Following a visual trajectory that begins in the mid-1930s, this article discusses advertising for cleaning products in order to trace the peculiar formation of the idea of hygiene and its ideological ties to the larger, more subliminal project of the consolidation of Italian racial identity as uniformly and permanently white. The author contends that the peculiar ubiquity of whiteness - simultaneously expansive yet fixed – was carried forth, among other things, through a project of “redemptive hygiene” that was, in turn, mediated by the influence of Fascist racialist models and reflected in the postwar culture of advertising, also in virtue of the expansion of new technologies in support of a mass-mediated national culture. After considering Gino Boccasile’s propaganda and commercial posters and a key example (the Calimero ad for AVA) from the 1960s, the article concentrates on the 2006-2007 advertising campaign by the multinational company Guaber for one of their brands, Coloreria Italiana. This last example shows how the racialization of the space of the domestic plays with the ambiguous turn of the post-racial in contemporary Italy, where race is unhinged from a familiar ground in order to appear, be consumed, and be washed away.

Childhood cancer is a rare disease that may be triggered prenatally. The few known causes of pediatric cancers include ionizing radiation, Down syndrome, and some genetic or chromosomal anomalies. Additional risk factors have been suggested, but due to the rarity of childhood cancers, it has been difficult to establish causes and hence targets for prevention. We investigated ultraviolet radiation (UVR), pesticides, and maternal dietary patterns as possible risk and protective factors. Studies have shown that higher solar UVR may be related to lower risk of some cancers in adults and children. In a large, population-based case-control study we tested the hypothesis that childhood cancers may be influenced by UVR. Cancers in children ages 0 to 5 years were identified from California Cancer Registry records for 1988-2007 and linked to birth certificate data. Controls were sampled from birth certificates. Based on birth address, we assigned UVR exposure using a geostatistical exposure model developed with data from the National Solar Radiation Database. Our preliminary findings suggest that UVR during pregnancy may decrease the odds of some childhood cancers. In the same study population we evaluated the associations of exposure to specific pesticide types during pregnancy with glial tumors in young children in California using a validated geographic exposure model. We observed increased odds of astrocytoma for residential pesticide exposure to herbicides, insecticides and fungicides, as well as for several chemical classes of pesticides. Additionally, using data from a multi-institutional case-control study of retinoblastoma in the United States and Canada, we investigated the association of maternal prenatal diet with the risk for unilateral retinoblastoma among children less 15 years of age. Previous studies have shown that mother's diet during pregnancy may affect her offspring's risk of cancer. Our results suggest that a dietary pattern with high fruit and vegetable consumption and low consumption of fried foods and sweets during pregnancy, as well as a dietary pattern with high fruit and vegetable consumption and low consumption of red and cured meats, may reduce the odds of unilateral retinoblastoma in offspring.

My dissertation examines how rural Southern farmers responded to exogenous changes to household incomes during the early twentieth century. I use a range of statistical approaches: Ordinary and Two Stage Least Squares, Probit, and instrumental variable Probit. Critically, the proxy for household incomes, cotton yields, is predicted using weather fluctuations. In chapter one, I find credit constrained households have lower school attendance rates following negative income shocks. In chapter two, I find the probability of farm wage work is negatively correlated with incomes in credit constrained households. In both chapters, I use black and tenant farmers as proxies for credit constrained households. In the final chapter, I find the probability of a lynching occurring in the local community increases after household incomes fall.

The size constraints of the nucleus necessitate condensation of eukaryotic DNA into chromatin. The fundamental subunit of chromatin is the nucleosome, ~147 bp of DNA wound about the histone octamer. Each octamer typically contains two copies each of the canonical histones H2A, H2B, H3 and H4. However, packaging DNA limits its availability to enzymes necessary for the maintenance and expression of our heritable material. More precisely, all chromatin-dependent processes--transcription, replication, recombination, and repair--are affected by the position and occupancy of nucleosomes. Given the transcriptional challenges inherent to DNA packaging, this dissertation documents studies aimed at addressing this fundamental question: How does a cell modify chromatin to achieve proper gene expression? To this end, I pursued functional studies in S. cerevisiae of a potential chromatin modifier, Yta7, and a novel chromatin modification, H2A.Z acetylation.

