy in a pregnancy complicated by GDM. A prospective longitudinal study design and recruitment by convenience sample was used. Data were obtained from 327 women and their babies. Diagnosis of GDM was made by a 75 gram oral glucose tolerance test (OGTT) using Australasian Diabetes in Pregnancy Society (ADIPS) criteria with the exception of seven women diagnosed on a blood glucose level >11.1mmol/l. Following consent of the women data were collected by a self report questionnaire and the medical record system at three points; at first intervention, following delivery and at the postpartum OGTT. Demographic, social, medical, maternal and neonatal outcome data were collected. The management protocol was similar for all of the women. Following nutritional intervention any woman who could not meet the glycemic targets of <= 5mmol/l fasting and/or <= 6.5mmol/l two hours postprandial was commenced on insulin therapy. The women had a mean age of 32 years, body mass index (BMI) of 25.7 and parity of 2 (range 1-12). Diagnosis was made at an average of 30 weeks and 70 women required insulin therapy with a mean dose of 34 IU per day, commencing at a mean of 31 weeks gestation. Mean birthweight was 3400G. Of the babies 12% were >4000G. Congenital abnormalities occurred in 3%, neonatal morbidities in 2% and there was 1 death in utero. Logistic regression analysis found the following significant associations: Increasing maternal BMI was related to increasing FPG levels at diagnosis and the requirement of higher insulin doses. There was a negative linear relationship to weight gain. Ethnicity was associated with maternal BMI and ethnicity with BMI was associated with birthweight in the specific ethnic group. BMI with insulin therapy as a covariate and the FPG value at OGTT were predictive of persistent glucose intolerance in 14% of women postpartum. Each value of the OGTT was a significant predictor of the need for insulin therapy as a function of the week of gestation. The FPG level was the statistical model of best fit. A 50% probability for requiring insulin was reached with a FPG at diagnosis of 4.0 mmol/l if tested at 10 weeks gestation, 5.1mmol/l at 20 weeks and 6.1 mmol/l at 30 weeks (p<.001). These results support the substantive research aim of the study. The model has the power to predict the probability (risk) of requiring insulin therapy based on the maternal FPG level at the OGTT according to the week of gestation. The study results demonstrate that glucose intolerance is linked to a number of adverse maternal and fetal outcomes in a continuous and graded fashion. The degree of reversibility of maternal and fetal risk through therapeutic interventions such as nutrition therapy, blood glucose monitoring, exercise and active patient participation aimed at improving glucose tolerance is unknown. Therefore, the rationale for, and feasibility of, new treatment strategies such as the application of this statistical model as a management approach require large scale randomised intervention studies, oriented toward measuring maternal and fetal outcomes amongst different populations.

Miami’s marketers have a long and successful history of creating and recreating imagery that draws visitors towards the "magic city" or the "tropical playground". This thesis investigates Miami’s marketing and its roots by analyzing the role and legacy of segregation in order to examine how tourism and its image relate to issues of exclusion and inequality. An inclusive rethinking of the definitions and usage of culture is then advocated as an important theoretical shift that could benefit development and revitalization in the city’s economically poorest neighborhoods. Analysis (through case studies, semi-structured interviews and GIS analysis) then shows how historic patterns of exclusion and adverse incorporation, especially in regard to tourism, are reproduced in much of Miami’s contemporary marketing, with the Greater Miami Convention and Visitors Bureau (GMCVB) playing an important role in this process. The Black community especially suffers greater levels of exclusion from Miami’s tourism and marketing and therefore has the most to gain from a shift in policy and perception. Community-based cultural tourism has functioned in various US cities as a tool to assist urban revitalization however Miami has yet to implement such a program. The results of this research suggest a number of recommendations for cultural tourism’s implementation in Miami, emphasizing the need for a community-based coalition of non-profit organizations utilizing governmental, marketing and creative/artistic partnerships.

