Applying Supervised Learning Algorithms and a New Feature Selection Method to Predict Coronary Artery Disease

Multidate imagery and satellite image derivatives such as vegetation and texture indices have been reported to improve image classification. However, the increase in additional predictor variables has also resulted in high data dimensionality and redundancy. Feature selection and extraction can be used to reduce high data dimensionality and minimize redundancy. The purpose of this chapter is to test whether feature selection can improve image classification. In this chapter, image classification will be performed using two different approaches. First, image classification is performed using the random forests (RF) classifier and multiple data sets (that consist of multidate Landsat 5 TM imagery, and vegetation and texture indices). Second, image classification is performed using the RF classifier with feature selection and multiple data sets. While the tutorial exercises indicate that feature selection did not improve image classification accuracy, it reduced the number of predictor variables.

Dry eye syndrome is one of the most frequently reported eye diseases in ophthalmological practice. The diagnosis of this disease is a challenging task due to its multifactorial etiology. One of the most applied tests is the manual classification of tear film images captured with the Doane interferometer. The interference phenomena in these images can be characterized as texture patterns, which can be automatically classified into one of the following categories: strong fringes, coalescing strong fringes, fine fringes, coalescing fine fringes, and debris. This work presents a method for classifying tear film images based on texture analysis using phylogenetic diversity indexes and Ripley's K function. The proposed method consists of six main steps: acquisition of the image dataset; segmentation of the region of interest; feature extraction using phylogenetic diversity indexes and Ripley's K function; feature selection using Greedy Stepwise; classification using the algorithms Support Vector Machine (SVM), Random Forest (RF), Naive Bayes (NB), Multilayer Perceptron (MLP), Random Tree (RT) and Radial Basis Function Network (RBFNet); and (6) validation of results. The best result, using the RF classifier, we obtained classification rates higher than 99% of accuracy with 0.843% of standard deviation, 0.999 of the area under the Receiver Operating Characteristics (ROC) curve, 0.995 of Kappa and 0.996 of F-Measure. The experimental results demonstrate that the proposed method is promising and can potentially be used by experts to accurately diagnose dry eye syndrome in tear film images.

Sentiment analysis adalah metode untuk memperoleh data dari berbagai platform yang tersedia di internet. Kemajuan teknologi memungkinkan mesin untuk mengenali suatu istilah yang dianggap sebagai opini positif maupun sebaliknya. Data-data dan opini tersebut berperan penting sebagai umpan balik produk, layanan, dan topik lainnya. Tanpa perlu memperoleh opini secara langsung dari masyarakat, pihak penyedia telah mendapatkan evaluasi yang penting guna mengembangkan diri. Bisnis perhotelan merupakan bidang yang terkait dengan jasa memberikan layanan pada pelanggan. Indikator keberlangsungan bisnis ini juga bergantung pada umpan balik pelanggannya dan dijadikan sebagai acuan untuk pengambilan kebijakan strategis. Teknik sentiment analysis berbasis Natural Language Processing dapat mengatasi permasalahan tersebut. Pada makalah ini prediksi dilakukan menggunakan classifier Random Forest (RF), sementara untuk merangkum kualitas classifier, digunakan kurva Receiver Operating Characteristic (ROC). Kurva ROC berupa grafik yang baik untuk merangkum kualitas classifier. Semakin tinggi kurva berada di atas garis diagonal, semakin baik prediksinya, dengan nilai kurva ROC yang diperoleh sebesar 0,90. Terlihat hasil ulasan terhadap opini pelanggan terhadap jasa dan pelayanan yang diberikan oleh hotel untuk kategori positif lebih banyak daripada kategori negatif. Polaritas dari ulasan diperoleh 68% ulasan pelanggan berada pada area positif dan 32% berada pada area negatif.

The random forest (RF) classifier, which is a combination of tree predictors, is one of the most powerful classification algorithms that has been recently applied for fault detection and diagnosis (FDD) of industrial processes. However, RF is still suffering from some limitations such as the noncorrelation between variables. These limitations are due to the direct use of variables measured at nodes and therefore the only use of static information from the process data. Thus, this article proposes two enhanced RF classifiers, namely the Euclidean distance based reduced kernel RF (RK-RF <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">ED</sub> ) and K-means clustering based reduced kernel RF (RK-RF <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">Kmeans</sub> ), for FDD. Based on the kernel principal component analysis, the proposed classifiers consist of two main stages: feature extraction and selection, and fault classification. In the first stage, the number of observations in the training data set is reduced using two methods: the first method consists of using the Euclidean distance as dissimilarity metric so that only one measurement is kept in case of redundancy between samples. The second method aims at reducing the amount of the training data based on the K-means clustering technique. Once the characteristics of the process are extracted, the most sensitive features are selected. During the second phase, the selected features are fed to an RF classifier. An emulated grid-connected PV system is used to validate the performance of the proposed RK-RF <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">ED</sub> and RK-RF <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">Kmeans</sub> classifiers. The presented results confirm the high classification accuracy of the developed techniques with low computation time.

