Three-dimensional virtual-reality surgical planning and soft-tissue prediction for orthognathic surgery

Complex maxillofacial malformations continue to present challenges in analysis and correction beyond modern technology. The purpose of this paper is to present a virtual-reality workbench for surgeons to perform virtual orthognathic surgical planning and soft-tissue prediction in three dimensions. A resulting surgical planning system, i.e., three-dimensional virtual-reality surgical-planning and soft-tissue prediction for orthognathic surgery, consists of four major stages: computed tomography (CT) data post-processing and reconstruction, three-dimensional (3-D) color facial soft-tissue model generation, virtual surgical planning and simulation, soft-tissue-change preoperative prediction. The surgical planning and simulation are based on a 3-D CT reconstructed bone model, whereas the soft-tissue prediction is based on color texture-mapped and individualized facial soft-tissue model. Our approach is able to provide a quantitative osteotomy-simulated bone model and prediction of postoperative appearance with photorealistic quality. The prediction appearance can be visualized from any arbitrary viewing point using a low-cost personal-computer-based system. This cost-effective solution can be easily adopted in any hospital for daily use.published_or_final_versio

Altered brain energetics induces mitochondrial fission arrest in Alzheimer's Disease.

Altered brain metabolism is associated with progression of Alzheimer's Disease (AD). Mitochondria respond to bioenergetic changes by continuous fission and fusion. To account for three dimensional architecture of the brain tissue and organelles, we applied 3-dimensional electron microscopy (3D EM) reconstruction to visualize mitochondrial structure in the brain tissue from patients and mouse models of AD. We identified a previously unknown mitochondrial fission arrest phenotype that results in elongated interconnected organelles, "mitochondria-on-a-string" (MOAS). Our data suggest that MOAS formation may occur at the final stages of fission process and was not associated with altered translocation of activated dynamin related protein 1 (Drp1) to mitochondria but with reduced GTPase activity. Since MOAS formation was also observed in the brain tissue of wild-type mice in response to hypoxia or during chronological aging, fission arrest may represent fundamental compensatory adaptation to bioenergetic stress providing protection against mitophagy that may preserve residual mitochondrial function. The discovery of novel mitochondrial phenotype that occurs in the brain tissue in response to energetic stress accurately detected only using 3D EM reconstruction argues for a major role of mitochondrial dynamics in regulating neuronal survival

Federated Cross Learning for Medical Image Segmentation

Federated learning (FL) can collaboratively train deep learning models using isolated patient data owned by different hospitals for various clinical applications, including medical image segmentation. However, a major problem of FL is its performance degradation when dealing with the data that are not independently and identically distributed (non-iid), which is often the case in medical images. In this paper, we first conduct a theoretical analysis on the FL algorithm to reveal the problem of model aggregation during training on non-iid data. With the insights gained through the analysis, we propose a simple and yet effective method, federated cross learning (FedCross), to tackle this challenging problem. Unlike the conventional FL methods that combine multiple individually trained local models on a server node, our FedCross sequentially trains the global model across different clients in a round-robin manner, and thus the entire training procedure does not involve any model aggregation steps. To further improve its performance to be comparable with the centralized learning method, we combine the FedCross with an ensemble learning mechanism to compose a federated cross ensemble learning (FedCrossEns) method. Finally, we conduct extensive experiments using a set of public datasets. The experimental results show that the proposed FedCross training strategy outperforms the mainstream FL methods on non-iid data. In addition to improving the segmentation performance, our FedCrossEns can further provide a quantitative estimation of the model uncertainty, demonstrating the effectiveness and clinical significance of our designs. Source code will be made publicly available after paper publication.Comment: 10 pages, 4 figure

Soft-tissue Driven Craniomaxillofacial Surgical Planning

In CMF surgery, the planning of bony movement to achieve a desired facial outcome is a challenging task. Current bone driven approaches focus on normalizing the bone with the expectation that the facial appearance will be corrected accordingly. However, due to the complex non-linear relationship between bony structure and facial soft-tissue, such bone-driven methods are insufficient to correct facial deformities. Despite efforts to simulate facial changes resulting from bony movement, surgical planning still relies on iterative revisions and educated guesses. To address these issues, we propose a soft-tissue driven framework that can automatically create and verify surgical plans. Our framework consists of a bony planner network that estimates the bony movements required to achieve the desired facial outcome and a facial simulator network that can simulate the possible facial changes resulting from the estimated bony movement plans. By combining these two models, we can verify and determine the final bony movement required for planning. The proposed framework was evaluated using a clinical dataset, and our experimental results demonstrate that the soft-tissue driven approach greatly improves the accuracy and efficacy of surgical planning when compared to the conventional bone-driven approach.Comment: Early accepted by MICCAI 202

Partial inhibition of mitochondrial complex I ameliorates Alzheimer\u27s disease pathology and cognition in APP/PS1 female mice.