M.S. / Bio-organic Chemistry / Single doses of tetrachlorobiphenyls, shown to be free of any chlorinated dibenzodioxins or dibenzofurans to a level of 1 ppm, were given to rhesus monkeys (Macaca mulatta) and the hepatic microsomal enzyme response measured periodically for 32 days. Liver biopsies, obtained by a closed needle technique, provided the tissue samples. Aryl hydrocarbon hydroxylase (measured as benzo[a]pyrene hydroxylase), aminopyrine - N - demethylase and cytochrome P-450 were measured on each sample. Animals treated with 25 mg/kg body weight of 2,5,2' ,5'- tetrachlorobiphenyl showed a marked increase in the demethylase activity, which peaked at 1 to 2 days after treatment, and had no effect on the x hydroxylase activity or the position of the absorption maximum of the CO difference spectrum of cytochrome P-450. This is phenobarbital like inductive behavior. The animals treated with 1 mg/kg body weight of 3, 4, 3’, 4’-tetrachlorobiphenyl showed a 3-methylcholanthrene type inductive profile. The hydroxylase activity was significantly increased and peaked at 2 days after treatment. The demethylase activity was not changed. The position of the cytochrome P-450 difference spectrum absorption maximum was shifted to 448 nm. The control animals received just the acetone / corn oil vehicle and showed no changes in any of the biochemical activities measured in the course of this experiment. This data supports the structure activity relationships, established in rats, for chlorobiphenyls as inducers of hepatic microsomal enzyme activity in rhesus monkeys.

Genetically determined differences in drug metabolism and disposition and drug targets play a pivotal role in the interindividual variability in the clinical outcome of antipsychotic treatment. The aim of this thesis was to study the impact of polymorphisms in genes involved in the pharmacokinetics and pharmacodynamics of antipsychotics, with special focus on their extrapyramidal and metabolic adverse effects. Polymorphisms in serotonin 2A and 2C receptor coding genes (HTR2A and HTR2C) were found to be associated with the risk to develop extrapyramidal side effects (EPS) in patients on short term perphenazine treatment. A further study in a larger group of patients on long term treatment with various classical antipsychotics confirmed the association between occurrence of EPS and HTR2C polymorphisms. In another study, dose corrected steady state serum clozapine and N-desmethylclozapine concentrations (C/D) and insulin elevation during clozapine therapy were found to correlate with CYP1A2 but not with CYP2D6 polymorphisms. Furthermore, HTR2C and HTR2A polymorphisms were found to have significant influences on BMI and C-peptide levels in patients treated with olanzapine and clozapine. Evaluation of the impact of polymorphisms in genes encoding CYP3A4, CYP3A5 and P-glycoprotein (ABCB1) in addition to CYP2D6 on the steady state plasma levels of risperidone, 9-hydroxyrisperidone and their active moiety revealed a significant influence of ABCB1 genotype on 9-hydroxyrisperidone and active moiety C/Ds, while CYP2D6 genotype associated with risperidone C/Ds but not with 9-hydroxyrisperidone or active moiety C/D. We have shown that polymorphisms in genes involved in the pharmacokinetics and the pharmacodynamics of antipsychotic drugs play a role in the occurrence of adverse effects, both EPS and metabolic disturbances, induced by antipsychotic treatment. Genotyping for HTR2A, HTR2C, CYP1A2, CYP2D6 and ABCB1 polymorphisms may therefore potentially provide useful information to identify patients at higher risk to develop EPS or metabolic adverse during schizophrenia treatment with antipsychotic drugs.