Considering the form diversity of tree species composition in the Bagong Mountain National Forest Park of China, we mapped tree species utilizing Machine Learning Algorithms (support vector machines (SVM) and random forest (RF) classifiers) based on the OHS-2 hyperspectral satellite image by different datasets which combined spectral information and hyperspectral-derived vegetation indices (VIs) for improving tree species classification and explored the best performance of them. To verify the improvement, the results of physically-based spectral classifiers (spectral angle mapper (SAM) and maximum likelihood (ML) classifiers) were applied to compare with the results of machine learning algorithms. The results indicated an overall accuracy of 94.01%, 96.08%, 82.9% and 79.3% for SVM, RF, SAM and ML classifiers of the best performance using different datasets. Highest accuracies resulted from two machine learning algorithms classifiers; SVM and RF compared to SAM and ML classifiers. Although SVM outperformed RF when using all hyperspectral bands and VIs, the overall accuracy of the RF classifier is higher when compared to the SVM classifier using VIs combined selected features. Meanwhile, the RF classifier performed better than SVM after removing the redundancy of spectral data in training samples. Moreover, the machine learning algorithms successfully classified a small number of tree species (Cedrus deodara and Pterocarya stenoptera C. DC.) in the study area, but the physical spectroscopy-based method failed to classify these species. Such integration strategy improved the effectiveness of enhancing the accuracy of tree species classification and mapping their distribution on broad spatial and temporal scales using machine learning algorithms and hyperspectral imagery.

Abstract. Random Forest is a supervised learning algorithm developed from decision trees with the application of boostrap aggregating (bagging). This method grows trees from decision trees to produce a forest or the best model called the random forest model. Tree growth is done with randomly selected data with returns through the bagging process. Random forest is considered to provide better performance results for diabetes data among other supervised learning methods, because random forest and has the lowest error rate compared to other methods. Random forest is also an important technique for medical data classification, especially for diagnosing diabetics. In this study, classification was carried out using Pima Indian Diabetes data, which is an American tribe that lives in Arizona and Mexico. Classification analysis was carried out using an algorithm to see the level of accuracy in random forest classification on Pima Indian diabetes data. The results show that the accuracy value of random forest classification is 74.78%, this value is in the accuracy category at the fair classification level. In this random forest classification, there are three main variables that become importance variables, namely glucose then BMI, and age.&#x0D; Abstract. Random Forest is a supervised learning algorithm developed from decision trees with the application of boostrap aggregating (bagging). This method grows trees from decision trees to produce a forest or the best model called the random forest model. Tree growth is done with randomly selected data with returns through the bagging process. Random forest is considered to provide better performance results for diabetes data among other supervised learning methods, because random forest and has the lowest error rate compared to other methods. Random forest is also an important technique for medical data classification, especially for diagnosing diabetics. In this study, classification was carried out using Pima Indian Diabetes data, which is an American tribe that lives in Arizona and Mexico. Classification analysis was carried out using an algorithm to see the level of accuracy in random forest classification on Pima Indian diabetes data. The results show that the accuracy value of random forest classification is 74.78%, this value is in the accuracy category at the fair classification level. In this random forest classification, there are three main variables that become importance variables, namely glucose then BMI, and age.

In this study, the relationship between natural gas (NG) data and gas-related environmental elements was performed using machine learning algorithms to predict the level of gas leakage risk without directly measuring gas leakage data. The study was based on open data provided by the server using the IoT-based remote control Picarro gas sensor specification. The naturel gas leaks into the air, it is a big problem for air pollution, environment and the health. The proposed method is multivariate outlier removing method based Random Forest (RF) classification for predicting risk of NG leak. After, unsupervised k-means clustering, the experimental dataset has done imbalanced data. Therefore, we focusing our proposed models can predict medium and high risk so best. In this case, we compared the receiver operating characteristic (ROC) curve, accuracy, area under the ROC curve (AUC), and mean standard error (MSE) for each classification model. As a result of our experiments, the evaluation measurements include accuracy, area under the ROC curve (AUC), and MSE; 99.71%, 99.57%, and 0.0016 for MOL_RF respectively.

Depression is an extremely serious illness of humans which causes constant mood swings and feelings of sadness. Nowadays, it is considered to be a deadly disorder in the world. At present, everyone from young to old is suffering from depression but most of them do not have the right idea about their mental state. Everyone needs to have a proper idea about their mental state. We will detect depression through a machine learning-based detection approach. Talking with psychologists and depressed people, we find some factors that are related to becoming depressed, and depending on those factors, information is collected from both depressed and non-depressed people. After applying preprocessing techniques, a processed dataset was created finally. Then, feature selection techniques were used. We applied eight machine learning algorithms and two feature selection methods to our dataset. We used k-nearest neighbor (k-NN), decision tree (DT), linear discriminant analysis (LDA), adaptive boosting (AB), support vector machine (SVM), naive Bayes (NB), random forest (RF), and logistic regression (LR) classifier. In our work, the RF classifier gave the best performance based on accuracy and the accuracy of the RF classifier was 96.00%.KeywordsMachine learningFeature selectionRandom forestSelectKBestDetectionDepression

