Artificial Intelligence for Identification of Images with Active Bleeding in Mesenteric and Celiac Arteries Angiography.

PURPOSE: The purpose of this study is to evaluate the efficacy of an artificial intelligence (AI) model designed to identify active bleeding in digital subtraction angiography images for upper gastrointestinal bleeding. METHODS: Angiographic images were retrospectively collected from mesenteric and celiac artery embolization procedures performed between 2018 and 2022. This dataset included images showing both active bleeding and non-bleeding phases from the same patients. The images were labeled as normal versus images that contain active bleeding. A convolutional neural network was trained and validated to automatically classify the images. Algorithm performance was tested in terms of area under the curve, accuracy, sensitivity, specificity, F1 score, positive and negative predictive value. RESULTS: The dataset included 587 pre-labeled images from 142 patients. Of these, 302 were labeled as normal angiogram and 285 as containing active bleeding. The model's performance on the validation cohort was area under the curve 85.0 ± 10.9% (standard deviation) and average classification accuracy 77.43 ± 4.9%. For Youden's index cutoff, sensitivity and specificity were 85.4 ± 9.4% and 81.2 ± 8.6%, respectively. CONCLUSION: In this study, we explored the application of AI in mesenteric and celiac artery angiography for detecting active bleeding. The results of this study show the potential of an AI-based algorithm to accurately classify images with active bleeding. Further studies using a larger dataset are needed to improve accuracy and allow segmentation of the bleeding.

Concurrence of High Fat Diet and APOE Gene Induces Allele Specific Metabolic and Mental Stress Changes in a Mouse Model of Alzheimer's Disease.

Aging is the main risk factor for neurodegenerative diseases, including Alzheimer's disease (AD). However, evidence indicates that the pathological process begins long before actual cognitive or pathological symptoms are apparent. The long asymptomatic phase and complex integration between genetic, environmental and metabolic factors make it one of the most challenging diseases to understand and cure. In the present study, we asked whether an environmental factor such as high-fat (HF) diet would synergize with a genetic factor to affect the metabolic and cognitive state in the Apolipoprotein E (ApoE4) mouse model of AD. Our data suggest that a HF diet induces diabetes mellitus (DM)-like metabolism in ApoE4 mice, as well as changes in ß-site amyloid precursor protein-cleaving enzyme 1 (BACE1) protein levels between the two ApoE strains. Furthermore, HF diet induces anxiety in this AD mouse model. Our results suggest that young ApoE4 carriers are prone to psychological stress and metabolic abnormalities related to AD, which can easily be triggered via HF nutrition.

PKR Inhibition Rescues Memory Deficit and ATF4 Overexpression in ApoE ε4 Human Replacement Mice.

Sporadic Alzheimer's disease (AD) is an incurable neurodegenerative disease with clear pathological hallmarks, brain dysfunction, and unknown etiology. Here, we tested the hypothesis that there is a link between genetic risk factors for AD, cellular metabolic stress, and transcription/translation regulation. In addition, we aimed at reversing the memory impairment observed in a mouse model of sporadic AD. We have previously demonstrated that the most prevalent genetic risk factor for AD, the ApoE4 allele, is correlated with increased phosphorylation of the translation factor eIF2α. In the present study, we tested the possible involvement of additional members of the eIF2α pathway and identified increased mRNA expression of negative transcription factor ATF4 (aka CREB2) both in human and a mouse model expressing the human ApoE4 allele. Furthermore, injection of a PKR inhibitor rescued memory impairment and attenuated ATF4 mRNA increased expression in the ApoE4 mice. The results propose a new mechanism by which ApoE4 affects brain function and further suggest that inhibition of PKR is a way to restore ATF4 overexpression and memory impairment in early stages of sporadic AD. Significance statement: ATF4 mRNA relative quantities are elevated in ApoE4 allele carriers compared with noncarrier controls. This is true also for the ApoE ε4 human replacement mice. ApoE4 mice injected with PKR inhibitor (PKRi) demonstrate a significant reduction in ATF4 expression levels 3 h after one injection of PKRi. Treatment of ApoE4 human replacement mice with the PKRi before learning rescues the memory impairment of the ApoE4 AD model mice. We think that these results propose a new mechanism by which ApoE4 affects brain function and suggest that inhibition of PKR is a way to restore memory impairment in early stages of sporadic AD.