Surgical Augmented Reality with Topological Changes

International audienceThe visualization of internal structures of organs in minimally invasive surgery is an important avenue for improving the perception of the surgeon, or for supporting planning and decision systems. However, current methods dealing with non-rigid augmented reality only provide augmentation when the topology of the organ is not modified. In this paper we solve this shortcoming by introducing a method for physics-based non-rigid augmented reality. Singularities caused by topo-logical changes are detected and propagated to the pre-operative model. This significantly improves the coherence between the actual laparascopic view and the model, and provides added value in terms of navigation and decision making. Our real time augmentation algorithm is assessed on a video showing the cut of a porcine liver's lobe in minimal invasive surgery

Augmented Reality during Cutting and Tearing of Deformable Objects

International audienceCurrent methods dealing with non-rigid augmented reality only provide an augmented view when the topology of the tracked object is not modified, which is an important limitation. In this paper we solve this shortcoming by introducing a method for physics-based non-rigid augmented reality. Singularities caused by topological changes are detected by analyzing the displacement field of the underlying deformable model. These topological changes are then applied to the physics-based model to approximate the real cut. All these steps, from deformation to cutting simulation, are performed in real-time. This significantly improves the coherence between the actual view and the model, and provides added value

Mexican tiger beetles

p. 231-309, [3] p. of plates : ill., maps ; 27 cm.Includes bibliographical references (p. 298-299)

Handling Topological Changes during Elastic Registration: Application to Augmented Reality in Laparoscopic Surgery

International audiencePurpose: Locating the internal structures of an organ is a critical aspect of many surgical procedures. Minimally invasive surgery, associated with augmented reality techniques, offers the potential to visualize inner structures, allowing for improved analysis, depth perception or for supporting planning and decision systems.Methods: Most of the current methods dealing with rigid or non-rigid augmented reality make the assumption that the topology of the organ is not modified. As surgery relies essentially on cutting and dissection of anatomical structures, such methods are limited to the early stages of the surgery.We solve this shortcoming with the introduction of a method for physics-based elastic registration using a single view from a monocular camera.Singularities caused by topological changes are detected and propagated to the pre-operative model. This significantly improves the coherence between the actual laparoscopic view and the model, and provides added value in terms of navigation and decision-making, e.g. by overlaying the internal structures of an organ on the laparoscopic view.Results: Our real time augmentation method is assessed on several scenarios, using synthetic objects and real organs. In all cases, the impact of our approach is demonstrated, both qualitatively and quantitatively.Conclusion: The presented approach tackles the challenge of localizing internal structures throughout a complete surgical procedure, even after surgical cuts. This information is crucial for surgeons to improve the outcome for their surgical procedure and avoid complications

Chrysina and Plusiotis of Mexico

8 p. : ill. ; 24 cm.Includes bibliographical references (p. 8)

Refinement of the associations between risk of colorectal cancer and polymorphisms on chromosomes 1q41 and 12q13.13

In genome-wide association studies (GWASs) of colorectal cancer, we have identified two genomic regions in which pairs of tagging-single nucleotide polymorphisms (tagSNPs) are associated with disease; these comprise chromosomes 1q41 (rs6691170, rs6687758) and 12q13.13 (rs7163702, rs11169552). We investigated these regions further, aiming to determine whether they contain more than one independent association signal and/or to identify the SNPs most strongly associated with disease. Genotyping of additional sample sets at the original tagSNPs showed that, for both regions, the two tagSNPs were unlikely to identify a single haplotype on which the functional variation lay. Conversely, one of the pair of SNPs did not fully capture the association signal in each region. We therefore undertook more detailed analyses, using imputation, logistic regression, genealogical analysis using the GENECLUSTER program and haplotype analysis. In the 1q41 region, the SNP rs11118883 emerged as a strong candidate based on all these analyses, sufficient to account for the signals at both rs6691170 and rs6687758. rs11118883 lies within a region with strong evidence of transcriptional regulatory activity and has been associated with expression of PDGFRB mRNA. For 12q13.13, a complex situation was found: SNP rs7972465 showed stronger association than either rs11169552 or rs7136702, and GENECLUSTER found no good evidence for a two-SNP model. However, logistic regression and haplotype analyses supported a two-SNP model, in which a signal at the SNP rs706793 was added to that at rs11169552. Post-GWAS fine-mapping studies are challenging, but the use of multiple tools can assist in identifying candidate functional variants in at least some cases