Anastomotic leakage (AL) is one of the commonest and most serious complications after rectal cancer surgery. The previous analyses on predictors for AL included small-scale patients, and their prediction models performed unsatisfactorily. Clinical data of 5,220 patients who underwent anterior resection for rectal cancer were scrutinized to create a prediction model via random forest classifier. Additionally, data of 836 patients served as the test dataset. Patients diagnosed with AL within 6 months' follow-up were recorded. A total of 20 candidate factors were included. Receiver operating characteristic (ROC) curve was conducted to determine the clinical efficacy of our model, and compare the predictive performance of different models. The incidence of AL was 6.2% (326/5,220). A multivariate logistic regression analysis and the random forest classifier indicated that sex, distance of tumor from the anal verge, bowel stenosis or obstruction, preoperative hemoglobin, surgeon volume, diabetes, neoadjuvant chemoradiotherapy, and surgical approach were significantly associated with AL. After propensity score matching, the temporary stoma was not identified as a protective factor for AL (P=0.58). Contrastingly, the first year of performing laparoscopic surgery was a predictor (P=0.009). We created a predictive random forest classifier based on the above predictors that demonstrated satisfactory prediction efficacy. The area under the curve (AUC) showed that the random forest had higher efficiency (AUC =0.87) than the nomogram (AUC =0.724). Our findings suggest that eight factors may affect the incidence of AL. Our random forest classifier is an innovative and practical model to effectively predict AL, and could provide rational advice on whether to perform a temporary stoma, which might reduce the rate of stoma and avoid the ensuing complications.

Co-operative co-evolution approach solves problems by breaking them into subproblems. The proposed framework for Clinical Decision Support System (CDSS) uses a co-operative coevolution approach which treats Feature Selection (FS) and Instance Selection (IS) as independent subproblems. FS and IS remove less relevant features and instances, respectively, thereby improving the overall performance of the system. In this work, both Feature and Instance selection are done using the wrapper approach, which uses co-operative co-evolution and random forest classifier. The reduced dataset is used to train a random forest classifier and this trained model helped in making clinical decisions. These decisions assist physicians as the second opinion for diagnosis and treatment. Wisconsin Diagnostic Breast Cancer (WDBC), Hepatitis, Pima Indian Diabetes (PID), Cleveland Heart Disease (CHD), Statlog Heart Disease (SHD), Vertebral Column, and Hepatocellular Carcinoma (HCC) datasets from the University of California Irvine (UCI) Machine Learning repository are used for experimentation. The proposed framework achieved an accuracy of 97.1%, 82.3%, 81.01%, 93.4%, 96.8%, 91.4%, and 72.2% for datasets WDBC, Hepatitis, PID, CHD, SHD, vertebral column, and HCC, respectively. The results prove that the CDSS-developed using co-operative coevolution can efficiently assist the physicians in decision-making.

