Real-time interactive isosurfacing: a new method for improving marching isosurfacing algorithm output and efficiency

Efficient rendering of a changing volumetric data-set is central to the development of effective medical simulations that incorporate haptic feedback. A new method referred to as real-time interactive isosurfacing (RTII) is described in this paper. RTII is an algorithm that can be applied to output from Marching Cubes-like algorithms to improve performance for real-time applications. The approach minimises processing by re-evaluating the isosurface around changing sub-volumes resulting from user interactions. It includes innovations that significantly reduce mesh complexity and improve mesh quality as triangles are created from the Marching Tetrahedra isosurfacing algorithm. Rendering efficiency is further improved over other marching isosurfacing algorithm outputs by maintaining an indexed triangle representation of the mesh. The effectiveness of RTII is discussed within the context of an endoscopic sinus surgery simulation currently being developed by the authors.     

Wildlife disease prevalence in human‐modified landscapes

Human‐induced landscape change associated with habitat loss and fragmentation places wildlife populations at risk. One issue in these landscapes is a change in the prevalence of disease which may result in increased mortality and reduced fecundity. Our understanding of the influence of habitat loss and fragmentation on the prevalence of wildlife diseases is still in its infancy. What is evident is that changes in disease prevalence as a result of human‐induced landscape modification are highly variable. The importance of infectious diseases for the conservation of wildlife will increase as the amount and quality of suitable habitat decreases due to human land‐use pressures. We review the experimental and observational literature of the influence of human‐induced landscape change on wildlife disease prevalence, and discuss disease transmission types and host responses as mechanisms that are likely to determine the extent of change in disease prevalence. It is likely that transmission dynamics will be the key process in determining a pathogen's impact on a host population, while the host response may ultimately determine the extent of disease prevalence. Finally, we conceptualize mechanisms and identify future research directions to increase our understanding of the relationship between human‐modified landscapes and wildlife disease prevalence. This review highlights that there are rarely consistent relationships between wildlife diseases and human‐modified landscapes. In addition, variation is evident between transmission types and landscape types, with the greatest positive influence on disease prevalence being in urban landscapes and directly transmitted disease systems. While we have a limited understanding of the potential influence of habitat loss and fragmentation on wildlife disease, there are a number of important areas to address in future research, particularly to account for the variability in increased and decreased disease prevalence. Previous studies have been based on a one‐dimensional comparison between unmodified and modified sites. What is lacking are spatially and temporally explicit quantitative approaches which are required to enable an understanding of the range of key causal mechanisms and the reasons for variability. This is particularly important for replicated studies across different host‐pathogen systems. Furthermore, there are few studies that have attempted to separate the independent effects of habitat loss and fragmentation on wildlife disease, which are the major determinants of wildlife population dynamics in human‐modified landscapes. There is an urgent need to understand better the potential causal links between the processes of human‐induced landscape change and the associated influences of habitat fragmentation, matrix hostility and loss of connectivity on an animal's physiological stress, immune response and disease susceptibility. This review identified no study that had assessed the influence of human‐induced landscape change on the prevalence of a wildlife sexually transmitted disease. A better understanding of the various mechanisms linking human‐induced landscape change and the prevalence of wildlife disease will lead to more successful conservation management outcomes.     

Disruption of barley immunity to powdery mildew by an in-frame Lys-Leu deletion in the essential protein SGT1

Barley (Hordeum vulgare L.) Mla (Mildew resistance locus a) and its nucleotide-binding, leucine-rich-repeat receptor (NLR) orthologs protect many cereal crops from diseases caused by fungal pathogens. However, large segments of the Mla pathway and its mechanisms remain unknown. To further characterize the molecular interactions required for NLR-based immunity, we used fast-neutron mutagenesis to screen for plants compromised in MLA-mediated response to the powdery mildew fungus, Blumeria graminis f. sp. hordei. One variant, m11526, contained a novel mutation, designated rar3 (required for Mla6 resistance3), that abolishes race-specific resistance conditioned by the Mla6, Mla7, and Mla12 alleles, but does not compromise immunity mediated by Mla1, Mla9, Mla10, and Mla13. This is analogous to, but unique from, the differential requirement of Mla alleles for the co-chaperone Rar1 (required for Mla12 resistance1). We used bulked-segregant-exome capture and fine mapping to delineate the causal mutation to an in-frame Lys-Leu deletion within the SGS domain of SGT1 (Suppressor of G-two allele of Skp1, Sgt1_{ΔKL308–309}), the structural region that interacts with MLA proteins. In nature, mutations to Sgt1 usually cause lethal phenotypes, but here we pinpoint a unique modification that delineates its requirement for some disease resistances, while unaffecting others as well as normal cell processes. Moreover, the data indicate that the requirement of SGT1 for resistance signaling by NLRs can be delimited to single sites on the protein. Further study could distinguish the regions by which pathogen effectors and host proteins interact with SGT1, facilitating precise editing of effector incompatible variants.     

