Application of the random forest algorithm to Streptococcus pyogenes response regulator allele variation: from machine learning to evolutionary models.
Ontology highlight
ABSTRACT:
SUBMITTER: Buckley SJ
PROVIDER: S-EPMC8209152 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Transcriptional enhancers play critical roles in regulation of gene expression, but their identification has remained a challenge. Recently, it was shown that enhancers in the mammalian genome are associated with characteristic histone modification patterns, which have been increasingly exploited for enhancer identification. However, only a limited number of histone modifications have previously been investigated for this purpose, leaving the questions answered whether there exist an optimal set of histone modifications that could improve the enhancer prediction. Here, we address this issue by exploring a rich dataset produced by the human Epigenome Roadmap Project. Specifically, we examined genome-wide profiles of 24 histone modifications in human embryonic stem cells and fibroblasts, and developed a Random-Forest based algorithm to integrate histone modification profiles for identification of enhancers.As a training set, we used histone modification profiles at genome-wide binding sites of p300 in the two cell types identified using ChIP-seq. We show that this algorithm not only leads to more accurate and precise prediction of enhancers than previous methods, but also helps identify an optimal set of three chromatin marks for enhancer prediction.
2012-05-10 | GSE37858 | GEO
Project description:Transcriptional enhancers play critical roles in regulation of gene expression, but their identification has remained a challenge. Recently, it was shown that enhancers in the mammalian genome are associated with characteristic histone modification patterns, which have been increasingly exploited for enhancer identification. However, only a limited number of histone modifications have previously been investigated for this purpose, leaving the questions answered whether there exist an optimal set of histone modifications that could improve the enhancer prediction. Here, we address this issue by exploring a rich dataset produced by the human Epigenome Roadmap Project. Specifically, we examined genome-wide profiles of 24 histone modifications in human embryonic stem cells and fibroblasts, and developed a Random-Forest based algorithm to integrate histone modification profiles for identification of enhancers.As a training set, we used histone modification profiles at genome-wide binding sites of p300 in the two cell types identified using ChIP-seq. We show that this algorithm not only leads to more accurate and precise prediction of enhancers than previous methods, but also helps identify an optimal set of three chromatin marks for enhancer prediction. ChIP-Seq Analysis of p300 in hESC H1 and IMR90 cells. Sequencing was done on the Illumina Genome Analyzer II platform for the H1 data and Illumina HiSeq for IMR90.Data was mapped to hg18 using Bowtie.
2012-05-09 | E-GEOD-37858 | biostudies-arrayexpress
Project description:tRNA fragments (tRFs) are a novel class of small RNAs comparable to the size and function of miRNAs. We and others have shown that tRFs are generally Dicer independent, can be found in abundance in the miRNA effector protein Ago, and can repress expression of specific genes that have complementarity to their 5’ seed-sequences. Given that this greatly expands the repertoire of small RNAs capable of post-transcriptional gene expression, it is important to predict tRF targets with confidence. Some attempts have been made to predict tRF targets, but are limited in the scope of tRF classes used in prediction or limited in feature selection. We hypothesized that established miRNA target prediction features applied to tRFs through a random forest machine learning algorithm will immensely improve tRF target prediction. Using this approach, we show significant improvements in tRF target prediction for all classes of tRFs and validate our predictions in two independent cell lines. Finally, using Gene Ontology analysis, we provide evidence that tRF-3009a targets may be involved in neural development. These improvements to tRF target prediction further our understanding of tRF function broadly across species and tRF types, and provide avenues for testing novel roles for tRFs in biology.
2022-05-16 | GSE189510 | GEO
Project description:ObjectiveTo explore the feasibility of using random forest (RF) machine learning algorithm in assessing normal and malignant peripheral pulmonary nodules based on in vivo endobronchial optical coherence tomography (EB-OCT).MethodsA total of 31 patients with pulmonary nodules were admitted to Department of Respiratory Medicine, Zhongda Hospital, Southeast University, and underwent chest CT, EB-OCT and biopsy. Attenuation coefficient and up to 56 different image features were extracted from A-line and B-scan of 1703 EB-OCT images. Attenuation coefficient and 29 image features with significant p-values were used to analyze the differences between normal and malignant samples. A RF classifier was trained using 70% images as training set, while 30% images were included in the testing set. The accuracy of the automated classification was validated by clinically proven pathological results.ResultsAttenuation coefficient and 29 image features were found to present different properties with significant p-values between normal and malignant EB-OCT images. The RF algorithm successfully classified the malignant pulmonary nodules with sensitivity, specificity, and accuracy of 90.41%, 77.87% and 83.51% respectively.ConclusionIt is clinically practical to distinguish the nature of pulmonary nodules by integrating EB-OCT imaging with automated machine learning algorithm. Diagnosis of malignant pulmonary nodules by analyzing quantitative features from EB-OCT images could be a potentially powerful way for early detection of lung cancer.
