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"Hart, George"
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The Dark Ecology of Naked Lunch
In this article, I argue that William S. Burroughs’ novel Naked Lunch engages in a “perverse aesthetics” that is analogous to Timothy Morton’s theory of dark ecology. The novel’s main themes of consumption and control are directly related to the Anthropocene’s twin disasters of global warming and mass extinction, and the trope for addiction, junk, reveals Burroughs’ deep analysis of the political and social forces that attempt to control life, what Burroughs calls biocontrol. By placing the novel’s obsession with hanging/lynching in the context of dark ecology, its critique of racism can also be seen as a critique of speciesism.
Journal Article
Ancient Egypt
Presents a photo essay on ancient Egypt and the people who lived there, documented through the mummies, pottery, weapons, and other objects they left behind.
Book
Inventing the Language to Tell It
From 1920 until his death in 1962, consciousness and its effect on the natural world was Robinson Jeffers's obsession. Understanding and explaining the biological basis of mind is one of the towering challenges of modern science to this day, and Jeffers's poetic experiment is an important contribution to American literary history no other twentieth-century poet attempted such a thorough engagement with a crucial scientific problem. Jeffers invented a sacramental poetics that accommodates a modern scientific account of consciousness, thereby integrating an essentially religious sensibility with science in order to discover the sacramentality of natural process and reveal a divine cosmos. There is no other study of Jeffers or sacramental nature poetry like this one. It proposes that Jeffers's sacramentalism emerged out of his scientifically informed understanding of material nature. Drawing on ecocriticism, religious studies, and neuroscience, Inventing the Language to Tell It shows how Jeffers produced the most compelling sacramental nature poetry of the twentieth century.
eBook
Indigenous caretaking of beargrass and the social and ecological consequences of adaptations to maintain beargrass weaving practices
Indigenous ecologies have persisted through major social and ecological changes including settler colonialism. Adaptations have been a necessary part of this resilience, however little attention has been given to the consequences of these adaptations for Indigenous Peoples and ecologies. Without exploring these consequences, we are left with an incomplete understanding of adaptation that potentially obscures social and ecological costs associated with resilience. Here we describe the contemporary caretaking of a culturally-significant plant used in weaving traditions called beargrass (Xerophyllum tenax Melanthiaceae), and discuss how adaptive practices to maintain biocultural connections to beargrass have influenced both socio-cultural and ecological systems. We ask: (1) How is beargrass stewarded and used today? (2) What are the adaptive practices that Indigenous communities in the Pacific Northwest have used to maintain cultural traditions through changing conditions? (3) What are some of the social and ecological consequences of these adaptations? Through semi-structured interviews with cultural practitioners we identified multiple reciprocal practices that form a basis of the caretaking relationship. In order to compensate for a lack of access to beargrass and lack of ability to exercise sovereignty in land management, practitioners described substituting other weaving materials for beargrass, as well as caretaking substitutions. These adaptations were not uniformly accepted and for some either represented significant cultural losses or placed additional burdens on communities. We also collected ecological field data on beargrass. Using structural equation modeling, we found that a key adaptive practice, the substitution of tree pruning for cultural fire, can replicate key short-term benefits of fire for beargrass populations, but does not appear to replicate longer term benefits. In sum, adaptive practices have allowed beargrass traditions to persist through colonialism, but cannot fully substitute for social and ecological benefits of pre-colonial caretaking, and also result in losses and/or additional burdens for communities. Investigating what adaptations to maintain resilience do in communities, and for whom, is necessary in order to fully appreciate the costs and benefits of adaptations that support resilience through various forms of perturbation.
Journal Article
Exercise training reduces resting heart rate via downregulation of the funny channel HCN4
Endurance athletes exhibit sinus bradycardia, that is a slow resting heart rate, associated with a higher incidence of sinus node (pacemaker) disease and electronic pacemaker implantation. Here we show that training-induced bradycardia is not a consequence of changes in the activity of the autonomic nervous system but is caused by intrinsic electrophysiological changes in the sinus node. We demonstrate that training-induced bradycardia persists after blockade of the autonomous nervous system
in vivo
in mice and
in vitro
in the denervated sinus node. We also show that a widespread remodelling of pacemaker ion channels, notably a downregulation of HCN4 and the corresponding ionic current,
I
f
. Block of
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f
abolishes the difference in heart rate between trained and sedentary animals
in vivo
and
in vitro
. We further observe training-induced downregulation of Tbx3 and upregulation of NRSF and miR-1 (transcriptional regulators) that explains the downregulation of HCN4. Our findings provide a molecular explanation for the potentially pathological heart rate adaptation to exercise training.
