Class of 2014 Abstract / Specific Aims: The purpose of this study was to assess pharmacists’, pharmacy technicians’, and pharmacy interns’ knowledge of current Centers for Disease Control and Prevention (CDC) immunization guidelines for pregnant women. Methods: Questionnaires administered to volunteers during the Arizona Pharmacy Association (AzPA) 2013 Annual Convention and Trade Show collected data showing the volunteers’ level of knowledge about current immunization guidelines; data on professional roles (pharmacist, pharmacy intern, or pharmacy technician), years in practice, current immunization certification status and activity, and practice setting were also collected. Main Results: Questionnaires were completed by 112 volunteers, including 48 pharmacists, 25 pharmacy technicians, and 39 pharmacy interns. The overall percentage of correct answers from all participants was 33%. Pharmacists, pharmacy technicians, and pharmacy interns had correct answer percentages of 41%, 16%, and 34%, respectively. Pharmacy practitioners who were state certified to perform immunizations performed statistically significantly better than the non-certified group (44.2% correct versus 33% correct, P=0.012). Practitioners who work at a practice site that provides immunizations were compared with practitioners who do not, with results trending toward statistical significance, but falling just short (45.7% correct versus 36% correct, P=0.054). Conclusion: The general level of knowledge about CDC immunization guidelines appears to be inadequate among the volunteer group of pharmacy practitioners, possibly leading to missed opportunities for needed immunizations.

Background: At a primary care center in Brooklyn, New York, approximately 27% of diabetic patients with abnormal Hgb A1C fail to return for follow-up appointments, as recommended by the Centers for Disease Control and Prevention (CDC). According to electronic medical records (EMR), healthcare providers demonstrated inconsistency in ordering and monitoring Hgb A1C and clinic follow-up appointments for patients. Purpose: The purpose of this quality improvement project was to determine retrospectively the healthcare providers’ ordering, monitoring, and follow-up appointments for adult diabetic patients with abnormal Hgb A1Cs; to develop and implement astandardized process for healthcare providers to monitor and follow these patients, especially those with possible nonclinic follow-up compliance and abnormal Hgb A1C; to determine prospectively healthcare providers’ ordering, monitoring, and follow-up appointments; and to evaluate the prospective charts to determine if Hgb AIC results changed from abnormal to normal or elevation over time until the next follow-up appointment.

A groundbreaking narrative, which would come to be known as the theory of “deaths of despair”, emerged in 2015 from a study by Case and Deaton analyzing mortality rates in the United States between 1999 and 2013. They found an increasing trend in all-cause mortality rates due to drug poisonings, alcohol-related liver disease, and suicides, which they called “deaths of despair”, among non-Hispanic (NH) white Americans aged 45 to 54—this age group was called the midlife. Case and Deaton’s findings and their narrative about the hypothetical causes of their findings garnered significant attention. The authors of this narrative hypothesized that the observed increases in mortality rates were due to white individuals in midlife increasingly suffering from “despair” and proposed a causal link between increasing “despair” rates and increased mortality rates only among white Americans in midlife. Case and Deaton did not provide a clear definition of “despair”; they presumed that white Americans in midlife were hopeless about their prospects for the future compared to what their parents had attained. This provocative narrative persisted and gained momentum because it functioned as an explanation of recent events like the 2016 U.S. presidential election, rise in white nationalism, and far right extremism. These white-related events were thought to be expressions of an agonizing, poor, under-educated generation of white Americans increasingly suffering from hypothetical feelings of "despair”, which have led them to self-destructive behaviors and premature death. However, no study has investigated the central claim of this theory: whether there is evidence of an association between increased “despair” rates and increased mortality rates only among white individuals in midlife, particularly for those with low education. Moreover, there is little evidence of their hypothesis of an increasing epidemic of “despair” affecting only white Americans in midlife, particularly those with low education. The theory of “deaths of despair” can be understood through Geoffrey Rose’s framework of causes of incidence and causes of cases, which highlights the difference between between-population and inter-individual causes of disease. Rose’s argues that causes of incidence explain the changes in outcome rates between populations, and may be uniform and imperceptible within populations. On the other hand, the causes of cases explain why some individuals within a population are susceptible or at high risk of the outcome. Like Rose’s causes of incidence, the authors of the theory of “deaths of despair” argue that “despair” increased between the midlife white American population in 1999 and in 2014, which led to increased mortality rates. Conversely, this theory does not claim that some individuals are at higher risk of death due to “despair”, which would be analogous to causes of cases. Therefore, the contrast of interest to test the central claim of Case and Deaton’s theory of “deaths of despair” is a between-population contrast (causes of incidence). As such, this dissertation aims to test the claims of the theory of “deaths of despair” proposed by Case and Deaton at the right level (causes of incidence). I began by conducting a scoping review of the current literature providing empirical support to the different elements of this theory: 1) socioeconomic causes as causes of “despair”, “diseases of despair”, “deaths of despair”, and all-cause mortality, and 2) “despair” as the cause of “diseases of despair”, “deaths of despair”, and all-cause mortality. I found 43 studies that I organized and displayed in two graphs according to Rose’s causes of cases (individual-level causes of “deaths of despair”) and causes of incidence (between-population level causes of “deaths of despair” rates). In each graph, I showed the number of studies that provided evidence for the individual- or population-level elements of the theory of “deaths of despair”. Of these 43 studies, I found that only 13 studies explicitly stated that they tested this theory. Three studies provided different definitions of “despair”, which did not align with the previous vague definition provided by Case and Deaton about white individuals’ hopeless about their prospects for the future. Most studies provided individual-level evidence for “despair” increasing the likelihood of death and despair-related outcomes, which is analogous to a type III error—a mismatch between the research question and the level at which the studies’ design and analyses were conducted to answer that question. Further, no study addressed at the right level—between populations—the central claim of the theory of “deaths of despair”. This led me to review the literature around concepts similar to “despair” and propose a suitable indicator to test the claims of the theory of “deaths of despair”. I leveraged data from the National Health Interview Survey and the Centers for Disease Control mortality data to test whether increases in the prevalence of “despair” were associated with increases in all-cause mortality rates only among white individuals in midlife and whether this effect was bigger among low educated white individuals. To obtain a valid estimate of this association, I adapted econometric methods to develop a valid estimator of the association between increasing “despair” prevalence and increased all-cause mortality rates. After adjusting for potential confounders at the between-population level, I found that the trends in the prevalence of “despair” were negligible across all race and ethnic groups and that an increasing trend could not be identified. Further, I found no evidence that increasing prevalences of “despair” were associated with increased all-cause mortality rates among NH white individuals in midlife, or that this association was more pronounced for those with low education. Lastly, I conducted a similar analysis looking at the association between increased prevalences of “despair” and increased rates of “deaths of despair”. I replicated Case and Deaton’s observed increased rates of “deaths of despair” among white individuals in midlife. However, I found no evidence that increased prevalences of “despair” were associated with increased “deaths of despair” rates among white individuals in midlife or that this association was higher for those with low education. Together, these findings suggest that the claims about the causes of increased mortality rates among white Americans in midlife are at best, questionable, and at worst, false. My aim with this work is to challenge and provide a critical examination of the theory of "deaths of despair", which has fueled the narrative of a suffering white generation and justified recent problematic events as white individuals lashing out for being forgotten to despair and die. While Case and Deaton’s observed rise in mortality rates among whites is a reproducible fact, their narrative ignores other evidence of white racial resentment as the cause of rise in mortality among white individuals. With this work, I intend to help stopping the perpetuation of narratives that favor structural whiteness by promoting an unsubstantiated narrative of psychosocial harm experienced by white Americans. Ultimately, I hope this work helps shift the focus in public health away from Case and Deaton's findings, which may overshadow and detract from the stark reality that mortality rates for Black individuals significantly exceed those for white individuals.

