CMS physics technical design report : Addendum on high density QCD with heavy ions

Peer reviewe

La dégénérescence maculaire liée à l'âge

Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in industrialized countries in individuals over 65 years of age. It is characterized by a progressive degenerative disorder of the macula, resulting in a loss of the central vision. There are two forms of AMD, the atrophic and the exudative form. A number of risk factors have been implicated in the onset of this condition. With the ageing of the population, the prevalence of AMD is steadily raising and is leading to a growing social and economical burden. Much research has been conducted to improve the diagnosis and management of people at risk of AMD and to develop new treatments. In this review we will discuss the risk factors associated with AMD, the clinical forms and their diagnosis, as well as the current and future therapeutic options.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Reduction of macular cysts after treatment with topical Dorzolamide in X-Linked Retinoschisis: A case report

P112info:eu-repo/semantics/nonPublishe

Necrotising retinopathy-like lesions as a manifestation of ocular sarcoidosis

Background: A 56-year-old Caucasian man presented with a 2-weeks history of decreased vision in the right eye. Vitritis, papillitis, cystoid macular oedema and inferior diffuse retinal infiltration were noticed. Extensive blood work-up, anterior chamber paracentesis with polymerase chain reaction (PCR) and Goldmann-Witmer coefficient, tuberculin skin test (PPD-test), fluorodeoxyglucose Positron Emission Tomography CT scan (FDG-PET/CT), lymph node biopsy and pars plana vitrectomy were performed. Results: Aqueous and vitreous samples were negative for an infectious and a lymphoproliferative etiology. Enlarged hilar and mediastinal lymph nodes were detected by FDG-PET/CT and subsequently biopsied, allowing to confirm the diagnosis of sarcoidosis. After a few months of oral corticosteroid therapy, the inflammation resolved completely and was replaced by atrophic retinal scars. Conclusion: Necrotising retinopathy-like lesions mimicking an infectious process or a lymphoproliferative disorder can be an atypical manifestation of ocular sarcoidosis.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Spectral domain optical coherence tomography findings in early deferoxamine maculopathy: Report of two cases

Purpose: To describe spectral domain optical coherence tomography features in two cases of early deferoxamine induced retinal toxicity. Methods: Two patients complained of sudden bilateral visual loss and dyschromatopsia. Both suffered from acute myelocytic leukemia with severe aplastic anemia and were treated with intravenous deferoxamine for 1 month. First ophthalmologic exploration and follow-up included fundoscopic examination, fluorescence angiography, fundus autofluorescence, and spectral domain optical coherence tomography. Results: Initially, both patients presented with a decreased visual acuity, inferior to 20/ 100. Fundus examination revealed a loss of transparency of the outer retina in the two cases. Autofluorescence pictures displayed hypoautofluorescence in the macular area, whereas fluorescein angiography unveiled an annular hyperfluorescence staining in the macular zone. Spectral domain optical coherence tomography showed a serous detachment of the neuroepithelium associated with photoreceptor outer segment elongation. Deferoxamine toxicity was immediately suspected and therapy promptly interrupted. One week later, both patients recovered visual acuity of 20/20 but retinal pigment epithelium (RPE) mottling was noticed in the macular areas. Spectral domain optical coherence tomography monitoring showed a progressive resolution of serous retinal detachment. Elongation of the photoreceptor outer segment disappeared but the RPE remained thickened, interrupted, and fragmented at different macular loci. Conclusion: Serous detachment of the neuroepithelium associated with photoreceptor outer segment elongation in the early stage of deferoxamine maculopathy is described for the first time. Early drug discontinuation allowed a fast resolution of the serous detachment but the typical RPE pigment mottling observed at the resolution phase was noticed 1 week later. Copyright ?by Ophthalmic Communications Society, Inc.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Clinical Phenotypes of Poppers Maculopathy and Their Links to Visual and Anatomic Recovery

SCOPUS: cp.jinfo:eu-repo/semantics/publishe

Long follow up of juvenile Idiopathic Arthritis Associated Uveitis

info:eu-repo/semantics/nonPublishe

New insight in understanding the contribution of SGLT1 in cardiac glucose uptake: evidence for a truncated form in mice and humans.

Although sodium-glucose co-transporter 1 (SGLT1) has been identified as one of the major SGLT isoforms expressed in the heart, its exact role remains elusive. Evidences using phlorizin, the most common inhibitor of SGLTs, suggested its role in glucose transport. However, phlorizin could also affect classical facilitated diffusion via glucose transporters (GLUTs), bringing into question the relevance of SGLT1 in overall cardiac glucose uptake. Accordingly, we assessed the contribution of SGLT1 in cardiac glucose uptake using the SGLT1 knock-out mouse model, which lacks exon 1. Glucose uptake was similar in cardiomyocytes isolated from SGLT1 knock-out (KO) and control littermate (WT) mice, either under basal state, insulin, or hyperglycemia. Similarly, in vivo basal and insulin-stimulated cardiac glucose transport measured by micro-PET scan technology did not differ between WT and KO mice. Micromolar concentrations of phlorizin had no impact on glucose uptake in either isolated WT or KO-derived cardiomyocytes. However, higher concentrations (1mM) completely inhibited insulin-stimulated glucose transport without affecting insulin signaling nor GLUT4 translocation, independently from cardiomyocyte genotype. Interestingly, we discover that mouse and human hearts expressed a shorter slc5a1 transcript, leading to SGLT1 protein lacking transmembrane domains and residues involved in glucose and sodium bindings. In conclusion, cardiac SGLT1 does not contribute to overall glucose uptake, probably due to the expression of slc5a1 transcript variant. The inhibitory effect of phlorizin on cardiac glucose uptake is SGLT1-independent and can be explained by GLUT transporter inhibition. These data open new perspectives in understanding the role of SGLT1 in the heart