Alzheimer\u27s Disease (AD) is a devastating neurodegenerative disorder without a cure. Here we show that mitochondrial respiratory chain complex I is an important small molecule druggable target in AD. Partial inhibition of complex I triggers the AMP-activated protein kinase-dependent signaling network leading to neuroprotection in symptomatic APP/PS1 female mice, a translational model of AD. Treatment of symptomatic APP/PS1 mice with complex I inhibitor improved energy homeostasis, synaptic activity, long-term potentiation, dendritic spine maturation, cognitive function and proteostasis, and reduced oxidative stress and inflammation in brain and periphery, ultimately blocking the ongoing neurodegeneration. Therapeutic efficacy in vivo was monitored using translational biomarkers FDG-PET, 31P NMR, and metabolomics. Cross-validation of the mouse and the human transcriptomic data from the NIH Accelerating Medicines Partnership-AD database demonstrated that pathways improved by the treatment in APP/PS1 mice, including the immune system response and neurotransmission, represent mechanisms essential for therapeutic efficacy in AD patients

Histopathology of Growth Anomaly Affecting the Coral, Montipora capitata: Implications on Biological Functions and Population Viability

Growth anomalies (GAs) affect the coral, Montipora capitata, at Wai'ōpae, southeast Hawai'i Island. Our histopathological analysis of this disease revealed that the GA tissue undergoes changes which compromise anatomical machinery for biological functions such as defense, feeding, digestion, and reproduction. GA tissue exhibited significant reductions in density of ova (66.1–93.7%), symbiotic dinoflagellates (38.8–67.5%), mesenterial filaments (11.2–29.0%), and nematocytes (28.8–46.0%). Hyperplasia of the basal body wall but no abnormal levels of necrosis and algal or fungal invasion was found in GA tissue. Skeletal density along the basal body wall was significantly reduced in GAs compared to healthy or unaffected sections. The reductions in density of the above histological features in GA tissue were collated with disease severity data to quantify the impact of this disease at the colony and population level. Resulting calculations showed this disease reduces the fecundity of M. capitata colonies at Wai'ōpae by 0.7–49.6%, depending on GA severity, and the overall population fecundity by 2.41±0.29%. In sum, GA in this M. capitata population reduces the coral's critical biological functions and increases susceptibility to erosion, clearly defining itself as a disease and an ecological threat

How Plastic Can Phenotypic Plasticity Be? The Branching Coral Stylophora pistillata as a Model System

Phenotypic plasticity enables multicellular organisms to adjust morphologies and various life history traits to variable environmental challenges. Here, we elucidate fixed and plastic architectural rules for colony astogeny in multiple types of colonial ramets, propagated by cutting from genets of the branching coral Stylophora pistillata from Eilat, the Red Sea. We examined 16 morphometric parameters on 136 one-year old S. pistillata colonies (of seven genotypes), originating from small fragments belonging, each, to one of three single-branch types (single tips, start-up, and advanced bifurcating tips) or to structural preparative manipulations (representing a single or two growth axes). Experiments were guided by the rationale that in colonial forms, complexity of evolving phenotypic plasticity can be associated with a degree of structural modularity, where shapes are approached by erecting iterative growth patterns at different levels of coral-colony organization. Analyses revealed plastic morphometric characters at branch level, and predetermined morphometric traits at colony level (only single trait exhibited plasticity under extreme manipulation state). Therefore, under the experimental manipulations of this study, phenotypic plasticity in S. pistillata appears to be related to branch level of organization, whereas colony traits are controlled by predetermined genetic architectural rules. Each level of organization undergoes its own mode of astogeny. However, depending on the original ramet structure, the spherical 3-D colonial architecture in this species is orchestrated and assembled by both developmental trajectories at the branch level, and traits at the colony level of organization. In nature, branching colonial forms are often subjected to harsh environmental conditions that cause fragmentation of colony into ramets of different sizes and structures. Developmental traits that are plastic, responding to fragment structure and are not predetermine in controlling astogeny, allow formation of species-specific architecture product through integrated but variable developmental routes. This adaptive plasticity or regeneration is an efficient mechanism by which isolated fragments of branching coral species cope with external environmental forces