Natural populations may be managed by humans for a number of reasons, with mathematical modelling playing an increasing role in the planning of such management and control strategies. In an increasingly heterogeneous, or `patchy' landscape, the interactions between distinct groups of individuals must be taken into account to predict meaningful management strategies. Invasive control strategies, involving reduction of populations, such as harvesting or culling have been shown to cause a level of disturbance, or spatial perturbation, to these groups, a factor which is largely ignored in the modelling literature. In this thesis, we present a series of deterministic, differential equation models which are used to investigate the impact of this disturbance in response to control. We address this impact in two scenarios. Firstly, in terms of a harvested population, where extinction must be prevented whilst maximising the yield obtained. Secondly, we address the impact of disturbance in an epidemic model, where the aim of the control strategy is to eradicate an endemic pathogen, or to prevent the invasion of a pathogen into a susceptible population. The movement of individuals between patches is modelled as both a constant rate, and a function which is increasing with population density. Finally, we discuss the 'optimal' control strategy in this context. We find that, whilst a population harvested from a coupled system is able to produce an inflated yield, this coupling can also cause the population to be more resistant to higher harvesting efforts, increasing the effort required to drive the population to extinction. Spatial perturbation raises this extinction threshold further still, providing a survival mechanism not only for the individuals that avoid being killed, but for the population as a whole. With regards to the eradication of disease, we show that disturbance may either raise or lower the pathogen exclusion threshold depending on the particular characteristics of the pathogen. In certain cases, we have shown that spatial perturbation may force a population to be susceptible to an infectious invasion where its natural carrying capacity would prevent this.

3 pp. / Mondell pine should not be planted within a mile of Comandra populations. Infection of pine occurs through needles by spores produced on Comandra, but spores produced on pine cannot re-infect pine. This article gives information about the disease cycle, the symptoms and prevention and control methods for blister rust.

Rapid blight is a new disease of cool season turf grasses that has occurred on over a dozen golf courses in Arizona. It is now known to be caused by Labyrinthula terrestris, an organism in a group referred to as the marine slime molds. A trial was conducted in fall 2003 and winter 2004 to evaluate efficacy of selected fungicides for control of rapid blight at a golf course in central Arizona with a previous history of disease. Plots were established in late October2003 on a practice green on which Bermuda was overseeded with Poa trivialis. Treatments included Compass, Insignia, Fore, Bordeaux, Kocide 2000, Microthiol Disperss, Ecoguard and Floradox in various combinations and application dates. Disease symptoms appeared about 6 weeks after the first mowing and were evaluated in mid January. Results indicate that applications of Fore, Insignia and tank mixes of Insignia and Compass with Fore gave excellent control. Bordeaux, Compass alone, Compass alternated with Fore, Insignia alone, and Kocide gave good control. Microthiol Disperss, Floradox and Ecoguard gave poor control.