Article Figures and data Abstract eLife digest Introduction Results Discussion Materials and methods Data availability References Decision letter Author response Article and author information Metrics Abstract End-stage kidney disease (ESKD) patients are at high risk of severe COVID-19. We measured 436 circulating proteins in serial blood samples from hospitalised and non-hospitalised ESKD patients with COVID-19 (n = 256 samples from 55 patients). Comparison to 51 non-infected patients revealed 221 differentially expressed proteins, with consistent results in a separate subcohort of 46 COVID-19 patients. Two hundred and three proteins were associated with clinical severity, including IL6, markers of monocyte recruitment (e.g. CCL2, CCL7), neutrophil activation (e.g. proteinase-3), and epithelial injury (e.g. KRT19). Machine-learning identified predictors of severity including IL18BP, CTSD, GDF15, and KRT19. Survival analysis with joint models revealed 69 predictors of death. Longitudinal modelling with linear mixed models uncovered 32 proteins displaying different temporal profiles in severe versus non-severe disease, including integrins and adhesion molecules. These data implicate epithelial damage, innate immune activation, and leucocyte–endothelial interactions in the pathology of severe COVID-19 and provide a resource for identifying drug targets. eLife digest COVID-19 varies from a mild illness in some people to fatal disease in others. Patients with severe disease tend to be older and have underlying medical problems. People with kidney failure have a particularly high risk of developing severe or fatal COVID-19. Patients with severe COVID-19 have high levels of inflammation, causing damage to tissues around the body. Many drugs that target inflammation have already been developed for other diseases. Therefore, to repurpose existing drugs or design new treatments, it is important to determine which proteins drive inflammation in COVID-19. Here, Gisby, Clarke, Medjeral-Thomas et al. measured 436 proteins in the blood of patients with kidney failure and compared the levels between patients who had COVID-19 to those who did not. This revealed that patients with COVID-19 had increased levels of hundreds of proteins involved in inflammation and tissue injury. Using a combination of statistical and machine learning analyses, Gisby et al. probed the data for proteins that might predict a more severe disease progression. In total, over 200 proteins were linked to disease severity, and 69 with increased risk of death. Tracking how levels of blood proteins changed over time revealed further differences between mild and severe disease. Comparing this data with a similar study of COVID-19 in people without kidney failure showed many similarities. This suggests that the findings may apply to COVID-19 patients more generally. Identifying the proteins that are a cause of severe COVID-19 – rather than just correlated with it – is an important next step that could help to select new drugs for severe COVID-19. Introduction Coronavirus disease (COVID-19), caused by the SARS-CoV-2 virus, displays wide clinical heterogeneity from asymptomatic to fatal disease. Patients with severe disease exhibit marked inflammatory responses and immunopathology. The mechanisms underlying this remain incompletely characterised, and the key molecular mediators are yet to be determined. The first treatment shown to reduce mortality from COVID-19 in randomised trials was dexamethasone (Horby et al., 2020), a corticosteroid that has broad non-specific effects on the immune system. Even with corticosteroid treatment, mortality in severe COVID-19 remains significant. There is a wide armamentarium of existing drugs that target inflammation more selectively, providing potential repurposing opportunities for the treatment of COVID-19. Recently, the REMAP-CAP trial has demonstrated efficacy of anti-IL6 receptor blockade in patients admitted to intensive care units with severe disease (Gordon et al., 2021). In order to select the most promising agents for future trials, we urgently need to better understand the molecular drivers of severe disease. Proteins are the effector molecules of biology and the targets of most drugs. Therefore, proteomic profiling to identify the key mediators of severe disease provides a valuable tool for identifying and prioritising potential drug targets (Suhre et al., 2021). Risk factors for severe or fatal COVID-19 include age, male sex, non-European ancestry, obesity, diabetes mellitus, cardiovascular disease, and immunosuppression (Williamson et al., 2020). End-stage kidney disease (ESKD) is one of the strongest risk factors for severe COVID-19 (estimated hazard ratio for death 3.69) (Williamson et al., 2020), and ESKD patients hospitalised with COVID-19 have a mortality of approximately 30% (Docherty et al., 2020; Corbett et al., 2020; Ng et al., 2020; Valeri et al., 2020). ESKD patients have a high prevalence of vascular and cardiometabolic disease (e.g. hypertension, ischaemic heart disease, diabetes), either as a result of the underlying cause of their renal disease or as a consequence of renal failure. In addition, ESKD results in both relative immunosuppression and chronic low-grade inflammation, which may impact viral defence and the host inflammatory response. Here we performed proteomic profiling of serial blood samples of ESKD patients with COVID-19, leveraging the unique opportunity for longitudinal sampling in both the outpatient and inpatient settings afforded by a large multi-ethnic haemodialysis cohort (Figure 1a). These data revealed 221 proteins that are dysregulated in COVID-19 versus matched non-infected ESKD patients. Using linear mixed models, joint models, and machine learning, we identified proteins that are markers of COVID-19 severity and risk of death. Finally, we characterised the temporal dynamics of the blood proteomic response during COVID-19 infection in ESKD patients, uncovering 32 proteins that display altered trajectories in patients with severe versus non-severe disease. Figure 1 with 1 supplement see all Download asset Open asset Study design. (a) Schematic representing a summary of the patient cohorts, sampling, and the major analyses. Blue and red stick figures represent outpatients and hospitalised patients, respectively. (b) Timing of serial blood sampling in relation to clinical course of COVID-19 (subcohort A). Black asterisks indicate when samples were obtained. Three patients were already in hospital prior to COVID-19 diagnosis (indicated by red bars). Results We recruited 55 ESKD patients with COVID-19 (subcohort A; Table 1). All patients were receiving haemodialysis prior to acquiring COVID-19. Blood samples were taken as soon as feasible following COVID-19 diagnosis. At time of initial sample, 30 patients were outpatients attending haemodialysis sessions and 25 were hospitalised inpatients (see Materials and methods, Figure 1). Following the initial blood sample, serial sampling was performed for 51/55 patients. We also recruited 51 non-infected haemodialysis patients as ESKD controls, mirroring the age, sex, and ethnicity distribution of the COVID-19 cases (Figure 1—figure supplement 1a–c). We used the Olink proteomics platform to measure 436 proteins (Supplementary file 1a) in 256 plasma samples from the COVID-19 patients and the 51 control samples. The proteins measured consisted of five multiplex 'panels' focussed on proteins relevant to immuno-inflammation, cardiovascular, and cardiometabolic disease. The 436 proteins assayed showed strong enrichment for immune-related proteins (Supplementary file 1b). Table 1 Characteristics of subcohort A. COVID-19-positive ESKD patients (n = 55)ESKD controls (n = 51) OverallPeak severity mild or moderate (n = 28)Peak severity severe or critical (n = 27)Age Median (IQR)72.2 62.5–77.373.4 65.5–76.468.5 61.8–78.870.1 62.2–75.1Sex M F39 (70.9%) 16 (29.1%)18 (64.3%) 10 (35.7%)21 (77.8%) 6 (22.2%)36 (70.6%) 15 (29.4%)Ethnicity White Black South Asian Asian (other) Other16 (29.1%) 8 (14.5%) 18 (32.7%) 4 (7.3%) 9 (16.4%)5 (17.9%) 5 (17.9%) 10 (35.7%) 1 (3.6%) 7 (25.0%)11 (40.7%) 3 (11.1%) 8 (29.6%) 3 (11.1%) 2 (7.4%)13 (25.5%) 8 (15.7%) 20 (39.2%) 3 (5.9%) 7 (13.7%)Diabetes34 (61.8%)*16 (57.1%)18 (66.7%)24 (47.1%)*Current smoker1 (1.8%)1 (3.6%)00ESKD cause DN Genetic GN HTN/vascular Other Unknown29 (52.7%) 1 (1.8%) 3 (5.5%) 5 (9.1%) 8 (14.5%) 9 (16.4%)14 (50.0%) 1 (3.6%) 1 (3.6%) 3 (10.7%) 5 (17.9%) 4 (14.3%)15 (55.6%) 0 2 (7.4%) 2 (7.4%) 3 (11.1%) 5 (18.5%)20 (39.2%) 1 (2.0%) 9 (17.6%) 7 (13.7%) 4 (7.8%) 10 (19.6%)Hospitalisation due to COVID-19†33 (60%)6 (21.4%)27 (100%)N/AFatal COVID-199 (16.3%)0 (0%)9 (33.3%)N/A DN = diabetic nephropathy. GN = glomerulonephritis. HTN = hypertension. IQR = inter-quartile range. 