![]() ![]() ![]() UC is therefore formed as a result of different etiologies, which influence the course and severity of subsequent illness. Solberg et al., 2009 reported that half of the patients may not respond to pharmacological treatment, resulting in a more complicated disease course. Only 30% and 15% of patients have aggressive or generalized colitis, respectively. ![]() Most patients with UC suffer from hemorrhagic diarrhea, and the clinical presentation is heterogeneous. Due to the phenotypic similarity of UC across the globe, environmental changes may also be responsible for the observed epidemiological trends. As IBD incidence increases in developing countries and phenotypes are similar between Asians and Westerners, ethnicity appears not to be an important factor in UC. Abraham and Kane., 2012 demonstrated in spite of having the same phenotype, extreme early-onset IBD may have a different pathophysiology from IBD of earlier onset. Healthcare and social costs are significant as a result of the excessive morbidity and mortality rate caused by UC. Conley et al., 2017 demonstrated by 2025, the population is expected to reach 30 million worldwide. Globally, the prevalence is high in developed countries, and is rapidly increasing in newly industrialized countries. Ī number of factors have been linked to this condition, including dysregulated immune response, altered microflora in the gut, genetic susceptibility, and environmental factors. 2015found that the ratio of neutrophils to lymphocytes could predict whether ulcerative colitis was in the active phase. In addition, diagnosis of digestive system diseases and evaluation of the prognosis of patients through inflammatory indicators and infiltration levels of immune cells. Prolonged inflammation will damage gastrointestinal function, such as causing abdominal pain, bleeding and other symptoms. It is a chronic immuno-mediated IBD, though its exact pathogenesis is not known. Ulcerative colitis (UC) was first discovered in 1859, and it is one of two main types of inflammatory bowel disease (IBD). To estimate the likelihood that each subtype of cuproptosis will occur in ulcerative colitis patients and their disease outcome, we developed a promising prediction model. We examined the complex relationship between cuproptosis and ulcerative colitis in a systematic manner. The nomogram and the calibration curve and decision curve analyses showed that the subtypes of ulcerative colitis had sufficient accuracy. There was a clear correlation between the differentially expressed genes in cluster 2 and the response of immune cells. The immune scores for Cluster2 were elevated. Both the residual error and root mean square error of the random forest machine model had clinical significance. Immune infiltration analysis indicated that different clusters exhibited significant heterogeneity. Two cuproptosis-associated molecular clusters were identified. Significant cuproptosis-related genes and immune response cells were detected between the ulcerative colitis and control groups. To assess the accuracy of the learning predictions, the nomogram and the calibration curve and decision curve analyses showed that the subtypes of ulcerative colitis have been accurately predicted. We identified the differentially expressed genes according to the clustering method, and the performance of the SVM model, the random forest model, the generalized linear model, and the limit gradient enhancement model were compared, and then the optimal machine model was selected. We examined clusters of cuproptosis related genes and immune cell infiltration molecules in 86 ulcerative colitis samples from the GSE179285 dataset. Ulcerative colitis is one of the two main forms of inflammatory bowel disease. Cuproptosis is reported to be a novel mode of cell death. ![]()
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