Parametric study of two planar high power flexible solar array concepts

The design parameters examined were: frequency, aspect ratio, packaging constraints, and array blanket flatness. Specific power-to-mass ratios for both solar arrays as a function of array frequency and array width were developed and plotted. Summaries of the baseline design data, developed equations, the computer program operation, plots of the parameters, and the process for using the information as a design manual are presented

Feasibility of Using Subject-Collected Dust Samples in Epidemiologic and Clinical Studies of Indoor Allergens

Studies of indoor allergen exposures are often limited by the cost and logistics of sending technicians to homes to collect dust. In this study we evaluated the feasibility of having subjects collect their own dust samples. The objectives were to compare allergen concentrations between subject- and technician-collected samples and to examine the sample return rate. Using a dust collection device and written instructions provided to them by mail, 102 subjects collected a combined dust sample from a bed and bedroom floor. Later the same day, a technician collected a side-by-side sample. Dust samples were weighed and analyzed for the cat allergen Fel d 1 and the dust mite allergen Der p 1. Fifty additional subjects who were enrolled by telephone were mailed dust collection packages and asked to return a dust sample and questionnaire by mail. A technician did not visit their homes. Correlations between subject- and technician-collected samples were strong for concentrations of Fel d 1 (r = 0.88) and Der p 1 (r = 0.87). With allergen concentrations dichotomized at lower limits of detection and clinically relevant thresholds, agreements between methodologies ranged from 91 to 98%. Although dust weights were correlated (r = 0.48, p < 0.001), subjects collected lighter samples. Among the group of 50 subjects, 46 returned a dust sample and completed questionnaire. The median number of days to receive a sample was 15. With some limitations, subject-collected dust sampling appears to be a valid and practical option for epidemiologic and clinical studies that report allergen concentration as a measure of exposure

The cytochrome p450 epoxygenase pathway regulates the hepatic inflammatory response in fatty liver disease

Fatty liver disease is an emerging public health problem without effective therapies, and chronic hepatic inflammation is a key pathologic mediator in its progression. Cytochrome P450 (CYP) epoxygenases metabolize arachidonic acid to biologically active epoxyeicosatrienoic acids (EETs), which have potent anti-inflammatory effects. Although promoting the effects of EETs elicits anti-inflammatory and protective effects in the cardiovascular system, the contribution of CYP-derived EETs to the regulation of fatty liver disease-associated inflammation and injury is unknown. Using the atherogenic diet model of non-alcoholic fatty liver disease/non-alcoholic steatohepatitis (NAFLD/NASH), our studies demonstrated that induction of fatty liver disease significantly and preferentially suppresses hepatic CYP epoxygenase expression and activity, and both hepatic and circulating levels of EETs in mice. Furthermore, mice with targeted disruption of Ephx2 (the gene encoding soluble epoxide hydrolase) exhibited restored hepatic and circulating EET levels and a significantly attenuated induction of hepatic inflammation and injury. Collectively, these data suggest that suppression of hepatic CYP-mediated EET biosynthesis is an important pathological consequence of fatty liver disease-associated inflammation, and that the CYP epoxygenase pathway is a central regulator of the hepatic inflammatory response in NAFLD/NASH. Future studies investigating the utility of therapeutic strategies that promote the effects of CYP-derived EETs in NAFLD/NASH are warranted

Metabolic reprogramming through fatty acid transport protein 1 (FATP1) regulates macrophage inflammatory potential and adipose inflammation