Endurance athletes are known to have a low resting heart rate. Here, D'Souza
et al.
propose that training-induced bradycardia is the result of electrophysiological changes in the sinus node, challenging the classical view that training-induced bradycardia is caused by increased activity of the autonomic nervous system.
Journal Article
RNAseq shows an all-pervasive day-night rhythm in the transcriptome of the pacemaker of the heart
Physiological systems vary in a day-night manner anticipating increased demand at a particular time. Heart is no exception. Cardiac output is primarily determined by heart rate and unsurprisingly this varies in a day-night manner and is higher during the day in the human (anticipating increased day-time demand). Although this is attributed to a day-night rhythm in post-translational ion channel regulation in the heart’s pacemaker, the sinus node, by the autonomic nervous system, we investigated whether there is a day-night rhythm in transcription. RNAseq revealed that ~ 44% of the sinus node transcriptome (7134 of 16,387 transcripts) has a significant day-night rhythm. The data revealed the oscillating components of an intrinsic circadian clock. Presumably this clock (or perhaps the master circadian clock in the suprachiasmatic nucleus) is responsible for the rhythm observed in the transcriptional machinery, which in turn is responsible for the rhythm observed in the transcriptome. For example, there is a rhythm in transcripts responsible for the two principal pacemaker mechanisms (membrane and Ca
2+
clocks), transcripts responsible for receptors and signalling pathways known to control pacemaking, transcripts from genes identified by GWAS as determinants of resting heart rate, and transcripts from genes responsible for familial and acquired sick sinus syndrome.
Journal Article
Simvastatin causes pulmonary artery relaxation by blocking smooth muscle ROCK and calcium channels: Evidence for an endothelium-independent mechanism
Simvastatin reduces pulmonary arterial pressure and right ventricular hypertrophy in animal models of pulmonary arterial hypertension (PAH) and is thought to restore endothelial dysfunction. In vivo effects of drugs are complicated by several factors and little is known of the direct effects of statins on pulmonary arteries. This study investigated the direct effects of simvastatin on pulmonary arteries isolated from rats with or without monocrotaline-induced PAH. Simvastatin suppressed contractions evoked by the thromboxane A2 receptor agonist U46619 (30 nM), the α1-adrenergic agonist phenylephrine (5 μM) and KCl (50 mM) by ~50% in healthy and diseased arteries, but did not reduce contraction evoked by sarco/endoplasmic reticulum ATPase blockers. It relaxed hypertensive arteries in the absence of stimulation. Removing the endothelium or inhibiting eNOS did not prevent the inhibition by simvastatin. Inhibiting RhoA/rho kinase (ROCK) with Y27632 (10 μM) suppressed contractions to U46619 and phenylephrine by ~80% and prevented their inhibition by simvastatin. Y27632 reduced KCl-induced contraction by ~30%, but did not prevent simvastatin inhibition. Simvastatin suppressed Ca2+ entry into smooth muscle cells, as detected by Mn2+ quench of fura-2 fluorescence. The calcium antagonist, nifedipine (1 μM), almost abolished K+-induced contraction with less effect against U46619 and phenylephrine. We conclude that simvastatin relaxes pulmonary arteries by acting on smooth muscle to interfere with signalling through G-protein coupled receptors and voltage-dependent Ca2+ entry. Its actions likely include inhibition of ROCK-dependent Ca2+ sensitisation and voltage-gated Ca2+ channels. These are likely to contribute to the beneficial effects of simvastatin in animal models of PAH.
Journal Article
Silencing miR-370-3p rescues funny current and sinus node function in heart failure
Bradyarrhythmias are an important cause of mortality in heart failure and previous studies indicate a mechanistic role for electrical remodelling of the key pacemaking ion channel HCN4 in this process. Here we show that, in a mouse model of heart failure in which there is sinus bradycardia, there is upregulation of a microRNA (miR-370-3p), downregulation of the pacemaker ion channel, HCN4, and downregulation of the corresponding ionic current,
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f
, in the sinus node. In vitro, exogenous miR-370-3p inhibits HCN4 mRNA and causes downregulation of HCN4 protein, downregulation of
I
f
, and bradycardia in the isolated sinus node. In vivo, intraperitoneal injection of an antimiR to miR-370-3p into heart failure mice silences miR-370-3p and restores HCN4 mRNA and protein and
I
f
in the sinus node and blunts the sinus bradycardia. In addition, it partially restores ventricular function and reduces mortality. This represents a novel approach to heart failure treatment.
Journal Article