Building a Web-Augmented Reality application for demonstration of kidney pathology for veterinary education.

Three-dimensional (3D) models created with computers and educational applications designed using such models are used in the medical field every day. However, there is a lack of macroscopic demonstration applications built with digital 3D models in the field of veterinary pathology. The aim is to build a fully interactive 3D educational web-based augmented reality application, to demonstrate macroscopic lesions in kidneys for educational purposes. We used open source and free software for all 3D modelling, Augmented Reality and website building. Sixteen 3D kidney pathology models were created. Kidney models modelled in 3D and published as WebAR are as follows: normal kidney, unilateral neurogenic shutdown with atrophy, hydronephrosis, hypercalcemia of malignancy tubular nephrosis, interstitial corticomedullary nephritis, renal infarct, multifocal petechial hemorrhages, polycystic kidneys, renal masses, multifocal nephritis, pigmentary nephrosis, papillary necrosis, glucose-related rapid autolysis (pulpy kidney), pyelonephritis, renomegaly and kidney stones. With the workflow shown here, it has been presented as a feasible model application for human pathology and presented to educators, researchers and developers who have 3D models and AR in their field of interest. To the best of the authors' knowledge, this is the first study on Web-Augmented Reality application for veterinary pathology education.

Astrocytes, microglia/macrophages, and neurons expressing Toll-like receptor 11 contribute to innate immunity against encephalitic Toxoplasma gondii infection.

Toll-like receptor 11 (TLR11) is a specific receptor for Toxoplasma gondii and uropathogenic Escherichia coli and has recently been identified in the mouse brain. In the present study, TLR11 gene expression was measured in the mouse brain by Real-time quantitative polymerase chain reaction (RT-PCR). Furthermore, the TLR11 protein expression profile was evaluated in neuroglia and neurons throughout the encephalitic period (10, 20, and 30days after inoculation) in mice with experimentally induced T. gondii infection. In the brains of experimental (n=21) and control (n=7) mice, TLR11, glial fibrillary acidic protein (GFAP), cd11b, NeuN, TLR11/GFAP+, TLR11/cd11b+, and TLR11/NeuN+ cells were investigated using either indirect single- or double-labeling immunoperoxidase staining. The results indicated that TLR11 gene expression increased during chronic toxoplasmic encephalitis, and there was a variable degree of TLR11 immunopositivity among cd11b+, GFAP+, and NeuN+ cells in the brain. On the tenth day of infection, there was a significant increase in TLR11 protein and gene expression, which remained stable during the later stages of infection. In this experimental model, TLR11 expression was induced in astrocytes, neurons, and microglia/macrophages during the immune response to T. gondii infection.