Bismuth Infusion of ABS Enables Additive Manufacturing of Complex Radiological Phantoms and Shielding Equipment.

Radiopacity is a critical property of materials that are used for a range of radiological applications, including the development of phantom devices that emulate the radiodensity of native tissues and the production of protective equipment for personnel handling radioactive materials. Three-dimensional (3D) printing is a fabrication platform that is well suited to creating complex anatomical replicas or custom labware to accomplish these radiological purposes. We created and tested multiple ABS (Acrylonitrile butadiene styrene) filaments infused with varied concentrations of bismuth (1.2-2.7 g/cm³), a radiopaque metal that is compatible with plastic infusion, to address the poor gamma radiation attenuation of many mainstream 3D printing materials. X-ray computed tomography (CT) experiments of these filaments indicated that a density of 1.2 g/cm³ of bismuth-infused ABS emulates bone radiopacity during X-ray CT imaging on preclinical and clinical scanners. ABS-bismuth filaments along with ABS were 3D printed to create an embedded human nasocranial anatomical phantom that mimicked radiological properties of native bone and soft tissue. Increasing the bismuth content in the filaments to 2.7 g/cm³ created a stable material that could attenuate 50% of 99mTechnetium gamma emission when printed with a 2.0 mm wall thickness. A shielded test tube rack was printed to attenuate source radiation as a protective measure for lab personnel. We demonstrated the utility of novel filaments to serve multiple radiological purposes, including the creation of anthropomorphic phantoms and safety labware, by tuning the level of radiation attenuation through material customization.

Under-correction of human myopia--is it myopigenic?: a retrospective analysis of clinical refraction data.

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<0.01); that is, the greater the under-correction, the greater the myopic progression. In addition, there was a significant positive correlation between myopia progression and subjective refraction (r=0.166, p=0.006); that is, the greater the degree of myopia, the greater the effect of under-correction. However, there was no significant correlation between myopia progression and either age (r=-0.11, p=0.86) or gender (r=-0.82, p=0.17). CONCLUSION: Under-correction of myopia produced a small but progressively greater degree of myopic progression than did full correction. The present finding is consistent with earlier clinical trials and modeling of human myopia.

Activation and trafficking of peritoneal B1a B-cells in response to amphibole asbestos.

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.