My studies on Yta7, a conserved bromodomain-containing protein with AAA-ATPase homology, identified this protein as a novel regulator of histone H3 eviction or degradation. Cells lacking Yta7 exhibited both increased levels of chromatin-incorporated histone H3 and decreased nucleosome spacing. Importantly, this modulation of H3 levels occurred post-transcriptionally. The yta7Δ mutant's transcriptional defects were partially suppressed by decreased dosage of histones H3 and H4, indicating the transcriptional impact of this increased nucleosome density. Additionally, Yta7 associated with inducible genes only upon transcriptional activation, with prominent enrichment within open reading frames. Yta7 and its ATPase function were required for the proper induction of these genes. Further, loss of local Yta7 activity resulted in a 5' to 3' gradient of H3 accumulation within a large open reading frame upon transcriptional activation, indicating a direct requirement for Yta7's regulation of H3 levels at that gene. In support of a direct mechanism of histone eviction or degradation by Yta7, Yta7 directly interacts with histone H3 in vitro. Further, over-expressing Yta7 resulted in a ~65% decrease in levels of chromatin-bound H3, as assayed by chromatin immunoprecipitation. Taken together, my studies support a model in which Yta7 utilizes the energy released upon ATP hydrolysis to evict and/or facilitate the degradation of histone H3. As bulk chromatin from cells without Yta7 exhibited increased nucleosome density and decreased dosage of either H3 or H4 suppresses the growth defect of the yta7Δ mutant, Yta7 presumably evicts or degrades an H3/H4 dimer or tetramer. Thus, these studies identified a protein that limited the extent of DNA packaging, thereby facilitating RNA polymerase activity upon transcription.

Restricting nucleosome density represents one mechanism for enabling transcriptional activation. Another possible mechanism is modifying the nucleosomes themselves, by covalently modifying the incorporated histones or changing which histones are incorporated. Although nucleosomes typically contain two copies of each canonical histone, histone variants, such as H2A.Z and H3.3, can be substituted at specific genomic locations for their cognate canonical histone. The histone H2A variant H2A.Z is conserved and essential in all multicellular eukaryotes assayed. Yeast cells lacking H2A.Z exhibit a broad range of chromatin-based phenotypes, including defective gene induction, genomic instability, and spreading of the Sir-silencing complex from heterochromatin into euchromatic domains. However, the importance of its N-terminal tail acetylations to these functions remained unclear. Therefore, I undertook studies to determine the genome-wide requirements for H2A.Z acetylation, assess the role of individual acetylation sites and identify which proteins might interpret these modifications.

My work on H2A.Z acetylation indicated that the transcriptome of cells lacking H2A.Z acetylation exhibited fewer expression defects than cells lacking H2A.Z. In contrast to proposed roles in transcriptional activation, cells lacking H2A.Z acetylation exhibited a bias toward up-regulation of genes. Genes that were down-regulated in these cells, however, were highly enriched for telomere-adjacent genes, consistent with Sir silencing antagonism or altered telomeric structure. In keeping with more recent work, my data supported a model of acetylation-site equivalence and additive activity of H2A.Z acetylation. Additionally, this work identified the double bromodomain-containing TFIID-associated Bdf1 as interacting with H2A.Z in an acetylation-dependent manner in vivo. As Bdf1 is required to inhibit Sir-complex spreading from the telomeres, this work provides insight into the potential mechanism of Bdf1's Sir complex antagonism. Further work will have to be performed to determine if the down-regulation of telomere-adjacent genes in cells that cannot acetylate H2A.Z is Sir-dependent and whether these genes' requirement for acetylated H2A.Z is a direct one. However, these studies on H2A.Z acetylation are consistent with a model in which H2A.Z acetylation prevents chromatin condensation by the Sir proteins, an alternative mechanism for maintaining proper gene expression.

This quasi-experimental study examined readers’ perceptions of content-evaluative metadiscourse—linguistic and rhetorical signals that indicate an author’s willingness (or lack thereof) to “own” the claims discussed in a text. Specific elements investigated in the study included hedging and boosting (markers of doubt or certainty), attitude markers, and attributions. Fifty-three participants were randomly assigned one of two versions of an article about “technophobia,” the first expressing a concerned, “technophobic” stance and the second expressing an optimistic, tech-enthusiast stance. Analysis of participants’ written responses plus twenty-eight retrospective text-based interviews revealed the relative saliency of specific linguistic cues on participants’ own personal attitudes regarding the topic, and on their perceptions of the author’s stance. The results are analyzed in terms of pedagogical implications, with particular emphasis on practices of rhetorical reading.

Case Report: Here we present a case of vitamin C and D deficiency in a previously healthy 26-year-old man during the coronavirus disease 2019 pandemic in urban America.

Conclusion: Severe nutritional deficiencies still exist today. Emergency clinicians should be aware of the signs and symptoms to promptly diagnose and initiate treatment.