'South Asian' represents individuals with Indian, Pakistani, or Bangladeshi ancestry. Subsets defined according to peak WHO severity over the course of the illness. N/A = not applicable. *One patient had type 1 diabetes, the remainder type 2. †3 patients were hospitalised prior to COVID-19 diagnosis. 8 patients diagnosed with COVID-19 as outpatients subsequently deteriorated were hospitalised. In addition, we performed the Olink proteomic assays in 52 serum samples from a separate set of 46 COVID-19-positive ESKD patients (subcohort B) and 11 serum samples from ESKD COVID-19-negative controls (a subset of the controls described above). For the large majority of patients in subcohort B, only a single timepoint was available. A higher proportion of these patients (41/46, 89%) were hospitalised and had severe disease (Table 2) than in subcohort A (Figure 1, Table 1). Table 2 Characteristics of subcohort B. COVID-19-positive ESKD patients (n = 46)COVID-19-negative ESKD controls (n = 11)*Age Median (IQR)64.3 60.3–73.071.6 (61.7–73.9)Sex M F32 (69.6%) 14 (30.4%)8 (72.3%) 3 (27.3%)Ethnicity White Black South Asian Asian (other) Other11 (23.9%) 8 (17.4%) 12 (26.1%) 7 (15.2%) 8 (17.4%)3 (27.3%) 3 (27.3%) 3 (27.3%) 0 2 (18.2%)Diabetes29 (63.0%)6 (54.5%)Current smoker2 (4.3%)0 (%)ESKD cause DN Genetic GN HTN/vascular Other Unknown19 (41.3%) 1 (2.2%) 7 (15.2%) 3 (6.5%) 3 (6.5%) 13 (28.3%)5 (45.5%) 0 1 (9.1%) 1 (9.1%) 2 (18.2%) 2 (18.2%)Hospitalisation due to COVID-1941 (89.1%)N/ASevere or critical COVID-1933 (71.7%)N/AFatal COVID-199 (19.6%)N/A DN = diabetic nephropathy. GN = glomerulonephritis. HTN = hypertension. IQR = inter-quartile range. 'South Asian' represents individuals with Indian, Pakistani, or Bangladeshi ancestry. Subsets defined according to peak WHO severity over the course of the illness. N/A = not applicable. *These 11 controls are a subset of the control patients used in subcohort A. Proteomic differences between COVID-19-positive and -negative ESKD patients Principal component analysis (PCA) of proteomic data from subcohort A demonstrated differences between samples from COVID-19-positive cases and controls, although the two groups did not separate into discrete clusters (Figure 2a,b). To examine the effects of COVID-19 on the plasma proteome, we performed a differential expression analysis in subcohort A between COVID-19 cases (n = 256 samples passing quality control [QC] from 55 patients) and non-infected ESKD controls (n = 51) using linear mixed models, which account for serial samples from the same individual (see Materials and methods). This revealed 221 proteins associated with COVID-19 (5% false discovery rate, FDR); the vast majority were upregulated, with only 40 downregulated (Figure 3a, Supplementary file 1c). In order to provide a succinct and standardised nomenclature, we report proteins by the symbols of the genes encoding them (see Supplementary file 1a for a mapping of symbols to full protein names). The most strongly upregulated proteins (in terms of fold change) were DDX58, CCL7, IL6, CXCL11, KRT19, and CXCL10, and the most strongly downregulated were SERPINA5, CCL16, FABP2, PON3, ITGA11, and MMP12 (Figure 3—figure supplement 1). Notably, many of the upregulated proteins were chemotaxins. Figure 2 with 2 supplements see all Download asset Open asset Principal component analysis. PC = principal component. Each point represents a sample. Colouring indicates COVID-19 status. The directions and relative sizes of the six largest PC loadings are plotted as arrows (middle column). (a, b) Subcohort A. Due to serial sampling, there are multiple samples for most patients. The proportion of variance explained in subcohort A by each PC is shown in parentheses on the axis labels. (c, d) Subcohort B. Samples are projected into the PCA coordinates from subcohort A. Figure 3 with 4 supplements see all Download asset Open asset Identification of dysregulated proteins. (a) Proteins upregulated (red) or downregulated (blue) in COVID-19-positive patients versus COVID-19-negative ESKD patients n = 256 plasma samples from 55 COVID-19-positive patients, versus n = 51 ESKD controls (one sample per control patient). (b) Proteins associated with disease severity associations of protein levels against WHO severity score at the time of sampling. Linear gradient indicates the effect size. A positive effect size (red) indicates that an increase in protein level is associated with increasing disease severity and a negative gradient (blue) the opposite. n = 256 plasma samples from 55 COVID-19-positive patients. For (a, b), p-values from linear mixed models after Benjamini–Hochberg adjustment; significance threshold = 5% FDR; dark-grey = non-significant. (c) Heatmap showing protein levels for selected proteins with strong associations with severity. Each column represents a sample (n = 256 COVID-19 samples and 51 non-infected samples). Each row represents a protein. Proteins are annotated using the symbol of their encoding gene. For the purposes of legibility, not all significantly associated proteins are shown; the heatmap is limited to the 17% most up- or downregulated proteins (by effect size) of those with a significant association. Proteins are ordered by hierarchical clustering. Samples are ordered by WHO severity at the time of blood sample ('Severity'). 'Overall course' indicates the peak WHO severity over the course of the illness. We observed that a high proportion of the measured proteins were associated with COVID-19. Given the highly targeted nature of the Olink panels that we used (enriched for immune and inflammation-related proteins), this was not surprising. Nevertheless, to ensure that the Benjamini–Hochberg adjustment of p-values was controlling the FDR at the 5% level, we performed two additional analyses (see Materials and methods). First, we estimated the FDR using an alternative method (the plug-in procedure ; Hastie et al., 2001); this confirmed appropriate FDR control. Second, we used permutation to estimate the distribution of the number of proteins expected to be declared significant under the null hypothesis of no association between any proteins and COVID-19. This showed that the probability of observing the number of differentially abundant proteins we identified was highly unlikely under the null (empirical p<1×10−5; Figure 3—figure supplement 2). Although our COVID-19-negative controls were well matched in terms of age, sex, and ethnicity (Figure 1—figure supplement 1a–c), perfect matching of comorbidities was not feasible in the context of the healthcare emergency at the time of patient recruitment. There was a higher prevalence of diabetes in the COVID-19 cases compared to the controls (61.8% versus 47.1%, respectively; Table 1). To evaluate whether differing rates of diabetes had impacted the proteins identified as differentially abundant between cases and controls, we performed a sensitivity analysis adding diabetes as an additional covariate in the linear mixed model. This did not materially affect our findings; estimated effect sizes and –log10 p-values from models with and without the inclusion of diabetes were highly correlated (Pearson r > 0.99, and r = 0.95, respectively; Figure 3—figure supplement 3a,b). Full results from both models are shown in Supplementary file 1c. Similarly, there were also differences in the underlying cause of ESKD in cases compared to controls (Table 1). We therefore performed a further sensitivity analysis adjusting for underlying cause of renal failure. This did not make any meaningful difference to our results (Figure 3—figure supplement 3c,d, Supplementary file 1c). We also considered the possibility that timing of haemodialysis might affect the plasma proteome. To minimise the impact of this, all samples were taken prior to haemodialysis. For the large majority (86.6%) of samples, the most recent haemodialysis was between 48 and 72 hr prior to blood draw. This consistency in timing of blood sampling reduces the potential for impact of this issue. Nevertheless, to evaluate whether timing of haemodialysis might have impacted our results, we performed a sensitivity analysis including time from last haemodialysis as a covariate. Our results were not materially affected by this, with −log10 p-values and estimated effect sizes very highly correlated with those obtained without inclusion of this covariate (Pearson r > 0.99 for effect size estimates and for −log10 p-values; Figure 3—figure supplement 4a,b, Supplementary file 1c). We used the smaller subcohort B (n = 52 serum samples from 46 patients with COVID-19; see Materials and methods) for validation. We first projected the data from subcohort B into the PCA space of subcohort A to examine how well the separation of cases and controls in the PCA space replicated (see Materials and methods). This revealed clearer separation of infected and non-infected patients than in subcohort A (Figure 