Publications by authors named "Yassin Djalali-Talab"

Background: To compare clinical, anatomical, and densitometric changes following Dresden (DCXL) vs. accelerated (ACXL) corneal UVA cross-linking (CXL; Avedro KXL, Geuder, Heidelberg, Germany) in progressive keratoconus (KC).

Methods And Material: In this retrospective study, we analyzed 20 patients following DCXL (3 mW/cm², 30 min, 5.

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Purpose: To compare results after ILM peeling and ILM inverted flap technique utilized the repair of full thickness macular holes, irrespective of their size.

Patients And Methods: Pre- and postoperative data of 109 patients who suffered from a full thickness macular hole were retrospectively analyzed. Forty-eight patients were treated with an inverted ILM flap technique, 61 patients were treated with ILM peeling.

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Background/purpose: To determine anatomical success and best-corrected visual acuity after secondary surgery with heavy silicone oil tamponade in patients with persistent full-thickness macular holes.

Methods: In this retrospective study, 63 eyes with persistent full-thickness macular holes after primary pars plana vitrectomy and internal limiting membrane peeling underwent secondary surgery with heavy silicone oil tamponade. Macular spectral domain optical coherence tomography and best-corrected visual acuity measurements were performed during the follow-up.

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Intraocular infections associated with Abiotrophia defectiva are rare. This article reports the case of a 57-year-old woman with endophthalmitis associated with Abiotrophia defectiva 3 months after uncomplicated cataract surgery combined with the implantation of a glaucoma gel-stent in the right eye. The patient had complained of redness of the right upper nasal conjunctiva and pain for 2 weeks prior to the endophthalmitis.

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Pigment epithelium-derived factor (PEDF) is a potent multifunctional protein that inhibits angiogenesis and has neurogenic and neuroprotective properties. Since the wet form of age-related macular degeneration is characterized by choroidal neovascularization (CNV), PEDF would be an ideal candidate to inhibit CNV and support retinal pigment epithelial (RPE) cells. However, its short half-life has precluded its clinical use.

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Purpose: To investigate the reliability of partial coherence laser interferometry for optical biometry in highly myopic eyes.

Methods: Axial length measurements by the IOLMaster (Carl Zeiss Meditec, Germany) with signal-to-noise ratio (SNR) ≥2 were performed in 52 consecutive myopic subjects with axial length ≥26.5 mm and 45 emmetropic patients before cataract surgery.

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Objective: Although junctional adhesion molecule (JAM)-C has been implicated in the control of inflammatory leukocyte recruitment, its role in neointima formation after arterial injury has not been elucidated.

Methods And Results: In apolipoprotein E-deficient (Apoe(-/-)) mice fed an atherogenic diet, antibody blockade of JAM-C significantly reduced neointimal hyperplasia after wire injury of carotid arteries without altering medial area and decreased neointimal macrophage but not smooth muscle cell (SMC) content. An increased expression of JAM-C was detected in colocalization with luminal SMCs 1 day after injury and neointimal SMCs after 3 weeks.

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Background: Although activation of the complement system has been implicated in the progression of human atherosclerosis, its function during arterial remodeling after injury has not been investigated. Here, we examined the contribution of the complement cascade to neointima formation in apolipoprotein E-deficient mice using a C1-esterase inhibitor (C1-inhibitor).

Methods And Results: Apolipoprotein E-deficient mice fed an atherogenic diet were subjected to wire-induced endothelial denudation of the carotid artery and treated with C1-inhibitor (Berinert; 15 IU i.

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The CXC ligand (CXCL)12/CXC receptor (CXCR)4 chemokine-receptor axis controls hematopoiesis, organ development, and angiogenesis, but its role in the inflammatory pathogenesis of atherosclerosis is unknown. Here we show that interference with Cxcl12/Cxcr4 by a small-molecule antagonist, genetic Cxcr4 deficiency, or lentiviral transduction with Cxcr4 degrakine in bone marrow chimeras aggravated diet-induced atherosclerosis in apolipoprotein E-deficient (Apoe-/-) or LDL receptor-deficient (Ldlr-/-) mice. Chronic blockade of Cxcr4 caused leukocytosis and an expansion of neutrophils and increased neutrophil content in plaques, associated with apoptosis and a proinflammatory phenotype.

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