Rove beetles (Osorius planifrons) can and often do cause extensive surface disruption on turf mowed at greens height. Two rates (1x and 2x of product label rate) of Crusade (fonophos), Sevin (carbaryl), DeltaGard (deltamethrin), and Chipco Choice (fipronil), were applied on September 28, 2001 on an SR1020 creeping bentgrass green. Percent rove beetle control was nearly 100% for DeltaGard at 9, 15 and 32 days after treatment, regardless of rate. Crusade had nearly 100% control at either rate at 9 days after treatment, which decreased slightly to 90-93% control by 15 days after treatment. Deltamethrin maintained 95% and 98% control at the 1x and 2x rates respectively, at the close of the test (32 DAT). Crusade maintained 93% and 98% control at the 1x and 2x rates at 32 DAT. Chipco Choice had a maximum control of 24% at 7 DAT when applied at the 1x rate, and a maximum control of 57% at 32 DAT when applied at the 2x rate. Sevin provided low levels of control which peaked at 53% at the 1x rate at 9 DAT, which decreased immediately afterwards. Delta-Gard and Crusade provided excellent control levels of rove beetles on SR1020 bentgrass greens.

Rapid blight is a new disease of cool season turf grasses that has occurred on several golf courses in Arizona over the past five years. It is now known to be caused by a Labyrinthula sp., an organism in a group referred to as the marine slime molds. A trial was conducted in fall 2002 to evaluate efficacy of selected fungicides for control of rapid blight at a golf course in central Arizona with a previous history of disease. Plots were established in October 2002 on a practice green on which Bermuda was overseeded with Poa trivialis. Treatments included Compass, Insignia, Fore, Eagle and Aqueduct in various combinations and application dates. Disease symptoms appeared several days after the first mowing and continued for over three months. Results indicate that both pre- and post-plant applications of Fore and post-plant applications of Insignia and Compass gave good control. The best results were obtained with the treatment of Fore combined with Compass that included a pre-plant application of Fore, or with post-plant application of Insignia.

A number of turfgrasses were screened in the greenhouse and laboratory for susceptibility to Labyrinthula terrestris, a new turfgrass pathogen that causes rapid blight of cool season turfgrasses. Salt tolerant varieties and warm season grasses such as Bermuda grass, tufted hairgrass, inland saltgrass, centipede grass, seashore paspalum and kikuyugrass were not susceptible; cool season grasses such as velvet bentgrass, annual ryegrass, perennial ryegrass, annual bluegrass, Kentucky bluegrass, and rough bluegrass were very susceptible.

Rapid blight disease is a potentially devastating disease on cool season overseed turfs when irrigated with saline water. A two year test was conducted on a closely mowed Tifgreen bermudagrass turf which was infected with visual symptoms of necrotic patches of turf, and various degrees of blighting. The test included a broad representation of turf species for overseeding in an effort to (1) determine selected specie/cultivar susceptibility and disease expression to rapid blight in the field and (2) survey and assess the association of laboratory isolate detection from field sampling, with disease occurrence and severity of expression of field maintained overseed turf. Over a two year period, Rapid blight, caused by Labyrinthula terrestris was capable of infesting most cool season grasses in this test. In year one, Dawson CRF, SRX 555 slender creeping red fescue, and SR 105210 slender creeping red fescue showed no positive lab detection results from field plots. In year two (2003-2004), only SRX 555 SLQ had only 1 plot known to carry Labyrinthula throughout the main infestation season. In year two, essentially all turf plots showed some symptomology of disease expression. This was confirmed by lab identification. Tiller infection rates varied from 2% to 80% infection in the lab from field samples. The relationship between tiller infection rates and field plot disease expression was determined by Pearson’s product and Spearman Rank correlation coefficients. Field plot disease scores were correlated with percent tiller infection rates, R² = -0.56 plot basis, and R² = –0.71 treatment mean basis, respectively. Spearman Rank correlation coefficients were R² =; -0.62 on a plot basis, and R² =–0.78 based on treatment means Agreement between the disease condition (yes/no) vs. lab findings (positive/negative) occurred on 51 of 59 plot cases, and was significant compared to chance alone occurrences. Over two years, entries which had low disease scores included Fult’s alkali grass, Dawson creeping red fescue, SRX 555 SLQ slender creeping red fescue, SR 5210 slender creeping red fescue, and Providence creeping bentgrass. Over two years, entries which produced high field disease rating scores included SR 3100 Hard fescue, TransEze intermediate ryegrass, SR 4400 perennial ryegrass, SR 7200 velvet bentgrass, SR 7100 colonial bentgrass, Sabre and Laser Poa trivialis, and Redtop.