Clinical characteristics of idiosyncratic drug reactions (IDRs) suggest that they are immune mediated. Penicillamine-induced autoimmunity in Brown Norway rats was used as a tool for mechanistic studies of this type of IDR. It has been shown that T helper 17 (Th17) cells play a central role in many types of autoimmune diseases. This study was designed to test whether Th17 cells are involved in the pathogenesis of penicillamine-induced autoimmunity. In sick animals, interleukin (IL) 6 and transforming growth factor-β1, known to be driving forces of Th17 differentiation, were consistently increased following penicillamine treatment. IL-17 and IL-22, characteristic cytokines produced by Th17 cells, were increased in sick animals. Furthermore, the percentage of IL-17-producing CD4 T cells was significantly increased, but only in sick animals. Retinoic acid, which has been reported to inhibit Th17 cell development, made the autoimmunity worse, increased IL-6 production, and did not decrease the number of Th17 cells. An infiltration of CD8 cytotoxic T cells in the liver suggests that they may be the key player in causing liver toxicity induced by D-penicillamine. Drug-induced liver injury (DILI) is one of the major causes of morbidity, mortality, and drug candidate failure. Recently, it has been suggested that Th17 cells may play an active role in inflammatory human liver diseases. In a study of patients being treated with isoniazid, some patients developed mild liver injury. The percentage of Th17 cells in the blood of these patients significantly increased when the ALT increased, and this suggests that they play a role in the mechanism of this liver injury. Furthermore, IL-10-producing T cells also increased and this may have prevented the development of severe liver injury. In another study, two hours after treatment of mice with acetaminophen there was a significant increase in Th17 cells in the liver. This rapid response suggests that Th17 cells can be part of the innate immune response to liver injury. Our data provided evidence that Th17 cells are involved in both “toxic” and idiosyncratic liver toxicity. This pathway could be a new target for the therapeutic interventions to treat DILI.

An animal model of nevirapine (NVP)-induced skin rash was used to test the hypothesis that sulfonation of 12-OH NVP, a metabolite of NVP proven essential for rash development, is the link between 12-OH NVP and the skin rash. Female Brown Norway (BN) rats were co-treated with NVP or 12-OH NVP and sulfation inhibitors dehydroepiandrosterone (DHEA) and salicylamide. Co-treatment with salicylamide markedly decreased formation of the sulfate conjugate but did not prevent development of the rash suggesting that the sulfate is not involved. However, it is not known whether the sulfate formation in the skin was affected. Co-treatments with DHEA decreased the sulfate formation and prevented the rash but also had other effects on NVP metabolism. This implies that the sulfate metabolite is responsible for the rash. Additional studies will be required to resolve these conflicting results.

An animal model of nevirapine (NVP)-induced skin rash was used to test the hypothesis that sulfonation of 12-OH NVP, a metabolite of NVP proven essential for rash development, is the link between 12-OH NVP and the skin rash. Female Brown Norway (BN) rats were co-treated with NVP or 12-OH NVP and sulfation inhibitors dehydroepiandrosterone (DHEA) and salicylamide. Co-treatment with salicylamide markedly decreased formation of the sulfate conjugate but did not prevent development of the rash suggesting that the sulfate is not involved. However, it is not known whether the sulfate formation in the skin was affected. Co-treatments with DHEA decreased the sulfate formation and prevented the rash but also had other effects on NVP metabolism. This implies that the sulfate metabolite is responsible for the rash. Additional studies will be required to resolve these conflicting results.

Essay One examines the asymmetric information problem between primary insurers and reinsurers in the reinsurance industry and contributes uniquely to the separation of adverse selection from moral hazard, if both are present. A two-period principal-agent model is set up to identify the signals of adverse selection and moral hazard generated by the actions of the primary insurer and to provide a basis for corresponding hypotheses for empirical testing. Using data from the National Association of Insurance Commissioners (NAIC) and A.M. Best Company, the empirical tests show that the problem of adverse selection exists in the reinsurance market between the affiliated insurers and non-affiliated reinsurers, and even between closely related affiliated insurers and reinsurers. There is no evidence indicating the presence of moral hazard in the reinsurance market. To address the issue of soaring property insurance premiums and coverage availability in states that are subject to hurricane risks, state and federal governments have not only regulated the private insurance market but have also intervened directly into markets by establishing government-funded insurance programs. With coexisting public and private insurance mechanisms and price regulation, the risk of cross subsidization and a subsequent moral hazard problem may arise. By using data from the Florida Citizens Insurance Corporation, the Florida Hurricane Catastrophe Fund, the Flood Insurance and the private homeowner insurance market in Florida from 1998 to 2007, the second essay examines the moral hazard problems arising from government regulation and involvement in the private insurance sector. In sum, the provision of national flood insurance is found to be positively related to the population growth in the state of Florida, which shows that state immigrants can take advantage of the lower cost of flood insurance when relocating in higher-risk areas. Further, we find that national flood insurance and the catastrophe fund complement the development of the private insurance sector, while the residual market hinders the development of private property insurance market.