24 research outputs found

    Love’s Transcendence and the Problem of Theodicy

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    L’enseignement et le soi

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    Le concept d’enseignement se trouve au centre des confĂ©rences faites par Levinas au CollĂšge philosophique et rĂ©cemment publiĂ©es. Cette notion est toujours prĂ©sente dans TotalitĂ© et Infini, mais semble disparaĂźtre ensuite de la philosophie de Levinas. Le but de ce travail est de comprendre pourquoi cela a lieu. En faisant un dĂ©tour par un texte de Levinas sur « JudaĂŻsme et Ă©ducation » de la mĂȘme pĂ©riode, il est possible de proposer que la notion d’éducation chez Levinas conduise Ă  une ambiguĂŻtĂ© au regard de la position du soi responsable faisant qu’il oscille entre l’accusatif et le datif. Cette ambiguĂŻtĂ© est la cause de son abandon plus tardif ou plutĂŽt : elle est rĂ©solue par la transformation de l’éducation en une instruction non mĂ©diate pour laquelle la rĂ©vĂ©lation de la loi est la figure paradigmatique.The concept of education is at the core of the newly published lectures that Levinas gave at the Philosophical College founded by Jean Wahl. The notion is still present in Totality and Infinity but seems to disappear later on in Levinas’ philosophy. The aim of my essay is to understand why this happens. Thanks to one of Levinas’ Jewish texts on Judaism and education from the same period, I suggest that the notion of “education” according to Levinas leads to an ambiguity with regard to the position of the responsible “Self”, making it oscillate between the accusative and the dative. This ambiguity causes its later abandonment or rather it is solved by transforming “education” into a non-mediated “instruction” to which the revelation of the law is the paradigmatic figure

    Det pĂŠdagogiske paradoks: - mellem Delfi og Sinai

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    Artiklen vil diskutere det pÊdagogiske paradoks primÊrt ud fra D. Benner. Artiklen hÊvder, at det pÊdagogiske paradoks hviler pÄ en forstÄelse af frihed, der hos Benner er underbelyst, og en idé om autenticitet, der ender i det isolerede Selv. Jeg foreslÄr her over for at studere appellens fÊnomen m.h.p. at indkredse en idé om frihed, der ikke udelukker enhver ydre indflydelse.The essay discuss the educational paradox primarely with D. Benner. The claim is that the educational paradox presupose a conception of freedom that in Benner remains unclear, and on an idea of authencity that ends in the isolated Self. In contrast to this, the essay propose to study the phenomenon of the appeal in order to encircle an idea of freedom that does not exclude exterior influence

    Is laparoscopic excision for superficial peritoneal endometriosis helpful or harmful?:Protocol for a double-blinded, randomised, placebo-controlled, three-armed surgical trial

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    INTRODUCTION: Placebo-controlled surgical designs are recommended to ascertain treatment effects for elective surgeries when there is genuine doubt about the effectiveness of the surgery. Some elective surgeries for pain have been unable to show an effect beyond sham surgery, suggesting contributions from contextual factors. However, the nature of contextual factors in elective surgery is largely unexplored. Further, methodological difficulties in placebo-controlled surgical trials impact the ability to estimate the effectiveness of a surgical procedure. These include an overall lack of testing the success of blinding, absence of comparison to a no-surgery control group and dearth of test for neuropathic pain. For women with peritoneal endometriosis, there is uncertainty regarding the pain-relieving effect of surgery. Surgery may put patients at risk of complications such as postsurgical neuropathic pain, without guarantees of sufficient pelvic pain relief. The planned placebo-controlled trial aims to examine the effect of surgery on pelvic pain, widespread pain and neuropathic pain symptoms in women with peritoneal endometriosis, and to test the contribution of contextual factors to pain relief. METHODS AND ANALYSIS: One hundred women with peritoneal endometriosis will be randomised to either diagnostic laparoscopy with excision of endometrial tissue (active surgery), purely diagnostic laparoscopy (sham surgery) or delayed surgery (no-surgery control group). Outcomes include pelvic pain relief, widespread pain, neuropathic pain symptoms and quality of life. Contextual factors are also assessed. Assessments will be obtained at baseline and 1, 3 and 6 months postrandomisation. Mixed linear models will be used to compare groups over time on all outcome variables. ETHICS AND DISSEMINATION: The trial is approved by the Regional Ethics Committee in the Central Denmark Region (1-10-72-152-20). The trial is funded by a PhD scholarship from Aarhus University, and supported by a grant from ‘Helsefonden’ (20-B-0448). Findings will be published in international peer-reviewed journals and disseminated at international conferences. TRIAL REGISTRATION NUMBER: NCT05162794

    Rotigaptide protects the myocardium and arterial vasculature from ischaemia reperfusion injury

