Stabilization of a Coupled Multidimensional System

We introduce a model of a vibrating multidimensional structure made of a n-dimensional body and a one dimensional rod. We actually consider the anisotropic elastodynamic system in the n-dimensional body and the Euler-Bernouilli beam in the one-dimensional rod. These equations are coupled via their boundaries. Using appropriate feedbacks on a part of the boundary we show the exponential decay of the energy of the system

Sur la controlabilité exacte de l’equation des plaques vibrantes

We define, for the trace of solution of vibrating plates equation, norms with initial conditions in no regular spaces. Then, we give the corresponding exact controllability results.On definit, pour la trace de la solution de certains modeles de plaques vibrantes, des normes avec des donn´ees initiales dans des espaces peu r´eguliers. Ensuite on d´eduit les th´eor`emes de contrˆolabilit´e correspondants.We define, for the trace of solution of vibrating plates equation, norms with initial conditions in no regular spaces. Then, we give the corresponding exact controllability results

IL10-driven STAT3 signalling in senescent macrophages promotes pathological eye angiogenesis

Macrophage dysfunction plays a pivotal role during neovascular proliferation in diseases of ageing including cancers, atherosclerosis and blinding eye disease. In the eye, choroidal neovascularization (CNV) causes blindness in patients with age-related macular degeneration (AMD). Here we report that increased IL10, not IL4 or IL13, in senescent eyes activates STAT3 signalling that induces the alternative activation of macrophages and vascular proliferation. Targeted inhibition of both IL10 receptor-mediated signalling and STAT3 activation in macrophages reverses the ageing phenotype. In addition, adoptive transfer of STAT3-deficient macrophages into eyes of old mice significantly reduces the amount of CNV. Systemic and CD163(+) eye macrophages obtained from AMD patients also demonstrate STAT3 activation. Our studies demonstrate that impaired SOCS3 feedback leads to permissive IL10/STAT3 signalling that promotes alternative macrophage activation and pathological neovascularization. These findings have significant implications for our understanding of the pathobiology of age-associated diseases and may guide targeted immunotherapy

Effects of lenten fasting on body composition and biochemical parameters

Background: The catholic lenten fasting is the period of 40 days of fasting that precedes Easter. It is one of religious fasting less documented in the scientific literature. Thus the aim of our study was to evaluate the evolution of anthropometric and body composition and biochemical profile during Catholic lenten fasting.Methods: We conducted a prospective study, which took place during the period between one week before at the end of lenten fasting. Eleven fasters (4 women and 7 men), aged between 18 and 59 years were included in present study. Anthropometric, body composition parameters and biochemical profile were evaluated one week before, at 15th day and at the end of Lenten fasting.Results: Weight, body mass index (BMI) and visceral fat decreased significantly at the end of Lenten fasting. Lipid profile changed significantly during this fasting period. Total cholesterol (TC), low density lipoprotein – cholesterol (LDL-C) and triglycerides decreased significantly with fasting. High density lipoprotein – cholesterol (HDL-C) was remained unchanged during this fasting period while TC/HDL ratio was significantly decreased at the end of Lent.Conclusions: Present study showed that the fasting of Lent seems to have beneficial effects on reducing cardiovascular risk factors. Further studies are required to better understand the physiological mechanisms involved for a therapeutic use

Impaired monocyte cholesterol clearance initiates age-related retinal degeneration and vision loss

Advanced age-related macular degeneration (AMD), the leading cause of blindness among people over 50 years of age, is characterized by atrophic neurodegeneration or pathologic angiogenesis. Early AMD is characterized by extracellular cholesterol-rich deposits underneath the retinal pigment epithelium (RPE) called drusen or in the subretinal space called subretinal drusenoid deposits (SDD) that drive disease progression. However, mechanisms of drusen and SDD biogenesis remain poorly understood. Although human AMD is characterized by abnormalities in cholesterol homeostasis and shares phenotypic features with atherosclerosis, it is unclear whether systemic immunity or local tissue metabolism regulates this homeostasis. Here, we demonstrate that targeted deletion of macrophage cholesterol ABC transporters A1 (ABCA1) and -G1 (ABCG1) leads to age-associated extracellular cholesterol-rich deposits underneath the neurosensory retina similar to SDD seen in early human AMD. These mice also develop impaired dark adaptation, a cardinal feature of RPE cell dysfunction seen in human AMD patients even before central vision is affected. Subretinal deposits in these mice progressively worsen with age, with concomitant accumulation of cholesterol metabolites including several oxysterols and cholesterol esters causing lipotoxicity that manifests as photoreceptor dysfunction and neurodegeneration. These findings suggest that impaired macrophage cholesterol transport initiates several key elements of early human AMD, demonstrating the importance of systemic immunity and aging in promoting disease manifestation. Polymorphisms in genes involved with cholesterol transport and homeostasis are associated with a significantly higher risk of developing AMD, thus making these studies translationally relevant by identifying potential targets for therapy

SARM1 depletion rescues NMNAT1-dependent photoreceptor cell death and retinal degeneration

Leber congenital amaurosis type nine is an autosomal recessive retinopathy caused by mutations of the NA