Writing the World: Ursula K. Le Guin and Margaret Atwood’s Literary Contributions to Ecofeminism

Along with the philosophical writings of ecofeminism’s greatest proponents and critics, the growth of ecofeminist philosophy has relied heavily on fiction writers. The term ecofeminism was coined in 1975, and the following year ecofeminism found fertile ground for exploration and growth in March Peircy’s science fiction novel, Woman on the Edge of Time (1976). The social, academic, and literary trends leading up to the emergence of ecofeminism, however, began well before 1975. Both Ursula K. Le Guin and Margaret Atwood are speculative fiction authors whose work before and after 1975 examines important ecofeminist topics and contributes to the growth of ecofeminist discussion. This thesis traces ecofeminist philosophy in Le Guin’s The Left Hand of Darkness (1969) and The Dispossessed (1974), and Atwood’s Surfacing (1972) and Oryx and Crake (2003) in an effort to explore the roots of the ecofeminist literary movement, examine its connection with and growth through speculative fiction, and gain insight into the roots of a movement which has important implications in an environmentally controversial future. Le Guin and Atwood are precocious ecofeminist authors whose early works handle topics such as technology, gender, demilitarization, ahistory, and the domination of both land and people. Because these matters are the founding issues of contemporary ecofeminism, an analysis of these authors provides context for where ecofeminism came from and where we can expect it to go

Population Health Solutions for Assessing Cognitive Impairment in Geriatric Patients.

In December 2017, the National Academy of Neuropsychology convened an interorganizational Summit on Population Health Solutions for Assessing Cognitive Impairment in Geriatric Patients in Denver, Colorado. The Summit brought together representatives of a broad range of stakeholders invested in the care of older adults to focus on the topic of cognitive health and aging. Summit participants specifically examined questions of who should be screened for cognitive impairment and how they should be screened in medical settings. This is important in the context of an acute illness given that the presence of cognitive impairment can have significant implications for care and for the management of concomitant diseases as well as pose a major risk factor for dementia. Participants arrived at general principles to guide future screening approaches in medical populations and identified knowledge gaps to direct future research. Key learning points of the summit included: recognizing the importance of educating patients and healthcare providers about the value of assessing current and baseline cognition;emphasizing that any screening tool must be appropriately normalized and validated in the population in which it is used to obtain accurate information, including considerations of language, cultural factors, and education; andrecognizing the great potential, with appropriate caveats, of electronic health records to augment cognitive screening and tracking of changes in cognitive health over time

Changes in smoking prevalence among U.S. adults by state and region: Estimates from the Tobacco Use Supplement to the Current Population Survey, 1992-2007

<p>Abstract</p> <p>Background</p> <p>Tobacco control policies at the state level have been a critical impetus for reduction in smoking prevalence. We examine the association between recent changes in smoking prevalence and state-specific tobacco control policies and activities in the entire U.S.</p> <p>Methods</p> <p>We analyzed the 1992-93, 1998-99, and 2006-07 Tobacco Use Supplement to the Current Population Survey (TUS-CPS) by state and two indices of state tobacco control policies or activities [initial outcome index (IOI) and the strength of tobacco control (SOTC) index] measured in 1998-1999. The IOI reflects cigarette excise taxes and indoor air legislation, whereas the SOTC reflects tobacco control program resources and capacity. Pearson Correlation coefficient between the proportionate change in smoking prevalence from 1992-93 to 2006-07 and indices of tobacco control activities or programs was the main outcome measure.</p> <p>Results</p> <p>Smoking prevalence decreased from 1992-93 to 2006-07 in both men and women in all states except Wyoming, where no reduction was observed among men, and only a 6.9% relative reduction among women. The percentage reductions in smoking in men and women respectively were the largest in the West (average decrease of 28.5% and 33.3%) and the smallest in the Midwest (18.6% and 20.3%), although there were notable exceptions to this pattern. The decline in smoking prevalence by state was correlated with the state's IOI in both women and men (r = -0.49, p < 0.001; r = -0.31, p = 0.03; respectively) and with state's SOTC index in women(r = -0.30, p = 0.03 0), but not men (r = -0.21, p = 0.14).</p> <p>Conclusion</p> <p>State level policies on cigarette excise taxes and indoor air legislation correlate strongly with reductions in smoking prevalence since 1992. Strengthening and systematically implementing these policies could greatly accelerate further reductions in smoking.</p

