Dying is not Death: The Difference between Blanchot’s Fiction and Hegel’s

<div>With “Literature and the Right to Death” (1948), Blanchot makes his most sustained contribution to the debate initiated in France by Kojève and Hippolyte concerning Hegel’s philosophy. At times Blanchot’s reading is</div><div>forced and idiosyncratic. Yet this reading has another motivation than the succinct and faithful paraphrase of the earlier thinker. Arguably Blanchot positions himself within Hegel’s terminology in order to rethink the sense of</div><div>the expression “the philosophy of art.” What is with Hegel an objective genitive becomes a subjective genitive. The rules therefore change. Whereas Hegel offers in his lectures on aesthetics an expatiation on art fixed under the gaze of philosophy, Blanchot installs art as the subject and submits the conventions and expectations of philosophical discourse to its procedures. In the light of this reversal, what might otherwise be judged a deviation or a lapse with respect to the genre of the philosophical essay can be seen to play its role in Blanchot’s reassessment of the relations between metaphysics and literature.</div

James Phillips. Heidegger’s Volk: Between National Socialism and Poetry. Stanford: Stanford UP, 2005 [Book review]

The space of the “in between” is a central figure in James Phillips’ study of Heidegger’s <i>Volk</i> (“the people”). Phillips’ reading of Heidegger manages to navigate a path between so many dangerous, because dogmatic, views of his engagement with National Socialism. The picture of Heidegger’s thought that Phillips constructs is one marked by <i>das Fremde</i> (the strange; the alien) and <i>Unheimlichkeit </i>(uncanniness, or the unhomeliness of that which lacks a home) that characterise Heidegger’s conception of Dasein’s poetic dwelling. The “in between” (80) which Heidegger’s thought inhabits is marked, on the one hand, by what in 1933 he saw to be the promise of National Socialism’s appeal to “the people,” and which he still saw in 1953 to be the movement’s “inner truth.” The other pole of the “in between” of Phillips’ study is that of Heidegger’s inevitable disillusionment with National Socialism, which his ontology exceeded but “could not leave... behind and cut itself off from” (53)

Additional file 1: Table S1. of Estimation of indices of health service readiness with a principal component analysis of the Tanzania Service Provision Assessment Survey

PCA loadings for Hospitals/Health Centers Principal Component , sorted by medical role in primary health care and size of coefficient. Table S2. PCA loadings for Hospitals/Health Centers Component 2, sorted by medical role in primary health care and size of coefficient. Table S3. PCA loadings for Dispensaries Principal Component, sorted by medical role in primary health care and size of coefficient. (DOCX 38 kb

Additional file 1: of A qualitative analysis of the effect of a community-based primary health care programme on reproductive preferences and contraceptive use among the Kassena-Nankana of northern Ghana

Interview guides. (DOC 43 kb

Crop rotation and agri-environment schemes determine bumblebee communities via flower resources

<p>The biodiversity (flower cover and bumblebees) and environmental data used in the analyses.</p

MOESM1 of A preliminary study of a novel emergency department nursing triage simulation for research applications

Additional file 1. Additional tables

Design, Synthesis, and Biological Evaluation of Novel Chromanone Derivatives as Multifunctional Agents for the Treatment of Alzheimer’s Disease

Based on a multitarget strategy, a series of novel chromanone–1-benzyl-1,2,3,6-tetrahydropyridin hybrids were identified for the potential treatment of Alzheimer’s disease (AD). Biological evaluation demonstrated that these hybrids exhibited significant inhibitory activities toward acetylcholinesterase (AChE) and monoamine oxidase B (MAO-B). The optimal compound C10 possessed excellent dual AChE/MAO-B inhibition both in terms of potency and equilibrium (AChE: IC50 = 0.58 ± 0.05 μM; MAO-B: IC50 = 0.41 ± 0.04 μM). Further molecular modeling and kinetic investigations revealed that compound C10 was a dual-binding inhibitor bound to both the catalytic anionic site and peripheral anionic site of AChE. In addition, compound C10 exhibited low neurotoxicity and potently inhibited AChE enzymatic activity. Furthermore, compound C10 more effectively protected against mitochondrial dysfunction and oxidation than donepezil, strongly inhibited AChE-induced amyloid aggregation, and moderately reduced glutaraldehyde-induced phosphorylation of tau protein in SH-SY5Y cells. Moreover, compound C10 displayed largely enhanced improvements in cognitive behaviors and spatial memory in a scopolamine-induced AD mice model with better efficacy than donepezil. Overall, the multifunctional profiles of compound C10 suggest that it deserves further investigation as a promising lead for the prospective treatment of AD

