Myo/Nog cells are nonprofessional phagocytes.

Myo/Nog cells were discovered in the chick embryo epiblast. Their expression of MyoD reflects a commitment to the skeletal muscle lineage and capacity to differentiate into myofibroblasts. Release of Noggin by Myo/Nog cells is essential for normal morphogenesis. Myo/Nog cells rapidly respond to wounding in the skin and eyes. In this report, we present evidence suggesting that Myo/Nog cells phagocytose tattoo ink in tissue sections of human skin and engulf cell corpses in cultures of anterior human lens tissue and magnetic beads injected into the anterior chamber of mice in vivo. Myo/Nog cells are distinct from macrophages in the skin and eyes indicated by the absence of labeling with an antibody to ionized calcium binding adaptor molecule 1. In addition to their primary roles as regulators of BMP signaling and progenitors of myofibroblasts, Myo/Nog cells behave as nonprofessional phagocytes defined as cells whose primary functions are unrelated to phagocytosis but are capable of engulfment.

Antibody-Conjugated, DNA-Based Nanocarriers Intercalated with Doxorubicin Eliminate Myofibroblasts in Explants of Human Lens Tissue.

Posterior capsule opacification (PCO) occurs in some adults and most children following cataract surgery. The fibrotic form of PCO arises, in part, from migratory, contractile myofibroblasts that deform the lens capsule and impair vision. In short-term cultures of human anterior lens tissue, myofibroblasts emerge from Myo/Nog cells that are identified with the G8 monoclonal antibody and by their expression of the MyoD transcription factor and bone morphogenetic protein inhibitor noggin. In this study, we tested the hypothesis that targeted depletion of Myo/Nog cells with the G8 monoclonal antibody (mAb) conjugated to three-dimensional DNA nanocarriers intercalated with doxorubicin (G8:3DNA:Dox) would prevent the accumulation of myofibroblasts in long-term, serum- and growth factor-free cultures of human lens tissue obtained by capsulorhexis. The mAb:nanocarrier complex was internalized into acidic compartments of the cell. G8:3DNA:Dox killed nearly all Myo/Nog cells without affecting the lens epithelial cells. In 30-day cultures, all G8-positive cells expressed noggin, and subpopulations had synthesized MyoD, sarcomeric myosin, and alpha smooth muscle actin (α-SMA). Myo/Nog cells responded to scratching of the lens epithelium by accumulating around the edges of the wound. Treatment with two doses of G8:3DNA:Dox completely eliminated G8+/α-SMA+ cells throughout the explant. These experiments demonstrate that Myo/Nog cells are the source of myofibroblasts in long-term cultures of anterior human lens tissue and mAb:3DNA nanocarriers specifically and effectively deliver cytotoxic cargo to a subpopulation of cells without off-target effects. G8:3DNA:Dox has the potential to reduce PCO following cataract surgery.

Correlation of macular thickness with visual fields in glaucoma patients and suspects.

PURPOSE: To provide a quantitative comparison of the retinal thickness in the macula, with Humphrey visual field (HVF) parameters and circumpapillary retinal nerve fiber layer (RNFL) defects, in glaucoma patients and suspects. PATIENTS AND METHODS: Retrospective statistical analysis of spectral domain optical coherence tomography (SD-OCT) compared with HVF mean deviation (MD) and pattern standard deviation (PSD) in 73 subjects who met the study criteria. Bivariate statistical analysis was performed. RESULTS: Macular thickness correlates with HVF deficits, with much worse MD (-6.8) and PSD (5.8) scores in subjects with average macular thickness <270 µm, compared with those >300 µm, (MD +0.4, PSD 1.7). Both the MD (P=0.0001) and PSD (P<0.0001) correlated with average macular thickness. In subjects with a difference of 3 or greater in the MD between the 2 eyes, there was a difference of 11 to 13 µm in average macular thickness. Asymmetry within the same eye, between the superior macula and inferior macula, correlated with a larger PSD in that eye. There was a strong correlation between RNFL defects and retinal thinning in the macula. CONCLUSIONS: SD-OCT measurements of retinal thickness in the macula correlate with HVF parameters and RNFL parameters in glaucoma patients and suspects. This correlation between visual field defects and macular thickness can help in confirming the existence and extent of the visual field defect.

Pediatric ophthalmology in the developing world.

PURPOSE OF REVIEW: It is estimated that of the 45 million people who are blind worldwide in 2000, 1.4 million are children from middle-income and low-income countries, the majority of whom live in the poorest regions of Africa and Asia. The focus of this paper is to discuss the status of pediatric ophthalmology in developing countries and the progress that has been made in the areas of avoidable childhood blindness and visual impairment, particularly corneal scarring as a result of vitamin A deficiency, congenital cataract and retinopathy of prematurity. In addition, we will review the prevalence of uncorrected refractive error and discuss the access to pediatric ophthalmologists in developing countries. RECENT FINDINGS: Some developing countries have begun incorporating vitamin A supplementation and measles immunizations and have seen a decrease in xerophthtalmia. With improvement in vitamin A status, cataract is becoming a more apparent cause of treatable childhood blindness. Amblyopia and uncorrected refractive errors are important and inexpensively treatable causes of visual impairment, with myopia being most common. As neonatal intensive care services in middle-income developing countries improve the survival of premature infants, retinopathy of prematurity is emerging as a significant cause of childhood blindness. SUMMARY: Childhood blindness and visual impairment in developing countries remains a significant public health issue, but recent initiatives have shown promise of future improvements.