2c,d), perhaps reflecting the higher proportion of hospitalised patients (41 of 46 patients) in subcohort B (Table 2). We next performed differential abundance analysis in subcohort B and found 201 proteins that were dysregulated in cases versus controls (5% FDR) (Supplementary file 1c). Of the 221 differentially abundant proteins from subcohort A, 150 (69.7%) were also identified in subcohort B at 5% FDR (Figure 4a). Effect sizes in each dataset showed a strong correlation (r = 0.80, Figure 4b). This demonstrates that our findings are highly reproducible despite differences in sample sizes and blood materials (plasma versus serum in subcohorts A and B, respectively). Figure 4 with 1 supplement see all Download asset Open asset Validation. (a) Overlap between the significant associations in the differential abundance analysis between ESKD patients with and without COVID-19 in subcohorts A and B. 5% FDR was used as the significance threshold in both analyses. (b) Comparison of estimated effect sizes for all 436 proteins in the differential abundance analyses (COVID-19 positive versus negative) in subcohort A and B. Each point represents a protein. Pearson's r is shown. Differential abundance analyses were performed using linear mixed models. Subcohort A analysis (plasma samples): 256 samples from 55 COVID-19 patients versus 51 non-infected patient samples (single time-point). Subcohort B (serum samples): 52 samples from 55 COVID-19 patients and 11 non-infected patient samples (single timepoint). Proteins associated with COVID-19 severity Examination of the principal components plot labelling samples by clinical severity at the time of sampling (defined by WHO severity scores, graded as mild, moderate, severe, or critical) demonstrated a gradient of COVID-19 severity, best captured by principal components 1 and 3 (Figure 2—figure supplement 1a). To determine the proteomic effects of COVID-19 severity, we tested for associations between proteins and WHO severity score at the time of blood sampling, using linear mixed models with severity encoded as an ordinal predictor (see Materials and methods). This analysis revealed 203 proteins associated with severity (Figure 3b, Supplementary file 1d). The majority of these were upregulated in more severe disease, with only 42 downregulated. A sensitivity analysis adjusting for time since last haemodialysis made no significant impact on our results (Figure 3—figure supplement 4c,d, Supplementary file 1d). Consistent with previous reports, we found that severe COVID-19 was characterised by elevated IL6. In addition, we observed a signature of upregulated monocyte chemokines (e.g. CCL2, CCL7, CXCL10), neutrophil activation and degranulation (e.g. PRTN3, MPO), and epithelial injury (e.g. KRT19, AREG, PSIP1, GRN). (Figures 3b,c and 5). SERPINA5 and leptin showed the greatest downregulation as COVID-19 severity increased (Figure 3b,c). Figure 5 Download asset Open asset proteins strongly associated with COVID-19 severity. showing distribution of plasma protein levels according to COVID-19 at the time of blood draw. indicate and inter-quartile range. n = 256 samples from 55 COVID-19 patients and 51 samples from non-infected patients. WHO severity indicates the clinical severity score of the patient at the time the sample was n = moderate n = severe n = critical n = 15 samples. monocyte markers of epithelial injury. two neutrophil and IL6. We next how the COVID-19 severity protein signature to the proteins that are differentially abundant between cases and The majority of proteins were also identified as differentially abundant in the COVID-19-positive versus -negative analysis (Figure fold for proteins in COVID-19 versus non-infected patients were correlated with effect sizes in the severity that the proteins most upregulated in cases versus controls also to the greatest in severe disease (Figure there were some (e.g. that were strongly associated with severity, not differentially expressed in infected versus non-infected patients (Figure Figure 6 Download asset Open asset Comparison of proteins differentially expressed in COVID-19 with those associated with clinical severity. (a) Overlap between the proteins significantly differentially expressed in COVID-19 (n = 256 COVID-19 samples and 51 non-infected versus those associated with severity n = 256 (subcohort A). 5% FDR was used as the significant in both analyses. (b) Comparison of effect sizes for each protein in the COVID-19-positive versus -negative analysis and severity analysis Each point represents a protein. Pearson's r is shown. (c) of proteins associated with severity, not significantly differentially abundant in the of all cases versus showing distribution of plasma protein levels according to COVID-19 at the time of blood draw. indicate and inter-quartile range. n = 256 samples from 55 COVID-19 patients and 51 samples from non-infected patients. WHO severity indicates the clinical severity score of the patient at the time the sample was n = moderate n = severe n = critical n = 15 samples. learning to predict COVID-19 severity PCA revealed that some samples from patients who had mild or moderate disease at the time of sampling with samples from patients with severe disease (Figure 2—figure supplement 1a). Examination of the same PCA plot labelling samples according to the clinical course by peak WHO severity score over the of the (Figure 2—figure supplement revealed that these samples from individuals who subsequently developed severe or critical disease. This that molecular may clinical To evaluate this we used learning to whether the proteomic signature of the first blood sample for each patient in our dataset could identify whether the patient either had severe COVID-19 at the time of sampling or severe disease in the differential expression analyses each protein of all proteins in the Using we a on the first sample for each COVID-19 patient to predict the clinical defined by peak WHO severity. For the purposes of this we clinical course into either WHO or The method in peak severity. using only predictors and clinical the method in peak severity. clinical proteins did not compared to using proteomic predictors that the information in the clinical predictors is captured at the proteomic we not that proteomic profiling is to clinical for risk during this the selected by the proteins of We therefore the to identify key proteins by (see Materials and methods, Supplementary file The most important proteins for the of or future severe disease were IL18BP, GDF15, KRT19, and (Figure is that this as a key of severe disease. Figure 7 with 1 supplement see all Download asset Open asset of severe COVID-19 and death. (a) The 12 most important proteins for clinical course (defined by peak COVID-19 WHO using a is important for it is to in many of and be to the have a The all was used as the (b) Proteins that are significant predictors of death n = 256 samples from 55 COVID-19-positive patients, of Risk estimates are from a joint model. indicate For proteins with a positive risk a higher to a high risk of and for proteins with negative Proteins associated with risk of death of 55 patients in subcohort A We therefore to identify proteins associated with risk of death. To the nature of protein for of we joint models, which linear mixed models and models et al., (see Materials and methods). This analysis identified proteins for which increased was associated with increased risk of death (Figure Supplementary file including and and 25 proteins for which increased was associated with risk of including and with clinical A number of clinical have associations with COVID-19 (e.g. elevated inflammatory and et al., 2020). We therefore compared our proteomic data from COVID-19 patients at each timepoint to clinical using linear mixed models (see Materials and methods). We found associations between plasma proteins and all clinical (Figure Supplementary file Many of these proteins were also markers of severity (e.g. IL6, KRT19, and were strongly associated with and and Of CCL7, a monocyte that was also identified as an important of severity by the was associated with monocyte and inflammatory neutrophil was associated with which IL6, and and with the and Figure 8 Download asset Open asset of clinical markers with plasma proteins. Proteins that are (red) or (blue) associated with clinical (5% p-values from differential abundance analysis using linear mixed models after Benjamini–Hochberg = non-significant. Two associations were found for shown – see Supplementary file Longitudinal analysis proteins with temporal profiles according to severity The immune response to infection is and therefore provide only the serial sampling in our dataset (Figure we the temporal of each protein and whether or not any protein trajectories in patients with a versus clinical This was a