Recessive mutations in SPTBN2 implicate β-III spectrin in both cognitive and motor development

β-III spectrin is present in the brain and is known to be important in the function of the cerebellum. Heterozygous mutations in SPTBN2, the gene encoding β-III spectrin, cause Spinocerebellar Ataxia Type 5 (SCA5), an adult-onset, slowly progressive, autosomal-dominant pure cerebellar ataxia. SCA5 is sometimes known as "Lincoln ataxia," because the largest known family is descended from relatives of the United States President Abraham Lincoln. Using targeted capture and next-generation sequencing, we identified a homozygous stop codon in SPTBN2 in a consanguineous family in which childhood developmental ataxia co-segregates with cognitive impairment. The cognitive impairment could result from mutations in a second gene, but further analysis using whole-genome sequencing combined with SNP array analysis did not reveal any evidence of other mutations. We also examined a mouse knockout of β-III spectrin in which ataxia and progressive degeneration of cerebellar Purkinje cells has been previously reported and found morphological abnormalities in neurons from prefrontal cortex and deficits in object recognition tasks, consistent with the human cognitive phenotype. These data provide the first evidence that β-III spectrin plays an important role in cortical brain development and cognition, in addition to its function in the cerebellum; and we conclude that cognitive impairment is an integral part of this novel recessive ataxic syndrome, Spectrin-associated Autosomal Recessive Cerebellar Ataxia type 1 (SPARCA1). In addition, the identification of SPARCA1 and normal heterozygous carriers of the stop codon in SPTBN2 provides insights into the mechanism of molecular dominance in SCA5 and demonstrates that the cell-specific repertoire of spectrin subunits underlies a novel group of disorders, the neuronal spectrinopathies, which includes SCA5, SPARCA1, and a form of West syndrome

NOX1 loss-of-function genetic variants in patients with inflammatory bowel disease.

Genetic defects that affect intestinal epithelial barrier function can present with very early-onset inflammatory bowel disease (VEOIBD). Using whole-genome sequencing, a novel hemizygous defect in NOX1 encoding NAPDH oxidase 1 was identified in a patient with ulcerative colitis-like VEOIBD. Exome screening of 1,878 pediatric patients identified further seven male inflammatory bowel disease (IBD) patients with rare NOX1 mutations. Loss-of-function was validated in p.N122H and p.T497A, and to a lesser degree in p.Y470H, p.R287Q, p.I67M, p.Q293R as well as the previously described p.P330S, and the common NOX1 SNP p.D360N (rs34688635) variant. The missense mutation p.N122H abrogated reactive oxygen species (ROS) production in cell lines, ex vivo colonic explants, and patient-derived colonic organoid cultures. Within colonic crypts, NOX1 constitutively generates a high level of ROS in the crypt lumen. Analysis of 9,513 controls and 11,140 IBD patients of non-Jewish European ancestry did not reveal an association between p.D360N and IBD. Our data suggest that loss-of-function variants in NOX1 do not cause a Mendelian disorder of high penetrance but are a context-specific modifier. Our results implicate that variants in NOX1 change brush border ROS within colonic crypts at the interface between the epithelium and luminal microbes

Common variation near CDKN1A, POLD3 and SHROOM2 influences colorectal cancer risk

We performed a meta-analysis of five genome-wide association studies to identify common variants influencing colorectal cancer (CRC) risk comprising 8,682 cases and 9,649 controls. Replication analysis was performed in case-control sets totaling 21,096 cases and 19,555 controls. We identified three new CRC risk loci at 6p21 (rs1321311, near CDKN1A; P = 1.14 × 10(-10)), 11q13.4 (rs3824999, intronic to POLD3; P = 3.65 × 10(-10)) and Xp22.2 (rs5934683, near SHROOM2; P = 7.30 × 10(-10)) This brings the number of independent loci associated with CRC risk to 20 and provides further insight into the genetic architecture of inherited susceptibility to CRC.Swedish Research Council et al.Manuscrip