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Neuropsychiatric complications of PD (e.g., depression) are primary contributors to reduced quality of life amongst people with PD (PWP). Thus, ongoing mental health research to develop effective treatments for psychiatric conditions associated with PD is crucial toward improving the lives of PWP. Common problems faced in mental health clinical trials include reluctance to take part in research, early dropout, and inaccurate and/or under-reporting of emotional concerns. These factors may impede the progress of clinical research, slowing development of effective mental health treatments for PWP. Developing a better understanding of these barriers represents important steps towards optimizing care for PWP. The objectives of this qualitative study were to 1) identify barriers and facilitators to participation in Parkinson’s Disease (PD) mental health research, 2) describe factors that influence study dropout, and 3) develop tools to enhance accuracy of self-report and participant retention in PD mental health clinical trials. The overall purpose of this research was to improve the quality of PD mental health research by gaining insight from direct engagement with PD advocates, including PWP and their carepartners. Three focus groups (N=16 total, 4-6 participants per group) were completed between December 2017 and March 2018 (Phase 1), transcribed, and analyzed via qualitative thematic analysis. Specific deliverables were developed in response to key themes, and two additional focus groups (Phase 2) were completed in June and July 2018 to gather further input and to revise research tools, methods, and procedures. Limited knowledge about the common and central role that neuropsychiatric symptoms play in overall PD management was identified as a key barrier to engagement. Perceived stigma was reported to be a major driver of self-report bias. Peer-to-peer research ambassador programs, improved educational materials regarding PD mental health, quarterly wellness newsletters, and mixed-media testimonials from prior study participants were examples of tools that may enhance the longevity and quality of PWP participation in mental health research, based on focus group results. Deliverables from this project may support the collection of high-quality clinical trial data, ultimately improving available mental health care resources for PWP.
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All life on Earth is dependent on biologically mediated electron transfer (i.e., redox) reactions that are not at thermodynamic equilibrium. Biological redox reactions originally evolved in prokaryotes and ultimately, over the first ~ 2.5 billion years of Earth’s history, formed a global electronic circuit. To maintain the circuit on a global scale requires that oxidants and reductants be transported; the two major planetary electron conductors that connect global metabolism are geological fluids - primarily the atmosphere and the oceans. Because all organisms exchange gases with the environment, the evolution of redox reactions has been a major force in modifying the chemistry at Earth’s surface. First, a review is given of the discovery and consequences of redox reactions in microbes with a specific focus on the co-evolution of life and geochemical phenomena. With the larger picture in mind, the focus is then directed specifically to one of the earliest metabolic pathways on Earth. The reduction of elemental sulfur. is an important energy-conserving pathway in prokaryotes inhabiting geothermal environments, where sulfur respiration contributes to sulfur biogeochemical cycling. Despite this, the pathways through which elemental sulfur is reduced to hydrogen sulfide remain unclear in most microorganisms. We integrated growth experiments using Thermovibrio ammonificans, a deep-sea vent thermophile that conserves energy from the oxidation of hydrogen and reduction of both nitrate and elemental sulfur, with comparative transcriptomic and proteomic approaches, coupled with scanning electron microscopy. Our results revealed that two members of the FAD-dependent pyridine nucleotide disulfide reductase family, similar to sulfide-quinone reductase (SQR) and to NADH-dependent sulfur reductase (NSR), respectively, are over-expressed during sulfur respiration. Scanning electron micrographs and sulfur sequestration experiments indicated that direct access of T. ammonificans to sulfur particles strongly promoted growth. The sulfur metabolism of T. ammonificans appears to require abiotic transition from bulk elemental sulfur to polysulfide to nanoparticulate sulfur at an acidic pH, coupled to biological hydrogen oxidation. A coupled biotic-abiotic mechanism for sulfur respiration is put forward, mediated by an NSR-like protein as the terminal reductase.