The objective of this research was to develop and validate a machine learning-based prediction model integrating clinical data, apparent diffusion coefficient (ADC) value, and diffusion- weighted imaging (DWI)-based radiomic features, aimed at assessing microsatellite instability (MSI) status in endometrial cancer (EC) patients. In total, 292 EC patients who underwent pelvic MRI scans participated in this study and were allocated into three distinct groups: an external validation cohort (n = 70), a testing cohort (n = 68), and a training cohort (n = 154). Preoperative clinical indicators, ADC metrics, and radiomic parameters extracted from DWI images were comprehensively evaluated. Feature selection was conducted using least absolute shrinkage and selection operator (LASSO) regression combined with Mann-Whitney U testing. Following feature selection, three distinct machine learning classifiers—support vector machine (SVM), random forest (RF), and logistic regression (LR)—were employed to develop predictive models. The performance and clinical utility of these models were subsequently examined through receiver operating characteristic (ROC) curves, calibration curves, and decision curve analysis (DCA). Among the evaluated methods, the RF model incorporating two clinical indicators, six radiomic parameters from DWI, and ADC values exhibited superior predictive ability. The areas under the ROC curves (AUC) reached 0.980 (95% CI: 0.944–0.996) in the training cohort, 0.852 (95% CI: 0.745–0.927) in the test cohort, and 0.938 (95% CI: 0.853–0.982) in the external validation cohort, respectively. These AUC values reflected better accuracy compared to separate predictive models employing only clinical factors, DWI radiomics, or ADC values (training cohort: AUC = 0.682, 0.925, and 0.851; test cohort: AUC = 0.663, 0.788, and 0.731; external validation cohort: AUC = 0.605, 0.872, and 0.828, respectively). Calibration curves indicated robust concordance, and DCA analysis confirmed that the model had substantial clinical applicability. A prediction model combining clinical factors, DWI radiomics features, and ADC values with machine learning algorithms can noninvasively assess MSI status in EC.

