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1.  Hand-gesture-based sterile interface for the operating room using contextual cues for the navigation of radiological images 
This paper presents a method to improve the navigation and manipulation of radiological images through a sterile hand gesture recognition interface based on attentional contextual cues. Computer vision algorithms were developed to extract intention and attention cues from the surgeon's behavior and combine them with sensory data from a commodity depth camera. The developed interface was tested in a usability experiment to assess the effectiveness of the new interface. An image navigation and manipulation task was performed, and the gesture recognition accuracy, false positives and task completion times were computed to evaluate system performance. Experimental results show that gesture interaction and surgeon behavior analysis can be used to accurately navigate, manipulate and access MRI images, and therefore this modality could replace the use of keyboard and mice-based interfaces.
doi:10.1136/amiajnl-2012-001212
PMCID: PMC3715344  PMID: 23250787
User-Computer Interface; computer vision system; infection control
2.  Vaccination for Invasive Canine Meningioma Induces in Situ Production of Antibodies Capable of Antibody-Dependent Cell-Mediated Cytotoxicity 
Cancer research  2013;73(10):2987-2997.
Malignant and atypical meningiomas are resistant to standard therapies and associated with poor prognosis. Despite progress in the treatment of other tumors with therapeutic vaccines, this approach has not been tested preclinically or clinically in these tumors. Spontaneous canine meningioma is a clinically meaningful but underutilized model for preclinical testing of novel strategies for aggressive human meningioma. We treated 11 meningioma-bearing dogs with surgery and vaccine immunotherapy consisting of autologous tumor cell lysate combined with toll-like receptor ligands. Therapy was well tolerated, and only one dog had tumor growth that required intervention, with a mean follow up of 585 days. Interferon gamma elaborating T cells were detected in the peripheral blood of two cases, but vaccine-induced tumor-reactive antibody responses developed in all dogs. Antibody responses were polyclonal, recognizing both intracellular and cell surface antigens, and heat shock protein 60 was identified as one common antigen. Tumor-reactive antibodies bound allogeneic canine and human meningiomas, demonstrating common antigens across breed and species. Histological analysis revealed robust infiltration of antibody-secreting plasma cells into the brain around the tumor in post-treatment compared to pre-treatment samples. Tumor-reactive antibodies were capable of inducing antibody dependent cell-mediated cytotoxicity to autologous and allogeneic tumor cells. These data demonstrate the feasibility and immunologic efficacy of vaccine immunotherapy for a large animal model of human meningioma and warrant further development towards human trials.
doi:10.1158/0008-5472.CAN-12-3366
PMCID: PMC3655124  PMID: 23471847
IM01 Animal/transgenic models for tumor immunobiology; CL07 Cancer Vaccines
3.  An ADAMTSL2 Founder Mutation Causes Musladin-Lueke Syndrome, a Heritable Disorder of Beagle Dogs, Featuring Stiff Skin and Joint Contractures 
PLoS ONE  2010;5(9):e12817.
Background
Musladin-Lueke Syndrome (MLS) is a hereditary disorder affecting Beagle dogs that manifests with extensive fibrosis of the skin and joints. In this respect, it resembles human stiff skin syndrome and the Tight skin mouse, each of which is caused by gene defects affecting fibrillin-1, a major component of tissue microfibrils. The objective of this work was to determine the genetic basis of MLS and the molecular consequence of the identified mutation.
Methodology and Principal Findings
We mapped the locus for MLS by genome-wide association to a 3.05 Mb haplotype on canine chromosome 9 (CFA9 (50.11–54.26; praw <10−7)), which was homozygous and identical-by-descent among all affected dogs, consistent with recessive inheritance of a founder mutation. Sequence analysis of a candidate gene at this locus, ADAMTSL2, which is responsible for the human TGFβ dysregulation syndrome, Geleophysic Dysplasia (GD), uncovered a mutation in exon 7 (c.660C>T; p.R221C) perfectly associated with MLS (p-value = 10−12). Murine ADAMTSL2 containing the p.R221C mutation formed anomalous disulfide-bonded dimers when transiently expressed in COS-1, HEK293F and CHO cells, and was present in the medium of these cells at lower levels than wild-type ADAMTSL2 expressed in parallel.
Conclusions/Significance
The genetic basis of MLS is a founder mutation in ADAMTSL2, previously shown to interact with latent TGF-β binding protein, which binds fibrillin-1. The molecular effect of the founder mutation on ADAMTSL2 is formation of disulfide-bonded dimers. Although caused by a distinct mutation, and having a milder phenotype than human GD, MLS nevertheless offers a new animal model for study of GD, and for prospective insights on mechanisms and pathways of skin fibrosis and joint contractures.
doi:10.1371/journal.pone.0012817
PMCID: PMC2941456  PMID: 20862248

Results 1-3 (3)