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By weight, this object is identified AE4. RIC only attests to various AE3 objects of this type. If mint mark is read correctly as SMNA, then this coin was minted in Nicomedia (cf. RIC VIII Nicomedia 49, 55); other possibilities are Heraclea (SMHA)(cf. RIC VIII Heraclea 45, 54, 59) and Cyzicus (SMKA)(cf. RIC VIII Cyzicus 48, 55, 63)
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Although sports are popular in North America, only a small research base examines the moral cultures of different sports. In this study, it was hypothesized that different sports have distinct moral cultures, that contact sports emphasize the care versus harm foundation from Moral Foundations Theory more than noncontact sports, and that contact sports emphasize morality more than noncontact sports in general. To investigate these questions, a corpus of transcribed athlete interviews was analyzed in accordance with the Moral Foundations Dictionary (MFD). A one-way ANOVA revealed that the seven sports examined (auto racing, baseball, basketball, football, golf, hockey, and tennis) significantly differed in their respective emphases on each of the moral foundations, as defined by the frequency of words from corresponding sections of the MFD used in that sport’s interviews relative to the total number of words in the interviews (care: F=108.1, sd=0.536; authority: F=46.63, sd=0.694; fairness: F=13.94, sd=0.314; purity: F=16.78, sd=0.240; ingroup: F=27.74, sd=0.492; p<0.001 for all foundations). T-tests were used to compare contact and noncontact sports’ relative frequencies of moral language use from the care category as well as their overall moral language use. The differences between contact and noncontact sports’ relative emphases on the care foundation, and morality in general, were both found to be significant (t=456.8, sd=0.1, p<0.001; t=5.718, sd=1.007, p=0.0168). These findings support the hypotheses that sports have distinct moral cultures, that contact sports emphasize the care foundation more than noncontact sports, and that contact sports emphasize morality more in general. These findings can guide future research on the effects that different sports have on their participants.
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In this dissertation, I examine how race has been molecularized through the hormone tes-tosterone and the impact that this process has had on the construction of racial disparities in prostate cancer between black and white men. While testosterone is widely conceptual-ized as a molecular marker of masculinity by both scientific and popular accounts, femi-nist science studies scholars have documented how these claims are both misleading and dangerous. Building from this foundational work, this project explores how testosterone has been both gendered and racialized by scientists over the course of the 20th-century. More specifically, biomedical researchers claim that racial differences in testosterone help explain racial disparities in prostate cancer between black and white men. This discourse endorses the theory that higher levels of testosterone, which has historically been a marker used to designate prostate cancer risk, must differ between black and white men and thus explain the persistence of prostate cancer disparities between these two groups. To examine the validity of these racialized claims, I use insights from science & technology studies, critical race theory, and social network analysis to critically evaluate the triangular linkages between testosterone, race, and prostate cancer in biomedical re-search. In my first analytic chapter, I examine the relationship between testosterone and race. To do this, I conduct a content analysis of 147 studies that evaluate population dif-ferences in testosterone. I find that, despite widespread claims that testosterone varies be-tween racial groups, the literature provides scant evidence to support these assertions. To demonstrate how population differences are enacted and reproduced, I use social net-work analysis to visualize a citation network of these data and trace how the racialization of testosterone circulates through scientific research. I identify three mechanisms – ambi-guity, absence and data recycling – to help explain how racial difference testing has con-tributed to preserving the cultural myth of testosterone as a molecular marker of racialized masculinity. Second, I evaluate the linkage between race and prostate cancer, looking to un-derstand how racial disparities in this disease are constructed. Biomedical and epidemio-logical researchers widely claim that African American men suffer from prostate cancer at two to three times the rate of white Americans. However, a critical review of this litera-ture finds that racial disparities in prostate cancer-specific mortality are largely explained by socioeconomic differences between the two groups. While scientists do discuss the ef-fects of socioeconomic inequalities in their work, researchers also suggest that black men’s more “aggressive biologies,” propelled by testosterone and other biological differ-ences, help explain why this group is more likely to experience earlier onset of disease, faster growing tumors and worse overall survival. These racialized claims shape group-differentiated patterns in