This study evaluates the impact of three Feature Selection (FS) algorithms in an Object Based Image Analysis (OBIA) framework for Very-High-Resolution (VHR) Land Use-Land Cover (LULC) classification. The three selected FS algorithms, Correlation Based Selection (CFS), Mean Decrease in Accuracy (MDA) and Random Forest (RF) based Recursive Feature Elimination (RFE), were tested on Support Vector Machine (SVM), K-Nearest Neighbor, and Random Forest (RF) classifiers. The results demonstrate that the accuracy of SVM and KNN classifiers are the most sensitive to FS. The RF appeared to be more robust to high dimensionality, although a significant increase in accuracy was found by using the RFE method. In terms of classification accuracy, SVM performed the best using FS, followed by RF and KNN. Finally, only a small number of features is needed to achieve the highest performance using each classifier. This study emphasizes the benefits of rigorous FS for maximizing performance, as well as for minimizing model complexity and interpretation.

Improving Subseasonal-to-Seasonal forecasts in predicting the occurrence of extreme precipitation events over the contiguous U.S. using machine learning models

BackgroundRetention in HIV care is essential to end the HIV epidemic and improve individual patient outcomes, yet 1/3 of people living with HIV in Maryland are not consistently retained in care. Predictive modeling using electronic health record (EHR) data is a promising strategy to identify patients at risk for lapses in care; however, existing efforts remain limited. Regional analyses using statewide health systems can uniquely inform local strategies by accounting for demographic, clinical, and structural variations. This study aimed to develop predictive models utilizing comprehensive EHR data from the University of Maryland Medical System (UMMS) to identify people living with HIV who are at risk of lapsing in care.Figure 1.Receiver Operating Characteristic (ROC) Curve demonstrating the performance of the Random Forest model in predicting lapses in HIV care. The model achieved an area under the curve (AUC) of 0.91, with high recall (98%) and precision (81%), indicating strong predictive capability for identifying patients at risk of lapsing in HIV care.Figure 2.SHAP summary illustrating the impact of key features on the Random Forest model's predictions of HIV care lapses. Each dot represents a patient encounter, with dot colors indicating feature value magnitude (high in red, low in blue).MethodsUtilizing EHR data from UMMS including HIV-related prescriptions, laboratory tests and clinical visits from adults receiving antiretroviral therapy from 1/2016-6/2024, we identified 8,518 patients with 205,633 encounters. Consolidating multiple encounters within 10 days as one encounter, and including only encounters preceding the last recorded encounter for both lapsed and non-lapsed groups, resulted in 4,735 patients. Of those, 2,667 (56%) had lapses - defined as not having an HIV-related clinical encounter within 12 months. We used a Random Forest classifier with extensive hyperparameter tuning via randomized search cross-validation. Model performance was assessed via the performance matrices and SHAP values for feature importance.ResultsThe Random Forest model demonstrated an AUC of 0.91 with 98% recall for lapses, and 81% precision (Figure 1). Feature importance analysis highlighted significant predictors, including time on treatment, age, BMI, alcohol use, employment status, racial demographics, and comorbidities such as hypertension and diabetes (Figure 2).ConclusionPredictive modeling using EHR data from a comprehensive statewide health system can effectively identify patients at risk for lapses in HIV care. Clinically actionable predictors, such as treatment duration, demographics, and specific health conditions, provide practical insights that can guide interventions to enhance patient retention and ultimately improve health outcomes for people living with HIV.DisclosuresAll Authors: No reported disclosures