Sufism and Liberation across the Indo-Afghan Border: 1880-1928

How do we understand links between sufism and pro-egalitarian revolutionary activism in the early twentieth century; and how did upland compositions of self and community help constitute revolutionary activism in South Asia more broadly? Using Pashto poetry as my archive I integrate a history of radical egalitarian thought and political practice to a holistic study of self-making; of imperial spatiality; and of shifting gradients of power in the regions between Kabul and Punjab. Amid a chaotic rise of new practices of imperial and monarchic hegemony around the turn of the twentieth century, I argue, older sedimentations of ‘devotee selfhood’ in the high valleys of eastern Afghanistan gave rise, in social spaces preserved by self-reflexive poetic practice and circulation, to conscious desires for avoidance of all forms of hierarchy or sovereignty, in favour of a horizontal politics of reciprocity. Such inchoate drives for freedom later played a role in constituting anti-statist revolutionary subjectivities across great geographical and social distance. From upland sufi roots they rippled outward to intersect with the work of transnational socialist and anti-imperialist militants in Indian nationalist circles too; and even influenced scholars at the heart of the nascent Afghan nation-state

Regulation of SIRT6 protein levels by nutrient availability

AbstractSirtuins have been shown to regulate life-span in response to nutritional availability. We show here that levels of the mammalian sirtuin, SIRT6, increased upon nutrient deprivation in cultured cells, in mice after fasting, and in rats fed a calorie-restricted diet. The increase in SIRT6 levels is due to stabilization of SIRT6 protein, and not via an increase in SIRT6 transcription. In addition, p53 positively regulates SIRT6 protein levels under standard growth conditions but has no role in the nutrient-dependent regulation of SIRT6. These observations imply that at least two sirtuins are involved in regulation of life-span by nutrient availability

Vascular Stenosis: An Introduction

International audienceAn arterial stenosis is a narrowing of the lumen that disturbs the local blood flow and precludes the adequate irrigation of perfused organs. A vascular stenosis can be extrinsic, which is caused by external compression (e.g., aneurysms and tumors), or intrinsic, currently related to atherosclerosis.Atherosclerosis is defined by an intramural retention of lipids coupled to inflammation and dyslipidemia. Atherosclerosis scatters throughout large and medium thick-walled systemic arteries, especially near and in branching regions. (Pulmonary arterial stenosis is a congenital defect.)Atherosclerosis is characterized by migration from the media, proliferation, and dedifferentiation of vascular smooth myocytes in the subendothelial layer, in addition to monocyte diapedesis and differentiation into macrophages. Both smooth myocytes and macrophages scavenge accumulated oxidized low-density lipoproteins (oxLDL) and transform into foam cells. Atherosclerosis produces symptoms when the arterial lumen is severely narrowed.Advanced atherosclerotic plaques can be destabilized, thereby being a source of clotting and subsequent emboli. Emboli block tissue perfusion in a smaller downstream artery, thereby causing ischemia and infarction.The treatment of stenotic arterial segments relies on surgical grafting or medical minimally invasive procedures such as stenting. However, both methods often lead to intimal hyperplasia resulting from uncontrolled proliferation of vascular smooth myocytes. Whereas atheroma evolves during a time magnitude order of 10 years, posttherapeutic intimal hyperplasia develops in a period of order 1 month.Successful stenting can be assumed as a procedure without strong endothelial injury. In other words, both delayed thrombosis and intimal hyperplasia result from stent deployment that more or less severely damages the vascular endothelium. To eliminate these complications, drug-eluting stents have been designed and fabricated. However, the antiproliferative drug not only blocks vascular smooth myocyte division but also precludes endothelium healing. In the absence of proper endothelial interface between blood and arterial wall, that is, when the local controller of blood coagulation and cell proliferation is missing, thrombosis and restenosis occur.Arterial stenoses have stimulated biomechanicians and applied mathematicians. They carried out flow visualization and pressure and velocity measurements in experimental models of stenoses with idealized, symmetrical or not, geometry. In parallel to technological improvements of medical imaging techniques, computational fluid dynamics, due to new numerical schemes and high-performance computing, enables to perform numerical tests on subject-specific compartments of the blood circulation, after 3D reconstruction, rather than focusing on more or less short arterial, branched or not, segments. In addition, the drug release from drug-eluting stents is investigated using mathematical models