the use of prostate-specific antigen screening, racially-specific treatment guidelines, and variability in the distribution of hormone-based pharmaceuticals and surgical interventions. Ultimately, I argue that biomedical researchers’ focus on ex-plaining prostate cancer through racial differences in biology (i.e. testosterone) ultimately leads to the misallocation of funding away from addressing the structural causes that drive these disparities in the first place. In the final analytic chapter, I investigate the linkage between testosterone and prostate cancer to see how this association has changed over time. By examining changes in scientific consensus over time, I demonstrate that the association between testosterone and prostate cancer has undergone a radical paradigm shift over the past 25 years. While high levels of testosterone were considered a robust indicator of prostate cancer risk for more than seven decades, most biomedical experts now argue that clinically low levels of testosterone may, in fact, be a more accurate risk factor for diagnosing this disease. Alt-hough prostate cancer researchers have moved towards consensus, this paradigm shift has not carried over to impact all domains of research in the same way. For example, today’s most widely used clinical guidelines on testosterone replacement therapies explicitly ad-vise clinicians not to prescribe testosterone to African American men because of their in-creased risk of prostate cancer. These guidelines are not only predicated on the assump-tion that black and white men have different testosterone levels, but also on the antiquat-ed theory that higher levels of testosterone contribute to prostate carcinogenesis, which unjustly withholds testosterone therapies from black men. In response to these findings, I call for the Endocrine Society to reassess their guidelines to reflect a more equitable poli-cy on testosterone replacement therapies, which relies on the best available evidence on the topic. Together, these chapters demonstrate that molecularization and racialization are co-constitutive processes that shape the contours of today’s biomedical markets, includ-ing the “gold-standards” of evidence-based medicine and access to hormone-based phar-maceuticals for black and white men across the United States. In the conclusion, I discuss how my work speaks to scholars working in science & technology studies as well as the literatures on the medicalization and pharmaceuticalization of race. Furthermore, I outline how my work affects biomedical research on testosterone. Most notably, I argue that those responsible for constructing the Endocrine Society’s clinical guidelines on testos-terone replacement therapies need to revise their recommendations to remove race as a ba-sis for withholding pharmaceuticals from black consumers. While it is crucial to recognize and assess the potential risks of hormone-based pharmaceuticals, using race as a basis for (not) disseminating medical treatment perpetuates the legacy of scientific racism and un-justly bars important resources from patients who may benefit from the use of testos-terone replacement therapies.
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Superinductors are inductors whose microwave characteristic impedances are greater than the resistance quantum, $R_{Q}=h/(2e)^{2}approx6.5kOmega$. They can be implemented using Josephson junction chains and high kinetic inductance nanowires. In this dissertation, we explore applications of superinductors in both implementations in superconducting quantum circuits. The dissertation consists of three parts. In the first part, we discuss the fluxon-parity-protected qubit consisting of a Cooper-pair box (CPB) shunted by a superinductor made of a chain of coupled asymmetric Superconducting Quantum Interference Devices (CASQUIDs). The spectroscopic measurement of a prototype of the fluxon-parity-protected qubit was performed. We observed almost complete suppression of the single fluxon tunneling across the CPB due to the destructive Aharonov-Casher interference when the offset charge on the CPB island was set to $e$ mod(2$e$). A fluxon-parity-protected qubit with a higher superinductance can potentially be used to perform fault-tolerant Clifford gates. In the second part, we studied the microwave losses in high-kinetic-inductance granular Aluminum films using superconducting coplanar-waveguide (CPW) resonators made of the films. We observed that the intrinsic losses in these resonators at low temperatures were limited by resonator coupling to the two-level systems (TLS) in the environment. The demonstrated internal quality factors are comparable with those for CPW resonators made of conventional superconductors. The characterized granular Aluminum films can be used to fabricate superinductors for a wide range of applications in quantum metrology and quantum information processing. In the third part, we discuss the one-dimensional Josephson metamaterial made of a similar structure as the superinductor used in the fluxon-parity-protected qubit. The metamaterial demonstrated strong Kerr nonlinearity with the Kerr constant tunable over a wide range from positive to negative values by the magnetic field. The metamaterial is promising for use as an active medium for quantum-limited Josephson traveling-wave parametric amplifiers.
