An association of various blood types and the 2019 novel coronavirus disease (COVID-19) has been found in a number of publications. The aim of this literature review is to summarize key findings related to ABO blood types and COVID-19 infection rate, symptom presentation, and outcome. Summarized findings include associations between ABO blood type and higher infection susceptibility, intubation duration, and severe outcomes, including death. The literature suggests that blood type O may serve as a protective factor, as individuals with blood type O are found COVID-19 positive at far lower rates. This could suggest that blood type O individuals are less susceptible to infection, or that they are asymptomatic at higher rates and therefore do not seek out testing. We also discuss genetic associations and potential molecular mechanisms that drive the relationship between blood type and COVID-19. Studies have found a strong association between a locus on a specific gene cluster on chromosome three (chr3p21.31) and outcome severity, such as respiratory failure. Cellular models have suggested an explanation for blood type modulation of infection, evidencing that spike protein/Angiotensin-converting enzyme 2 (ACE2)-dependent adhesion to ACE2-expressing cell lines was specifically inhibited by monoclonal or natural human anti-A antibodies, so individuals with non-A blood types, specifically O, or B blood types, which produce anti-A antibodies, may be less susceptible to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection due to the inhibitory effects of anti-A antibodies.
Epilepsy is among the most common serious disabling disorders of the brain, and the global burden of epilepsy exerts a tremendous cost to society. Most people with epilepsy have acquired forms of the disorder, and the development of antiepileptogenic interventions could potentially prevent or cure epilepsy in many of them. However, the discovery of potential antiepileptogenic treatments and clinical validation would require a means to identify populations of patients at very high risk for epilepsy after a potential epileptogenic insult, to know when to treat and to document prevention or cure. A fundamental challenge in discovering biomarkers of epileptogenesis is that this process is likely multifactorial and crosses multiple modalities. Investigators must have access to a large number of high quality, well-curated data points and study subjects for biomarker signals to be detectable above the noise inherent in complex phenomena, such as epileptogenesis, traumatic brain injury (TBI), and conditions of data collection. Additionally, data generating and collecting sites are spread worldwide among different laboratories, clinical sites, heterogeneous data types, formats, and across multi-center preclinical trials. Before the data can even be analyzed, these data must be standardized. The Epilepsy Bioinformatics Study for Antiepileptogenic Therapy (EpiBioS4Rx) is a multi-center project with the overarching goal that epileptogenesis after TBI can be prevented with specific treatments. The identification of relevant biomarkers and performance of rigorous preclinical trials will permit the future design and performance of economically feasible full-scale clinical trials of antiepileptogenic therapies. We have been analyzing human data collected from UCLA and rat data collected from the University of Eastern Finland, both centers collecting data for EpiBioS4Rx, to identify biomarkers of epileptogenesis. Big data techniques and rigorous analysis are brought to longitudinal data collected from humans and an animal model of TBI, epilepsy, and their interaction. The prolonged continuous data streams of intracranial, cortical surface, and scalp EEG from humans and an animal model of epilepsy span months. By applying our innovative mathematical tools via supervised and unsupervised learning methods, we are able to subject a robust dataset to recently pioneered data analysis tools and visualize multivariable interactions with novel graphical methods.
With COVID-19 cases rising rapidly, deep learning has emerged as a promising diagnosis technique. However, identifying the most accurate models to characterize COVID-19 patients is challenging because comparing results obtained with different types of data and acquisition processes is non-trivial. In this paper we designed, evaluated, and compared the performance of 20 convolutional neutral networks in classifying patients as COVID-19 positive, healthy, or suffering from other pulmonary lung infections based on Chest CT scans, serving as the first to consider the EfficientNet family for COVID-19 diagnosis and employ intermediate activation maps for visualizing model performance. All models are trained and evaluated in Python using 4173 Chest CT images from the dataset entitled “A COVID multiclass dataset of CT scans,” with 2168, 758, and 1247 images of patients that are COVID-19 positive, healthy, or suffering from other pulmonary infections, respectively. EfficientNet-B5 was identified as the best model with an F1 score of 0.9769±0.0046, accuracy of 0.9759±0.0048, sensitivity of 0.9788±0.0055, specificity of 0.9730±0.0057, and precision of 0.9751± 0.0051. On an alternate 2-class dataset, EfficientNetB5 obtained an accuracy of 0.9845±0.0109, F1 score of 0.9599±0.0251, sensitivity of 0.9682±0.0099, specificity of 0.9883±0.0150, and precision of 0.9526 ± 0.0523. Intermediate activation maps and Gradient-weighted Class Activation Mappings offered human-interpretable evidence of the model’s perception of ground-class opacities and consolidations, hinting towards a promising use-case of artificial intelligence-assisted radiology tools. With a prediction speed of under 0.1 seconds on GPUs and 0.5 seconds on CPUs, our proposed model offers a rapid, scalable, and accurate diagnostic for COVID-19.
BackgroundTraumatic brain injury (TBI) causes early seizures and is the leading cause of post-traumatic epilepsy. We prospectively assessed structural imaging biomarkers differentiating patients who develop seizures secondary to TBI from patients who do not.DesignMulticentre prospective cohort study starting in 2018. Imaging data are acquired around day 14 post-injury, detection of seizure events occurred early (within 1 week) and late (up to 90 days post-TBI).ResultsFrom a sample of 96 patients surviving moderate-to-severe TBI, we performed shape analysis of local volume deficits in subcortical areas (analysable sample: 57 patients; 35 no seizure, 14 early, 8 late) and cortical ribbon thinning (analysable sample: 46 patients; 29 no seizure, 10 early, 7 late). Right hippocampal volume deficit and inferior temporal cortex thinning demonstrated a significant effect across groups. Additionally, the degree of left frontal and temporal pole thinning, and clinical score at the time of the MRI, could differentiate patients experiencing early seizures from patients not experiencing them with 89% accuracy.Conclusions and relevanceAlthough this is an initial report, these data show that specific areas of localised volume deficit, as visible on routine imaging data, are associated with the emergence of seizures after TBI.
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