OBJECTIVE: A novel approach to regulate obesity-associated adipose inflammation may be through metabolic reprogramming of macrophages (MΦs). Broadly speaking, MΦs dependent on glucose are pro-inflammatory, classically activated MΦs (CAM), which contribute to adipose inflammation and insulin resistance. In contrast, MΦs that primarily metabolize fatty acids are alternatively activated MΦs (AAM) and maintain tissue insulin sensitivity. In actuality, there is much flexibility and overlap in the CAM-AAM spectrum in vivo dependent upon various stimuli in the microenvironment. We hypothesized that specific lipid trafficking proteins, e.g. fatty acid transport protein 1 (FATP1), would direct MΦ fatty acid transport and metabolism to limit inflammation and contribute to the maintenance of adipose tissue homeostasis. METHODS: Bone marrow derived MΦs (BMDMs) from Fatp1 (-/-) and Fatp1 (+/+) mice were used to investigate FATP1-dependent substrate metabolism, bioenergetics, metabolomics, and inflammatory responses. We also generated C57BL/6J chimeric mice by bone marrow transplant specifically lacking hematopoetic FATP1 (Fatp1 (B-/-)) and controls Fatp1 (B+/+). Mice were challenged by high fat diet (HFD) or low fat diet (LFD) and analyses including MRI, glucose and insulin tolerance tests, flow cytometric, histologic, and protein quantification assays were conducted. Finally, an FATP1-overexpressing RAW 264.7 MΦ cell line (FATP1-OE) and empty vector control (FATP1-EV) were developed as a gain of function model to test effects on substrate metabolism, bioenergetics, metabolomics, and inflammatory responses. RESULTS: Fatp1 is downregulated with pro-inflammatory stimulation of MΦs. Fatp1 (-/-) BMDMs and FATP1-OE RAW 264.7 MΦs demonstrated that FATP1 reciprocally controled metabolic flexibility, i.e. lipid and glucose metabolism, which was associated with inflammatory response. Supporting our previous work demonstrating the positive relationship between glucose metabolism and inflammation, loss of FATP1 enhanced glucose metabolism and exaggerated the pro-inflammatory CAM phenotype. Fatp1 (B-/-) chimeras fed a HFD gained more epididymal white adipose mass, which was inflamed and oxidatively stressed, compared to HFD-fed Fatp1 (B+/+) controls. Adipose tissue macrophages displayed a CAM-like phenotype in the absence of Fatp1. Conversely, functional overexpression of FATP1 decreased many aspects of glucose metabolism and diminished CAM-stimulated inflammation in vitro. FATP1 displayed acyl-CoA synthetase activity for long chain fatty acids in MΦs and modulated lipid mediator metabolism in MΦs. CONCLUSION: Our findings provide evidence that FATP1 is a novel regulator of MΦ activation through control of substrate metabolism. Absence of FATP1 exacerbated pro-inflammatory activation in vitro and increased local and systemic components of the metabolic syndrome in HFD-fed Fatp1 (B-/-) mice. In contrast, gain of FATP1 activity in MΦs suggested that Fatp1-mediated activation of fatty acids, substrate switch to glucose, oxidative stress, and lipid mediator synthesis are potential mechanisms. We demonstrate for the first time that FATP1 provides a unique mechanism by which the inflammatory tone of adipose and systemic metabolism may be regulated

Institutional creativity and pathologies of potential space: The modern university

This paper proposes the applicability of object relations psychoanalytic conceptions of dialogue (Ogden, 1986, 1993) to thinking about relationships and relational structures and their governance in universities. It proposes that: the qualities of dialogic relations in creative institutions are the proper index of creative productivity; that is of, as examples, ’thinking’ (Evans, 2004), ’emotional learning’ (Salzberger-Wittenburg et al., 1983) or ’criticality’ (Barnett, 1997); contemporary institutions’ explicit preoccupation in assuring, monitoring and managing creative ’dialogue’ can, in practice, pervert creative processes and thoughtful symbolic productivity, thus inhibiting students’ development and the quality of ’thinking space’ for teaching and research. In this context the paper examines uncanny and perverse connections between Paulo Freire’s (1972) account of educational empowerment and dialogics (from his Pedagogy of the oppressed) to the consumerist (see, for example, Clarke & Vidler, 2005) rhetoric of student empowerment, as mediated by some strands of managerialism in contemporary higher education. The paper grounds its critique of current models of dialogue, feedback loops, audit and other mechanisms of accountability (Power, 1997; Strathern, 2000), in a close analysis of how creative thinking emerges. The paper discusses the failure to maintain a dialogic space in humanities and social science areas in particular, exploring psychoanalytic conceptions from Donald Winnicott (1971), Milner (1979), Thomas Ogden (1986) and Csikszentmihalyi (1997). Coleridge’s ideas about imagination as the movement of thought between subjective and objective modes are discussed in terms of both intra- and inter-subjective relational modes of ’dialogue’, which are seen as subject to pathology in the pathologically structured psychosocial environment. Current patterns of institutional governance, by micromanaging dialogic spaces, curtail the ’natural’ rhythms and temporalities of imagination by giving an over-emphasis to the moment of outcome, at the expense of holding the necessary vagaries of process in the institutional ’mind’. On the contrary, as this paper argues, creative thinking lies in sporadic emergences at the conjunction of object/(ive) outcome and through (thought) processes