PI3Kγ is a molecular switch that controls immune suppression

Macrophages play critical, but opposite, roles in acute and chronic inflammation and cancer1,2,3,4,5. In response to pathogens or injury, inflammatory macrophages express cytokines that stimulate cytotoxic T cells, whereas macrophages in neoplastic and parasitic diseases express anti-inflammatory cytokines that induce immune suppression and may promote resistance to T cell checkpoint inhibitors1,2,3,4,5,6,7. Here we show that macrophage PI 3-kinase γ controls a critical switch between immune stimulation and suppression during inflammation and cancer. PI3Kγ signalling through Akt and mTor inhibits NFκB activation while stimulating C/EBPβ activation, thereby inducing a transcriptional program that promotes immune suppression during inflammation and tumour growth. By contrast, selective inactivation of macrophage PI3Kγ stimulates and prolongs NFκB activation and inhibits C/EBPβ activation, thus promoting an immunostimulatory transcriptional program that restores CD8+ T cell activation and cytotoxicity. PI3Kγ synergizes with checkpoint inhibitor therapy to promote tumour regression and increased survival in mouse models of cancer. In addition, PI3Kγ-directed, anti-inflammatory gene expression can predict survival probability in cancer patients. Our work thus demonstrates that therapeutic targeting of intracellular signalling pathways that regulate the switch between macrophage polarization states can control immune suppression in cancer and other disorders

Sputtering Erosion Measurement on Boron Nitride as a Hall Thruster Material

The durability of a high-powered Hall thruster may be limited by the sputter erosion resistance of its components. During normal operation, a small fraction of the accelerated ions will impact the interior of the main discharge channel, causing its gradual erosion. A laboratory experiment was conducted to simulate the sputter erosion of a Hall thruster. Tests of sputter etch rate were carried out using 300 to 1000 eV Xenon ions impinging on boron nitride substrates with angles of attack ranging from 30 to 75 degrees from horizontal. The erosion rates varied from 3.41 to 14.37 Angstroms/[sec(mA/sq cm)] and were found to depend on the ion energy and angle of attack, which is consistent with the behavior of other materials

Sublethal concentrations of diverse gold compounds inhibit mammalian cytosolic thioredoxin reductase (TrxR1)

Thioredoxin reductase (TrxR) reduces thioredoxin (Trx), thereby contributing to cellular redox balance, facilitating the synthesis of deoxy-ribose sugars for DNA synthesis, and regulating redox-sensitive gene expression. Auranofin is a gold compound that potently inhibits TrxR. This inhibition is one suspected mechanism of auranofin’s therapeutic benefit in the treatment of rheumatoid arthritis. The use of other gold compounds to treat cancer or inflammatory disease may rely on their ability to inhibit TrxR. In the current study, we tested the hypothesis that a variety of gold compounds may inhibit TrxR. Methods: We exposed rat-TrxR1 to auranofin, gold sodium thiomalate, sodium aurothiosulfate, triphenyl phosphine gold chloride, or gold acetate, and measured TrxR activity ex vivo. We then compared TrxR1 inhibitory levels of gold compounds to those that inhibited mitochondrial activity of THP1 monocytes and OSC2 epithelial cells, estimated by succinate dehydrogenase activity. Results: All gold compounds inhibited TrxR1 at concentrations ranging from 5 to 4000 nM (50% inhibitory concentration). The oxidation state of gold did not correlate with inhibitory potency, but ligand configuration was important. Au(I)-phosphine compounds (triphenyl phosphine gold chloride and auranofin) were the most potent inhibitors of TrxR. All TrxR1 inhibitory concentrations were sublethal to mitochondrial activity in both THP1 and OSC2 cells. Conclusions: Diverse types of gold compounds may be effective inhibitors of TrxR1 at concentrations that do not suppress cellular mitochondrial function. Inhibition may be optimized to some degree by altering the ligand configuration of the compounds. These results support future study of a variety of Au compounds for therapeutic development as inhibitors of TrxR1