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    Aim: Ischaemia-reperfusion injury (IRI) causes impaired endothelial function and is a major component of the adverse effects of reperfusion following myocardial infarction. Rotigaptide increases gap junction conductance via connexin-43. We tested the hypothesis that rotigaptide reduces experimental myocardial infarction size and ameliorates endothelial IRI in humans. Methods: Myocardial infarction study: porcine myocardial infarction was achieved by catheter-induced occlusion of the left anterior descending artery. In a randomized double-blind study, rotigaptide (n = 9) or placebo (n = 10) was administered intravenously as a 10 min bolus prior to reperfusion and continuously during 2 h of reperfusion. Myocardial infarction size (IS) was assessed as proportion of the area at risk (AAR). Human translational study: forearm IRI was induced in the presence or absence of intra-arterial rotigaptide. In a randomized double-blind study, forearm arterial blood flow was measured at rest and during intra-arterial infusion of acetylcholine (5–20 Όg min–1; n = 11) or sodium nitroprusside (2–8 mg min–1; n = 10) before and after intra-arterial infusion of placebo or rotigaptide, and again following IRI. Results: Myocardial infarction study: Rotigaptide treatment was associated with a reduction of infarct size (IS/AAR[%]: 18.7 ± 4.1 [rotigaptide] vs. 43.6 ± 4.2 [placebo], P = 0.006). Human translational study: Endothelium-dependent vasodilatation to acetylcholine was attenuated after ischaemia-reperfusion in the presence of placebo (P = 0.007), but not in the presence of rotigaptide (P = NS). Endothelium-independent vasodilatation evoked by sodium nitroprusside was unaffected by IRI or rotigaptide (P = NS). Conclusions: Rotigaptide reduces myocardial infarction size in a porcine model and protects from IRI-related endothelial dysfunction in man. Rotigaptide may have therapeutic potential in the treatment of myocardial infarction

    Abnormal increase in urinary aquaporin-2 excretion in response to hypertonic saline in essential hypertension

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    <p>Abstract</p> <p>Background</p> <p>Dysregulation of the expression/shuttling of the aquaporin-2 water channel (AQP2) and the epithelial sodium channel (ENaC) in renal collecting duct principal cells has been found in animal models of hypertension. We tested whether a similar dysregulation exists in essential hypertension.</p> <p>Methods</p> <p>We measured urinary excretion of AQP2 and ENaC ÎČ-subunit corrected for creatinine (u-AQP2<sub>CR</sub>, u-ENaC<sub>ÎČ-CR</sub>), prostaglandin E2 (u-PGE<sub>2</sub>) and cyclic AMP (u-cAMP), fractional sodium excretion (FE<sub>Na</sub>), free water clearance (C<sub>H2O</sub>), as well as plasma concentrations of vasopressin (AVP), renin (PRC), angiotensin II (Ang II), aldosterone (Aldo), and atrial and brain natriuretic peptide (ANP, BNP) in 21 patients with essential hypertension and 20 normotensive controls during 24-h urine collection (baseline), and after hypertonic saline infusion on a 4-day high sodium (HS) diet (300 mmol sodium/day) and a 4-day low sodium (LS) diet (30 mmol sodium/day).</p> <p>Results</p> <p>At baseline, no differences in u-AQP2<sub>CR </sub>or u-ENaC<sub>ÎČ-CR </sub>were measured between patients and controls. U-AQP2<sub>CR </sub>increased significantly more after saline in patients than controls, whereas u-ENaC<sub>ÎČ-CR </sub>increased similarly. The saline caused exaggerated natriuretic increases in patients during HS intake. Neither baseline levels of u-PGE<sub>2</sub>, u-cAMP, AVP, PRC, Ang II, Aldo, ANP, and BNP nor changes after saline could explain the abnormal u-AQP2<sub>CR </sub>response.</p> <p>Conclusions</p> <p>No differences were found in u-AQP2<sub>CR </sub>and u-ENaC<sub>ÎČ-CR </sub>between patients and controls at baseline. However, in response to saline, u-AQP2<sub>CR </sub>was abnormally increased in patients, whereas the u-ENaC<sub>ÎČ-CR </sub>response was normal. The mechanism behind the abnormal AQP2 regulation is not clarified, but it does not seem to be AVP-dependent.</p> <p>Clinicaltrial.gov identifier</p> <p><a href="http://www.trialregister.nl/trialreg/admin/rctview.asp?TC=00345124">NCT00345124</a>.</p

    Increased renal sodium absorption by inhibition of prostaglandin synthesis during fasting in healthy man. A possible role of the epithelial sodium channels

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    <p>Abstract</p> <p>Background</p> <p>Treatment with prostaglandin inhibitors can reduce renal function and impair renal water and sodium excretion. We tested the hypotheses that a reduction in prostaglandin synthesis by ibuprofen treatment during fasting decreased renal water and sodium excretion by increased absorption of water and sodium via the aquaporin2 water channels and the epithelial sodium channels.</p> <p>Methods</p> <p>The effect of ibuprofen, 600 mg thrice daily, was measured during fasting in a randomized, placebo-controlled, double-blinded crossover study of 17 healthy humans. The subjects received a standardized diet on day 1, fasted at day 2, and received an IV infusion of 3% NaCl on day 3. The effect variables were urinary excretions of aquaporin2 (u-AQP2), the beta-fraction of the epithelial sodium channel (u-ENaCbeta), cyclic-AMP (u-cAMP), prostaglandin E2 (u-PGE2). Free water clearance (CH2O), fractional excretion of sodium (FENa), and plasma concentrations of vasopressin, angiotensin II, aldosterone, atrial-, and brain natriuretic peptide.</p> <p>Results</p> <p>Ibuprofen decreased u-AQP2, u-PGE2, and FENa at all parts of the study. During the same time, ibuprofen significantly increased u-ENaCbeta. Ibuprofen did not change the response in p-AVP, u-c-AMP, urinary output, and free water clearance during any of these periods. Atrial-and brain natriuretic peptide were higher.</p> <p>Conclusion</p> <p>During inhibition of prostaglandin synthesis, urinary sodium excretion decreased in parallel with an increase in sodium absorption and increase in u-ENaCbeta. U-AQP2 decreased indicating that water transport via AQP2 fell. The vasopressin-c-AMP-axis did not mediate this effect, but it may be a consequence of the changes in the natriuretic peptide system and/or the angiotensin-aldosterone system</p> <p>Trial Registration</p> <p>Clinical Trials Identifier: NCT00281762</p
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