Classifying shoulder implants in X-ray images using deep learning.

Total Shoulder Arthroplasty (TSA) is a type of surgery in which the damaged ball of the shoulder is replaced with a prosthesis. Many years later, this prosthesis may be in need of servicing or replacement. In some situations, such as when the patient has changed his country of residence, the model and the manufacturer of the prosthesis may be unknown to the patient and primary doctor. Correct identification of the implant's model prior to surgery is required for selecting the correct equipment and procedure. We present a novel way to automatically classify shoulder implants in X-ray images. We employ deep learning models and compare their performance to alternative classifiers, such as random forests and gradient boosting. We find that deep convolutional neural networks outperform other classifiers significantly if and only if out-of-domain data such as ImageNet is used to pre-train the models. In a data set containing X-ray images of shoulder implants from 4 manufacturers and 16 different models, deep learning is able to identify the correct manufacturer with an accuracy of approximately 80% in 10-fold cross validation, while other classifiers achieve an accuracy of 56% or less. We believe that this approach will be a useful tool in clinical practice, and is likely applicable to other kinds of prostheses.

Complement C3 Is Activated in Human AD Brain and Is Required for Neurodegeneration in Mouse Models of Amyloidosis and Tauopathy.

Complement pathway overactivation can lead to neuronal damage in various neurological diseases. Although Alzheimer's disease (AD) is characterized by ß-amyloid plaques and tau tangles, previous work examining complement has largely focused on amyloidosis models. We find that glial cells show increased expression of classical complement components and the central component C3 in mouse models of amyloidosis (PS2APP) and more extensively tauopathy (TauP301S). Blocking complement function by deleting C3 rescues plaque-associated synapse loss in PS2APP mice and ameliorates neuron loss and brain atrophy in TauP301S mice, improving neurophysiological and behavioral measurements. In addition, C3 protein is elevated in AD patient brains, including at synapses, and levels and processing of C3 are increased in AD patient CSF and correlate with tau. These results demonstrate that complement activation contributes to neurodegeneration caused by tau pathology and suggest that blocking C3 function might be protective in AD and other tauopathies.