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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.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.Fifty of 63 eyes (79.4%) achieved anatomical success. In eyes achieving anatomical success, best-corrected visual acuity before primary vitreoretinal surgery was significantly better (0.77 [∼20/125 Snellen] ± 0.24 [1.3-0.3] logarithm of the minimum angle of resolution) compared with eyes not achieving anatomical success (0.88 [∼20/160 Snellen] ± 0.17 [1.1-0.6] logarithm of the minimum angle of resolution, P = 0.044). Minimum linear diameter of full-thickness macular holes was significantly smaller in eyes achieving anatomical success, both before primary (403.4 ± 128.7 [199.0-707.0] µ m vs. 568.1 ± 209.1 [307.0-953.0] µ m, P = 0.009) and secondary surgery (464.1 ± 215.0 [178.0-1,521.0] µ m vs. 663.3 ± 228.5 [451.0-1,301.0] µ m, P = 0.010). Patients remaining phakic during all three surgeries did not benefit from best-corrected visual acuity improvement, although anatomical success was achieved.Heavy silicone oil tamponade in secondary surgery for persistent full-thickness macular holes is a safe and efficient surgical method. Best-corrected visual acuity and minimum linear diameter before surgery may be indicators for anatomical success.

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. Axial length measurements and SNR were analyzed and compared among the two study groups. Results Axial length measurements were feasible in 46 of 52 (88.5%) highly myopic eyes and in 41 of 45 (91.1%) eyes with normal axial length. To achieve two reliable axial length values with SNR ≥2, a mean number of 2.06±0.25 measurements was necessary in myopic eyes and 2.10±0.37 in emmetropic counterparts. Mean SNR after two measurements was 4.98±2.44 in myopic eyes versus 5.56±2.32 in control eyes. Even though successful measurement was independent of preoperative visual acuity, patients with visual acuity better than 20/63 showed significantly higher SNR values. Conclusions Partial coherence laser interferometry shows satisfying feasibility and good signal quality for axial length determination in highly myopic eyes with stable retinal condition and clear media.

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. Blocking JAM-C inhibited monocytic cell arrest and leukocyte adhesion to carotid arteries perfused ex vivo and in vivo. Furthermore, monocyte adhesion to activated coronary artery SMCs under flow conditions in vitro was diminished by blocking JAM-C. Conclusions— Our data provide the first evidence for a crucial role of JAM-C in accelerated lesion formation and leukocyte recruitment in atherosclerosis-prone mice.

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. Whereas circulating neutrophils were recruited to atherosclerotic lesions, depletion of neutrophils reduced plaque formation and prevented its exacerbation after blocking Cxcr4. Disrupting Cxcl12/Cxcr4 thus promotes lesion formation through deranged neutrophil homeostasis, indicating that Cxcl12/Cxcr4 controls the important contribution of neutrophils to atherogenesis in mice

A 62-year-old man presented with mild left hemiparesis, headache, and blurred vision of his right eye. Ten days before, he had undergone thromboendarterectomy because of subtotal stenosis of his right internal carotid artery. MRI revealed confluent white matter edema together with focal hemorrhage consistent with cerebral hyperperfusion syndrome (CHS; figure 1). Likewise, funduscopy showed small retinal hemorrhages confined to the right eye (figure 2). Under careful blood pressure control, symptoms and brain edema fully resolved within weeks. CHS occurs in around 3% of patients undergoing carotid thromboendarterectomy and can induce severe neurologic deficits.1 Rarely, hyperperfusion also involves the ipsilateral eye.2