Huanglongbing (HLB), also known as citrus greening disease or yellow dragon disease, is the most destructive disease of citrus worldwide. In the United States, Huanglongbing is associated with infection of the phloem-restricted bacterium Candidatus Liberibacter asiaticus (CLas). This pathogenic agent is transmitted by the Asian citrus psyllid (ACP; Diaphorina citri Kuwayama) which feeds directly on the phloem of diseased citrus plants, ingesting CLas in the process, and transmits the pathogen into the phloem of a new tree during subsequent feeding. Symptoms of infection with CLas can take months to years to develop which allows asymptomatic trees to act as sources of inoculum for dissemination of the pathogen. When symptoms do appear, the disease is associated with asymmetric leaf chlorosis (‘yellow mottle’), twig dieback, sparsely foliated trees, and production of fruit that is lopsided, bitter, and green even when ripe; symptoms ultimately culminate with premature tree death.

To date, most efforts to understand the plant’s early response to CLas introduce the pathogen by grafting diseased plant material onto healthy trees instead of using the pathogen’s natural ACP vector. To fully understand HLB, it is necessary to know how citrus responds to the psyllid vector and how that response differs when ACP are harboring CLas and introducing it into the plant. The purpose of this dissertation was to address this under-explored area of literature by characterizing the early leaf response of greenhouse citrus trees to exposure to ACP with or without CLas (Chapter 2) and to assess the translatability of ACP-inoculation greenhouse studies to trends observed in HLB field studies (Chapter 3).

In the first study (Chapter 2), we used transcriptomics, proteomics, and metabolomics to identify how exposure to ACP with or without CLas impacts the metabolism of citrus leaves for one year. Two hundred CLas-positive or CLas-negative ACP were introduced to pairs of Madam Vinous sweet orange (Citrus sinensis (L.) Osbeck) trees. Two weeks later, collection of leaf samples began and took place every two weeks for 52 weeks. The resulting analysis utilized transcriptomic data from four timepoints, proteomic data from six timepoints, and metabolomic data from 14 timepoints to gain insights into the response of trees over time. The results of this study indicated that the initial plant response of ACP-vectored CLas infection is primarily due to exposure to ACP and to a lesser extent, the presence or absence of CLas. Additionally, it demonstrated the complexity of this disease by identifying only 17 transcripts, one protein, and no metabolites that were consistently differentially accumulated between trees exposed to CLas-positive or CLas-negative ACP during the first 16 weeks post-exposure to psyllids. By using a controlled greenhouse environment to investigate the citrus response, we were able to clearly characterize changes in citrus leaf cellular metabolism due to these stimuli.

To understand the translatability of our results to real-world situations, a subsequent investigation was carried out to compare the metabolomic results of our greenhouse study to CLas-infected citrus grove trees from Texas (Chapter 3). Metabolomic data from symptomatic grove trees and non-infected screenhouse trees was previously acquired from southern Texas and reported as part of a multi-laboratory investigation to evaluate different early HLB detection techniques. By comparing the metabolic trends in response to ACP-inoculated CLas infection in greenhouse versus field trees, it was possible to understand how well controlled greenhouse studies reflect disease progression relative to what is actually occurring in the field. Overall, the results of this dissertation identified changes in citrus leaf metabolism due to ACP with or without CLas (Chapter 2) and examined the overlap and discrepancies between ACP-transmitted CLas infection between greenhouse and field studies (Chapter 3). The outcomes of the investigations conducted here can be used to refine molecular targets for early disease detection, development of resistant cultivars, and to inform a broader understanding of plant-microbe and plant-vector interactions.

Disruption of protein homeostasis, leading to accumulation of insoluble high molecular weight protein complexes containing the Huntingtin (HTT) protein and SUMOylated proteins, and transcriptional dysregulation are key features in Huntington’s disease (HD). Genetic modifiers contributing to HD age of onset have recently been identified and have critical roles in DNA damage repair (DDR) pathways. The mechanisms involved in DDR rely strongly on signaling cascades and post-translational modifications such as SUMO to maintain genomic integrity. Further, the Huntingtin (HTT) protein itself scaffolds DDR proteins. We previously showed that striatal reduction of the E3 SUMO ligase PIAS1 was neuroprotective and modulated disease associated pathologies including accumulation of mutant HTT in a mouse model of HD. However, the exact mechanistic contributions of PIAS1 towards HD pathogenesis have not yet been fully elucidated. To further evaluate PIAS1 function in the context of HD, knock-down was investigated in human patient medium spiny neurons differentiated from induced pluripotent stems cells and two disease mouse models. My findings suggest that PIAS1 functions as a key regulator of post-translational modification and protein homeostasis in HD neurons and mediates the functional activity of the transcription-coupled DNA damage repair complex in the striatum. Reduction of PIAS1 facilitated DNA repair, normalized aberrant transcriptional profiles related to synaptic function, and may stabilize the CAG-repeat within HTT. The results of this research provide the first mechanistic link between SUMOylation and DNA damage repair in the central nervous system. Specifically, they provide insight into how DNA damage repair pathways and post-translational modifications might contribute towards HD, and overall for targeting pathway mediators to restore homeostatic balance, with broad implications for HD and other neurodegenerative diseases.