A variable cytoplasmic domain segment is necessary for γ-protocadherin trafficking and tubulation in the endosome/lysosome pathway

Clustered protocadherins (Pcdhs) are arranged in gene clusters (α, β, and γ) with variable and constant exons. Variable exons encode cadherin and transmembrane domains and ~90 cytoplasmic residues. The 14 Pcdh-αs and 22 Pcdh-γs are spliced to constant exons, which, for Pcdh-γs, encode ~120 residues of an identical cytoplasmic moiety. Pcdh-γs participate in cell-cell interactions but are prominently intracellular in vivo, and mice with disrupted Pcdh-γ genes exhibit increased neuronal cell death, suggesting nonconventional roles. Most attention in terms of Pcdh-γ intracellular interactions has focused on the constant domain. We show that the variable cytoplasmic domain (VCD) is required for trafficking and organelle tubulation in the endolysosome system. Deletion of the constant cytoplasmic domain preserved the late endosomal/lysosomal trafficking and organelle tubulation observed for the intact molecule, whereas deletion or excision of the VCD or replacement of the Pcdh-γA3 cytoplasmic domain with that from Pcdh-α1 or N-cadherin dramatically altered trafficking. Truncations or internal deletions within the VCD defined a 26-amino acid segment required for trafficking and tubulation in the endolysosomal pathway. This active VCD segment contains residues that are conserved in Pcdh-γA and Pcdh-γB subfamilies. Thus the VCDs of Pcdh-γs mediate interactions critical for Pcdh-γ trafficking.     

Approaches for Addressing Life Cycle Assessment Data Gaps for Bio‐based Products

There is an increasing need for life cycle data for bio‐based products, which becomes particularly evident with the recent drive for greenhouse gas reporting and carbon footprinting studies. Meeting this need is challenging given that many bio‐products have not yet been studied by life cycle assessment (LCA), and those that have are specific and limited to certain geographic regions. In an attempt to bridge data gaps for bio‐based products, LCA practitioners can use either proxy data sets (e.g., use existing environmental data for apples to represent pears) or extrapolated data (e.g., derive new data for pears by modifying data for apples considering pear‐specific production characteristics). This article explores the challenges and consequences of using these two approaches. Several case studies are used to illustrate the trade‐offs between uncertainty and the ease of application, with carbon footprinting as an example. As shown, the use of proxy data sets is the quickest and easiest solution for bridging data gaps but also has the highest uncertainty. In contrast, data extrapolation methods may require extensive expert knowledge and are thus harder to use but give more robust results in bridging data gaps. They can also provide a sound basis for understanding variability in bio‐based product data. If resources (time, budget, and expertise) are limited, the use of averaged proxy data may be an acceptable compromise for initial or screening assessments. Overall, the article highlights the need for further research on the development and validation of different approaches to bridging data gaps for bio‐based products.     

Genetic interactions with mutations affecting septin assembly reveal ESCRT functions in budding yeast cytokinesis

Membrane trafficking via targeted exocytosis to the Saccharomyces cerevisiae bud neck provides new membrane and membrane-associated factors that are critical for cytokinesis. It remains unknown whether yeast plasma membrane abscission, the final step of cytokinesis, occurs spontaneously following extensive vesicle fusion, as in plant cells, or requires dedicated membrane fission machinery, as in cultured mammalian cells. Components of the endosomal sorting complexes required for transport (ESCRT) pathway, or close relatives thereof, appear to participate in cytokinetic abscission in various cell types, but roles in cell division had not been documented in budding yeast, where ESCRTs were first characterized. By contrast, the septin family of filament-forming cytoskeletal proteins were first identified by their requirement for yeast cell division. We show here that mutations in ESCRT-encoding genes exacerbate the cytokinesis defects of cla4Δ or elm1Δ mutants, in which septin assembly is perturbed at an early stage in cell division, and alleviate phenotypes of cells carrying temperature-sensitive alleles of a septin-encoding gene, CDC10. Elevated chitin synthase II (Chs2) levels coupled with aberrant morphogenesis and chitin deposition in elm1Δ cells carrying ESCRT mutations suggest that ESCRTs normally enhance the efficiency of cell division by promoting timely endocytic turnover of key cytokinetic enzymes.