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<p>The inactivation of ribosomal protein S6 kinase 1 (S6K1) recapitulates aspects of caloric restriction and mTORC1 inhibition to achieve prolonged longevity in invertebrate and mouse models. In addition to delaying normative aging, inhibition of mTORC1 extends the shortened lifespan of yeast, fly, and mouse models with severe mitochondrial disease. Here we tested whether disruption of S6K1 can recapitulate the beneficial effects of mTORC1 inhibition in the Ndufs4 knockout (NKO) mouse model of Leigh Syndrome caused by Complex I deficiency. These NKO mice develop profound neurodegeneration resulting in brain lesions and death around 50–60 days of age. Our results show that liver-specific, as well as whole body, S6K1 deletion modestly prolongs survival and delays onset of neurological symptoms in NKO mice. In contrast, we observed no survival benefit in NKO mice specifically disrupted for S6K1 in neurons or adipocytes. Body weight was reduced in WT mice upon disruption of S6K1 in adipocytes or whole body, but not altered when S6K1 was disrupted only in neurons or liver. Taken together, these data indicate that decreased S6K1 activity in liver is sufficient to delay the neurological and survival defects caused by deficiency of Complex I and suggest that mTOR signaling can modulate mitochondrial disease and metabolism via cell non-autonomous mechanisms.</p

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<p>The inactivation of ribosomal protein S6 kinase 1 (S6K1) recapitulates aspects of caloric restriction and mTORC1 inhibition to achieve prolonged longevity in invertebrate and mouse models. In addition to delaying normative aging, inhibition of mTORC1 extends the shortened lifespan of yeast, fly, and mouse models with severe mitochondrial disease. Here we tested whether disruption of S6K1 can recapitulate the beneficial effects of mTORC1 inhibition in the Ndufs4 knockout (NKO) mouse model of Leigh Syndrome caused by Complex I deficiency. These NKO mice develop profound neurodegeneration resulting in brain lesions and death around 50–60 days of age. Our results show that liver-specific, as well as whole body, S6K1 deletion modestly prolongs survival and delays onset of neurological symptoms in NKO mice. In contrast, we observed no survival benefit in NKO mice specifically disrupted for S6K1 in neurons or adipocytes. Body weight was reduced in WT mice upon disruption of S6K1 in adipocytes or whole body, but not altered when S6K1 was disrupted only in neurons or liver. Taken together, these data indicate that decreased S6K1 activity in liver is sufficient to delay the neurological and survival defects caused by deficiency of Complex I and suggest that mTOR signaling can modulate mitochondrial disease and metabolism via cell non-autonomous mechanisms.</p

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<p>The inactivation of ribosomal protein S6 kinase 1 (S6K1) recapitulates aspects of caloric restriction and mTORC1 inhibition to achieve prolonged longevity in invertebrate and mouse models. In addition to delaying normative aging, inhibition of mTORC1 extends the shortened lifespan of yeast, fly, and mouse models with severe mitochondrial disease. Here we tested whether disruption of S6K1 can recapitulate the beneficial effects of mTORC1 inhibition in the Ndufs4 knockout (NKO) mouse model of Leigh Syndrome caused by Complex I deficiency. These NKO mice develop profound neurodegeneration resulting in brain lesions and death around 50–60 days of age. Our results show that liver-specific, as well as whole body, S6K1 deletion modestly prolongs survival and delays onset of neurological symptoms in NKO mice. In contrast, we observed no survival benefit in NKO mice specifically disrupted for S6K1 in neurons or adipocytes. Body weight was reduced in WT mice upon disruption of S6K1 in adipocytes or whole body, but not altered when S6K1 was disrupted only in neurons or liver. Taken together, these data indicate that decreased S6K1 activity in liver is sufficient to delay the neurological and survival defects caused by deficiency of Complex I and suggest that mTOR signaling can modulate mitochondrial disease and metabolism via cell non-autonomous mechanisms.</p