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Influenza is a highly contagious respiratory disease, which can have severe impacts on human health. Influenza type B is traditionally known as the seasonal flu and is the main source for annually occurring influenza outbreaks. The Non-Structural protein 1 of influenza B (NS1B) is a highly conserved protein that the influenza virus produces post infection. NS1B is hypothesized to inhibit the innate immune system via interactions with the RIG-I activation pathway. NS1B has been known to bind dsRNA via its N-terminal domain (NS1B-NTD) for decades, but recently a second RNA binding site was discovered on the C-terminal domain of NS1B (NS1B-CTD). Due to the high conservation of NS1B, its ability to inhibit the innate immune system, and the recent discovery of a second RNA binding domain, this dissertation research focused on the biological function of this second RNA binding site. We discovered a surprising novel blunt-end binding orientation of the NS1B-CTD by dsRNA. We then looked at the connection between RIG-I’s well-known ability to detect and bind triphosphorylated-5’ hairpin RNA (3P-5’-hpRNA) with a much higher affinity than OH-5’ hairpin RNA (OH-5’ hpRNA). We discovered similar binding affinity changes and characteristics with NS1BCTD and the 3P-5’-hpRNA/OH-5’ hpRNA. When the second RNA binding site in NS1B was mutated in transgenic influenza B viruses, we observed reduction in the ability of the virus to suppress Rig-I activation, as Rig-I induced phosphorylation of IRF3 was no longer suppressed flowing virus infection. Our results suggests that the function of the second RNA binding site in the CTD of wildtype NS1B is to outcompete RIG-I for its RNA substrates, typically 5’ triphosphorylaed vRNA molecules. Based on these studies we propose that NS1B-CTD acts as a sensory domain with high specificity for vRNA molecules, which form a “panhandle dsRNA duplex structure” with a unique 3P-5’ modification not found in host cells. This interaction functions to prevent activation of Rig-I, and the innate host immune response.
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Perennial ryegrass (Lolium perenne L.) is a widely used cool-season turfgrass species. The primary breeding objectives for turf-type perennial ryegrass include improving tolerance to abiotic and biotic factors such as salinity stress and dollar spot disease, which is caused by Clarireedia jacksonii C. Salgado, L.A. Beirn, B.B. Clarke, and J.A. Crouch. These types of traits are often quantitatively inherited and present difficulties for the phenotypic selection breeding technique. Quantitative trait locus (QTL) mapping has been implemented in modern plant breeding programs as a basis for marker-assisted selection for complex, quantitatively inherited traits. The preliminary components for QTL mapping include developing an appropriate mapping population and constructing a genetic linkage map that is densely populated with markers. After these prerequisite tasks have been completed, and phenotypic data for the traits of interest have been collected, QTL analyses may be conducted. The purpose of this dissertation was to exploit the QTL mapping technique for developing molecular breeding tools to help improve these complex traits in perennial ryegrass. The specific research objectives of this work were (i) to develop a diverse perennial ryegrass mapping population that would accommodate QTL mapping studies for salinity tolerance and dollar spot resistance in perennial ryegrass, (ii) to construct a high-density, single nucleotide polymorphism (SNP)-based genetic linkage map for perennial ryegrass, (iii) to conduct QTL analyses for salinity tolerance, dollar spot resistance, and growth habit morphology traits in perennial ryegrass. For the first objective, candidate parental genotypes were selected from a large population of perennial ryegrass clones in the Rutgers turfgrass breeding program. These genotypes were studied for response to salinity stress and dollar spot disease. Additionally, phenotypic variation in growth habit and leaf color was also observed among the candidate parental genotypes. Although these two traits were not of primary interest in developing the mapping population, they were also considered when pairing parents for cross-fertilization events. Nine biparental crosses were made in the summer of 2016. The selected population consisted of 118 pseudo-F2 progeny derived from a cross between 15-8325 (maternal parent, referenced as I06) and 15-8343 (paternal parent, referenced as A89). Thus, the population is commonly referenced as the I06 × A89 perennial ryegrass mapping population and is comprised of the 2 parent genotypes and 118 progeny genotypes. For the second objective, greater than 1.8 Gb of raw sequencing reads were generated for the 2 parent genotypes and the 118 progeny genotypes from the I06 × A89 population. In addition to the SNP markers that