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Purpose: To investigate retrospectively, based on routine clinical records in an optometric office, the effect of refractive under-correction of the myopic spectacle prescription on myopic progression in children and young adults. Methods: Patient records of children and young-adult myopes in a private optometric practice in Glendale, Arizona, USA, were initially reviewed to identify those that met the criteria. Information collected from the patient records included: age, gender, the dates and number of their visits (more than one visit was required for use of the data), final prescription, and non-cycloplegic subjective refraction. For each patient visit, the difference in spherical equivalent (SE) between the subjective refraction for maximum visual acuity and the final prescription was calculated for both the left and right eyes. Myopia progression was defined as the difference in SE between the final subjective refraction of the previous visit and that of the subsequent visit. Based on the study criteria, a total of 275 patient visits were obtained from the data collected in 76 patients. Results: A significant positive correlation was found between the magnitude of under-correction of the refractive error and myopic progression (r = 0.301, p

B1a B-cells are concentrated in peritoneal and pleural cavities, are producers of 'natural auto-antibodies', and have been implicated in autoimmune responses. Their numbers are increased in humans and mice with systemic autoimmune diseases, but their role in the immune pathology is not known. Asbestos causes pulmonary, pleural, and peritoneal pathologies by accessing these tissues after inhalation. Amphibole asbestos has been shown to elicit immune dysfunction, including chronic inflammation, fibrosis, and autoantibody production. This study tested the hypothesis that asbestos affects immune dysfunction by activating B1a B-cells to traffic to secondary lymphatic tissue. C57Bl/6 mice were exposed to amphibole asbestos (Libby 6-Mix) either endotracheally or intraperitoneally, and the B1a B-cells in pleural or peritoneal compartments were tested by multi-parameter flow cytometry. Adoptive transfer of peritoneal lymphocytes from CD45.1 transgenic to wild-type mice was used to track the migration. The percentage and numbers of B1a B-cells in pleural and peritoneal cavities decreased 3-6 days following exposure. During that time, asbestos exposure led to a decrease in cells expressing alpha-4 (α4) integrin and MHC II antigen. Peritoneal cells treated in vitro showed decreased α4 integrin with no change in CD5, IgM, or MHC II antigen. Therefore, B1a cells (IgM(+), CD5(+), MHC II(+)) traffic from the peritoneal cavity following loss of α4 integrin expression. Following adoptive transfer into the peritoneum of asbestos-exposed mice, CD45.1(+) B1a cells were detected in the spleen and mesenteric lymph nodes after 3 days, peaking at 6 days. Interestingly, the percentage of splenic suppressor B-cells (IgM(+), CD5(+), CD11b(+), CD1d(+)) decreased following amphibole exposure, demonstrating that the B1a cells did not contribute to an increased pool of suppressive B-cells. These results show that B1a B-cells respond to asbestos exposure by trafficking to secondary lymphatic tissue where they may affect ultimate immune dysfunction.