Female senior secondary physics students’ engagement in science: a qualitative study of constructive influences

Background: Prompted by fewer females compared to males enrolling in physics and advanced mathematics at both secondary and university levels, our research investigated the views and experiences of female students currently studying upper secondary school physics. We interviewed 18 female students about influences they considered important to their own science education, interest in science, and future science-related aspirations. Our purpose was to identify the experiences that these students most strongly associated with the generation and maintenance of their engagement in science, particularly represented in this research by their enrolment in upper secondary physics. Results: The research team used a systematic, iterative process to identify the main themes in the transcribed interview data. We identified the influence each girl reported as the strongest (ranked first). We also combined all influences that the participants had nominated, regardless of their ranking, to further examine all factors participants suggested as influential in their sustained engagement in school science (represented by their decision to study upper secondary physics). Systematic analysis of the interview data confirms that the influences on these females’ choices to study physics at upper secondary originate from a combination of their teachers, their school’s science culture, members of their family, the participants themselves and their peers. Conclusions: The interviews highlighted the idiographic complexities in understanding the wide range of important influences on these students studying physics at upper secondary school and their engagement in science. The unique contribution of this work is giving voice to the participants and reflecting on what these high achieving females have to say about the influential factors in their decisions to pursue science. Supportive teachers and the school science culture play essential roles, and other cultural and/or social factors such as family members and peers are identified as important. References to the culture and expectations of the school, family holidays, and conversations with siblings are support factors that seem to interact and overlap. At the same time, the importance of policy-amenable factors such as competent and caring science teachers, and science-supportive school cultures should be emphasised and encouraged

Effect of Soluble Epoxide Hydrolase on the Modulation of Coronary Reactive Hyperemia: Role of Oxylipins and PPARγ

Coronary reactive hyperemia (CRH) is a physiological response to ischemic insult that prevents the potential harm associated with an interruption of blood supply. The relationship between the pharmacologic inhibition of soluble epoxide hydrolase (sEH) and CRH response to a brief ischemia is not known. sEH is involved in the main catabolic pathway of epoxyeicosatrienoic acids (EETs), which are converted into dihydroxyeicosatrienoic acids (DHETs). EETs protect against ischemia/reperfusion injury and have numerous beneficial physiological effects. We hypothesized that inhibition of sEH by t-AUCB enhances CRH in isolated mouse hearts through changing the oxylipin profiles, including an increase in EETs/DHETs ratio. Compared to controls, t-AUCB–treated mice had increased CRH, including repayment volume (RV), repayment duration, and repayment/debt ratio (p \u3c 0.05). Treatment with t-AUCB significantly changed oxylipin profiles, including an increase in EET/DHET ratio, increase in EpOME/DiHOME ratio, increase in the levels of HODEs, decrease in the levels of mid-chain HETEs, and decrease in prostanoids (p \u3c 0.05). Treatment with MS-PPOH (CYP epoxygenase inhibitor) reduced CRH, including RV (p \u3c 0.05). Involvement of PPARγ in the modulation of CRH was demonstrated using a PPARγ-antagonist (T0070907) and a PPARγ-agonist (rosiglitazone). T0070907 reduced CRH (p \u3c 0.05), whereas rosiglitazone enhanced CRH (p \u3c 0.05) in isolated mouse hearts compared to the non-treated. These data demonstrate that sEH inhibition enhances, whereas CYP epoxygenases-inhibition attenuates CRH, PPARγ mediate CRH downstream of the CYP epoxygenases-EET pathway, and the changes in oxylipin profiles associated with sEH-inhibition collectively contributed to the enhanced CRH