were generated in this study, a set of framework simple sequence repeat (SSR) markers from previous studies were also used for linkage map construction. Two linkage maps, one for each parent, were developed. After screening markers for polymorphisms, segregation distortion, redundancy, and insufficient grouping support, 848 SNP markers and 52 SSR markers were included in the marker dataset for parent I06 while 769 SNP markers and 35 SSR markers were included in the marker dataset for parent A89. The 900 markers included in the I06 dataset mapped to a total distance of 677.5 cM with an average marker density of 0.75 cM. The 804 markers included in the A89 dataset mapped to a total distance of 687.9 cM with an average marker density of 0.86 cM. For the third objective, the I06 × A89 population was evaluated for the traits of salinity tolerance, dollar spot resistance, and growth habit morphology using multiple field trials during 2017 and 2018 at the Rutgers Plant Science Research and Extension Farm in Adelphia, NJ. Subsequently, QTL analyses were conducted with the individual I06 and A89 parent maps and phenotypic data for the traits of interest.The QTL analyses for salinity tolerance resulted in the identification of fifteen major-effect QTL and forty-three minor-effect QTL. Eleven salinity tolerance QTL were identified using two distinct assessment methods for salinity tolerance, seven salinity tolerance QTL were identified at multiple environmental locations, and one salinity tolerance QTL was identified on both parent maps. The QTL analyses for dollar spot resistance resulted in the identification of twelve major-effect QTL and nine minor-effect QTL. Coincident dollar spot resistance QTL were mapped to four distinct genomic regions and were consistently identified using multiple evaluation methods for dollar spot severity and/or multiple environments. The growth habit morphology QTL analyses resulted in the identification of twenty-one major effect QTL and seven minor-effect QTL. Four growth habit morphology QTL were identified across multiple environments, and two growth habit morphology QTL were significantly associated with multiple morphological traits. These are the first reported efforts for QTL mapping of salinity tolerance and dollar spot resistance in perennial ryegrass. Further, this is the first report of QTL mapping for growth habit traits in turf-type perennial ryegrass. These findings will be useful for future studies involving development of marker-assisted selection techniques for breeding applications, gene and mechanism discovery, and comparative genomics investigations using closely related plant species. These efforts will be used to develop improved perennial ryegrass cultivars, which will ultimately contribute to the sustainability of the turfgrass industry. Moreover, the I06 × A89 perennial ryegrass population will be useful to further study these and additional traits in perennial ryegrass, and the high-density genetic linkage map constructed herein will be a valuable resource for future QTL studies in turf-type perennial ryegrass breeding.
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Within the Peace River Oil Sands patch of Alberta, Canada, white settlers actively avoid awareness of the pollution and social violence their Indigenous neighbors experience daily. To do so, they erect racial boundaries that separate them from their Indigenous Other with violent consequences. Their avoidance both produces and is enabled through a settler coloniality – a racial hierarchy that allocates political, economic, and cultural power inequitably to privilege settlers and marginalize Indigenous nations, better securing state and industry access to natural resource regions. This allocation of power drives the formation of the Canadian nation-state and provides significant material benefit to its white citizens, but often to the detriment of First Nations communities. Application of theory from environmental anthropology, critical Native and race studies, and decolonial and phenomenological methods reveals that processes of historical narration, spatial practice, and Anglo-Canadian perception of Indigenous bodies and space work concurrently to reproduce the settler coloniality that allows tar sands development to expand in the absence of local political opposition. I conclude that settlers’ refusal to cross the boundaries they create denies them the ability to see Indigenous neighbors in their full humanity, reinforces stereotypes, and thus prolongs environmental injustice in settler societies. This argument is driven by an engaged praxis, meant to assist in dismantling harmful racial boundaries across settler nations; that wherever Indigenous nations, peoples of color, and settlers live together we achieve the cessation of the social and environmental violence that justice, reconciliation, and human rights all demand.
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