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

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

Antibiotic susceptibility profile of Streptococcus pneumoniae isolated from acute respiratory infection in Dakar: a cross sectional study

Streptococcus pneumoniae is a pathogen causing pneumonia, meningitis, otitis and bacteraemia. Nowadays, S. pneumoniae is developing antibacterial resistance, particularly for those with reduced susceptibility to penicillin. The objective of this study was to assess the susceptibility profile of S. pneumoniae strains isolated from acute respiratory infections (ARIs) in children younger than 5 years of age in Dakar, Senegal. S. pneumoniae strains were isolated from broncho-alveolar lavages (BALs), nasopharyngeal swabs, and middle ear secretion from children in the Paediatric Department of Abass Ndao University Teaching Hospital and Paediatric Department of Roi Baudouin Hospital in Dakar, Senegal. The strains were cultivated on Columbia agar supplemented with 5% of horse blood and gentamicin (6 mg/L). Antibiotic susceptibility testing was performed using E-test method. A total of 34 strains of S. pneumoniae were isolated and identified in this study, among them 7 strains (20.58%) showed penicillin-resistance. Antibiotics such as amoxicillin/clavulanic acid (MIC90=0.036 μg/mL), cefuroxim (MIC90=0.38 μg/mL), cefixim (MIC90=1.5 μg/mL), as well as macrolides (azithromycin MIC90=1.5 μg/mL, clarithromycin MIC90=0.125 μg/mL) and fluoroquinolone (levofloxacin MIC90=1 μg/mL, ofloxacin MIC90=2 μg/mL) were mostly active. However, all S. pneumoniae strains were resistant to sulfamethoxazole/trimethoprim (MIC90: 32 μg/mL). Except of S. pneumoniae strains penicillin-resistance or reduced susceptibility, most strains were susceptible to β-lactams antibiotics commonly used in ARI treatment. Continuous surveillance of antimicrobial resistance patterns of pneumococcus strains is still crucial for effective control of ARIs in children

GDF15 is elevated in mice following retinal ganglion cell death and in glaucoma patients

Glaucoma is the second leading cause of blindness worldwide. Physicians often use surrogate endpoints to monitor the progression of glaucomatous neurodegeneration. These approaches are limited in their ability to quantify disease severity and progression due to inherent subjectivity, unreliability, and limitations of normative databases. Therefore, there is a critical need to identify specific molecular markers that predict or measure glaucomatous neurodegeneration. Here, we demonstrate that growth differentiation factor 15 (GDF15) is associated with retinal ganglion cell death. Gdf15 expression in the retina is specifically increased after acute injury to retinal ganglion cell axons and in a murine chronic glaucoma model. We also demonstrate that the ganglion cell layer may be one of the sources of secreted GDF15 and that GDF15 diffuses to and can be detected in aqueous humor (AH). In validating these findings in human patients with glaucoma, we find not only that GDF15 is increased in AH of patients with primary open angle glaucoma (POAG), but also that elevated GDF15 levels are significantly associated with worse functional outcomes in glaucoma patients, as measured by visual field testing. Thus, GDF15 maybe a reliable metric of glaucomatous neurodegeneration, although further prospective validation studies will be necessary to determine if GDF15 can be used in clinical practice

Infiltration of Proinflammatory M1 Macrophages into the Outer Retina Precedes Damage in a Mouse Model of Age-Related Macular Degeneration

Age-related macular degeneration (AMD) is a major cause of blindness in the developed world. Oxidative stress and inflammation are implicated in AMD, but precise mechanisms remain poorly defined. Carboxyethylpyrrole (CEP) is an AMD-associated lipid peroxidation product. We previously demonstrated that mice immunized with CEP-modified albumin developed AMD-like degenerative changes in the outer retina. Here, we examined the kinetics of lesion development in immunized mice and the presence of macrophages within the interphotoreceptor matrix (IPM), between the retinal pigment epithelium and photoreceptor outer segments. We observed a significant and time-dependent increase in the number of macrophages in immunized mice relative to young age-matched controls prior to overt pathology. These changes were more pronounced in BALB/c mice than in C57BL/6 mice. Importantly, IPM-infiltrating macrophages were polarized toward the M1 phenotype but only in immunized mice. Moreover, when Ccr2-deficient mice were immunized, macrophages were not present in the IPM and no retinal lesions were observed, suggesting a deleterious role for these cells in our model. This work provides mechanistic evidence linking immune responses against oxidative damage with the presence of proinflammatory macrophages at sites of future AMD and experimentally demonstrates that manipulating immunity may be a target for modulating the development of AMD