backgroundIn general, academic but not community endoscopists have demonstrated adequate endoscopic differentiation accuracy to make the 'resect and discard' paradigm for diminutive colorectal polyps workable. Computer analysis of video could potentially eliminate the obstacle of interobserver variability in endoscopic polyp interpretation and enable widespread acceptance of 'resect and discard'. study design and methods We developed an artificial intelligence (AI) model for real-time assessment of endoscopic video images of colorectal polyps. A deep convolutional neural network model was used. Only narrow band imaging video frames were used, split equally between relevant multiclasses. Unaltered videos from routine exams not specifically designed or adapted for AI classification were used to train and validate the model. The model was tested on a separate series of 125 videos of consecutively encountered diminutive polyps that were proven to be adenomas or hyperplastic polyps. results The AI model works with a confidence mechanism and did not generate sufficient confidence to predict the histology of 19 polyps in the test set, representing 15% of the polyps. For the remaining 106 diminutive polyps, the accuracy of the model was 94% (95% CI 86% to 97%), the sensitivity for identification of adenomas was 98% (95% CI 92% to 100%), specificity was 83% (95% CI 67% to 93%), negative predictive value 97% and positive predictive value 90%. conclusions An AI model trained on endoscopic video can differentiate diminutive adenomas from hyperplastic polyps with high accuracy. Additional study of this programme in a live patient clinical trial setting to address resect and discard is planned. IntroductIonEndoscopists combine their knowledge of the spectrum of endoscopic appearances of precancerous lesions with meticulous mechanical exploration and cleaning of mucosal surfaces to maximise lesion detection during colonoscopy. An extension of detection is endoscopic prediction of lesion histology, including differentiation of precancerous lesions from non-neoplastic lesions, and prediction of deep submucosal invasion of cancer.1 2 Image analysis can guide whether lesion removal is necessary and direct an endoscopist to the best resection method. 1-3Image analysis during colonoscopy has achieved increasing acceptance as a means to accurately predict the histology of diminutive lesions, 4 5 which have minimal risk of cancer, 6 so that these diminutive lesions could be resected and discarded without pathological assessment or left in place without resection in the case of diminutive distal colon hyperplastic polyps.3 Discarding most diminutive lesions without pathological assessment has the potential for large cost saving with minimal risk.
Numerous studies have implicated bacteria in cardiovascular disease, but there is a paucity of information on the mechanism involved. In this study we show how the common oral bacterium Streptococcus sanguis can directly interact with platelets, resulting in activation and aggregate formation. Platelet aggregation was dependent on glycoprotein IIb/IIIa (GPIIb/ IIIa) and thromboxane. Platelets could also directly bind to S sanguis, but this interaction was not inhibited by GPIIb/IIIa antagonists. Antibodies to GPIb could inhibit both platelet aggregation and platelet adhesion to bacteria. This suggested a direct interaction between GPIb and S sanguis; however, this interaction did not require von Willebrand factor, the normal ligand for GPIb. By use of a range of monoclonal antibodies to GPIb and the enzyme mocharagin, which cleaves GPIb at amino acid 282, the interaction was localized to a region within the N-terminal 1-225 portion of GPIb␣. Furthermore S sanguis failed to induce aggregation of platelets from a patient with BernardSoulier disease, the organism bound to Chinese hamster ovary cells transfected with the GPIb␣ gene but did not bind to mock-transfected cells and biotin-labeled S sanguis cells bound to purified GPIb in ligand blots. It is suggested that the interaction between S sanguis and GPIb is important in the pathogenesis of infective endocarditis and may also play a contributory role in some cases of myocardial infarction. ( IntroductionRecent reports suggest a role for infectious agents in cardiovascular disease. Much of this work is in the form of clinical evidence of infection [1][2][3][4][5][6] or the effect of antibiotics on the incidence of cardiovascular disease. 7,8 Although studies have found evidence of bacteria in atherosclerotic plaques, 1,2,4,5,9-13 their role in the etiology of cardiovascular disease is uncertain. In contrast, the role of bacteria in infective endocarditis is well established and the molecular mechanisms involved may also occur in other forms of cardiovascular disease.Infective endocarditis involves inflammation of the heart valves due to infection and if untreated can lead to valve failure and death. In most cases there is one or more predisposing factors, which results in damage to the endothelium on or adjacent to the valves. This area of damage becomes covered with a platelet-fibrin vegetation and these can become colonized by bacteria that gain access to the blood. The 2 species most commonly involved are Streptococcus sanguis 14 and Staphylococcus aureus. 15 Historically oral streptococci have been referred to as Streptococcus viridans, but this name was never accepted as a recognized taxon because of the biochemical and serologic heterogeneity among isolates. Subsequent detailed biochemical and genetic studies allowed the definition of at least 17 taxa within what was originally called S viridans. However, the term viridans has survived but is now used as viridans group of streptococci to recognize the existence of various taxa and S sanguis is one taxon w...
Background and Purpose-Aspirin resistance may be relatively common and associated with adverse outcome.Meta-analysis has clearly shown that 75 mg plain aspirin is the lowest effective dose; however, it is not known whether the recent increased use of enteric-coated aspirin could account for aspirin resistance. This study was designed to determine whether enteric-coated aspirin is as effective as plain aspirin in healthy volunteers. Methods-Seventy-one healthy volunteers were enrolled in 3 separate bioequivalence studies. Using a crossover design, each volunteer took 2 different aspirin preparations. Five aspirin preparations were evaluated, 3 different enteric-coated 75-mg aspirins, dispersible aspirin 75 mg and asasantin (25-mg standard release aspirin plus 200-mg modified-release dipyridamole given twice daily). Serum thromboxane (TX) B 2 levels and arachidonic acid-induced platelet aggregation were measured before and after 14 days of treatment. Results-All other aspirin preparations tested were inferior to dispersible aspirin (PϽ0.001) in their effect on serum TXB 2 level. Treatment failure (Ͻ95% inhibition serum TXB 2 formation) occurred in 14 subjects, none of whom were taking dispersible aspirin. Mean weight for those demonstrating treatment failure was greater than those with complete TXB 2 (Ͼ99%) inhibition (PϽ0.001). Using logistic regression analysis an 80-kg subject had a 20% probability of treatment failure. Asasantin was the most potent preparation in terms of inhibition of platelet aggregation. Conclusions-Equivalent doses of the enteric-coated aspirin were not as effective as plain aspirin. Lower bioavailability of these preparations and poor absorption from the higher pH environment of the small intestine may result in inadequate platelet inhibition, particularly in heavier subjects. (Stroke. 2006;37:2153-2158.)
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