| S-EPMC8719667 | biostudies-literature
Project description:Novel Coronavirus pandemic, which negatively affected public health in social, psychological and economical terms, spread to the whole world in a short period of 6 months. However, the rate of increase in cases was not equal for every country. The measures implemented by the countries changed the daily spreading speed of the disease. This was determined by changes in the number of daily cases. In this study, the performance of the Random Forest (RF) machine learning algorithm was investigated in estimating the near future case numbers for 190 countries in the world and it is mapped in comparison with actual confirmed cases results. The number of confirmed cases between 23/01/2020 - 17/06/2020 were divided into 3 main sub-datasets: training sub-data, testing sub-data (interpolation data) and estimating sub-data (extrapolation data) for the random forest model. At the end of the study, it has been found that R2 values for testing sub-data of RF model estimates range between 0.843 and 0.995 (average R2= 0.959), and RMSE values between 141.76 and 526.18 (mean RMSE = 259.38); and that R2 values for estimating sub-data range between 0.690 and 0.968 (mean R2 = 0.914), and RMSE values between 549.73 and 2500.79 (mean RMSE = 909.37). These results show that the random forest machine learning algorithm performs well in estimating the number of cases for the near future in case of an epidemic like Novel Coronavirus, which outbreaks suddenly and spreads rapidly.
| S-EPMC7439995 | biostudies-literature
Project description:Since 2017, we have used IonTorrent NGS platform in our hospital to diagnose and treat cancer. Analyzing variants at each run requires considerable time, and we are still struggling with some variants that appear correct on the metrics at first, but are found to be negative upon further investigation. Can any machine learning algorithm (ML) help us classify NGS variants? This has led us to investigate which ML can fit our NGS data and to develop a tool that can be routinely implemented to help biologists. Currently, one of the greatest challenges in medicine is processing a significant quantity of data. This is particularly true in molecular biology with the advantage of next-generation sequencing (NGS) for profiling and identifying molecular tumors and their treatment. In addition to bioinformatics pipelines, artificial intelligence (AI) can be valuable in helping to analyze mutation variants. Generating sequencing data from patient DNA samples has become easy to perform in clinical trials. However, analyzing the massive quantities of genomic or transcriptomic data and extracting the key biomarkers associated with a clinical response to a specific therapy requires a formidable combination of scientific expertise, biomolecular skills and a panel of bioinformatic and biostatistic tools, in which artificial intelligence is now successful in developing future routine diagnostics. However, cancer genome complexity and technical artifacts make identifying real variants challenging. We present a machine learning method for classifying pathogenic single nucleotide variants (SNVs), single nucleotide polymorphisms (SNPs), multiple nucleotide variants (MNVs), insertions, and deletions detected by NGS from different types of tumor specimens, such as: colorectal, melanoma, lung and glioma cancer. We compared our NGS data to different machine learning algorithms using the k-fold cross-validation method and to neural networks (deep learning) to measure the performance of the different ML algorithms and determine which one is a valid model for confirming NGS variant calls in cancer diagnosis. We trained our machine learning with 70% of our data samples, extracted from our local database (our data structure had 7 parameters: chromosome, position, exon, variant allele frequency, minor allele frequency, coverage and protein description) and validated it with the 30% remaining data. The model offering the best accuracy was chosen and implemented in the NGS analysis routine. Artificial intelligence was developed with the R script language version 3.6.0. We trained our model on 70% of 102,011 variants. Our best error rate (0.22%) was found with random forest machine learning (ntree = 500 and mtry = 4), with an AUC of 0.99. Neural networks achieved some good scores. The final trained model with the neural network achieved an accuracy of 98% and an ROC-AUC of 0.99 with validation data. We tested our RF model to interpret more than 2000 variants from our NGS database: 20 variants were misclassified (error rate < 1%). The errors were nomenclature problems and false positives. After adding false positives to our training database and implementing our RF model routinely, our error rate was always < 0.5%. The RF model shows excellent results for oncosomatic NGS interpretation and can easily be implemented in other molecular biology laboratories. AI is becoming increasingly important in molecular biomedical analysis and can be very helpful in processing medical data. Neural networks show a good capacity in variant classification, and in the future, they may be useful in predicting more complex variants.
| S-EPMC8575902 | biostudies-literature
Project description:BACKGROUND:Aggregated claims data on medication are often used as a proxy for the prevalence of diseases, especially chronic diseases. However, linkage between medication and diagnosis tend to be theory based and not very precise. Modelling disease probability at an individual level using individual level data may yield more accurate results. METHODS:Individual probabilities of having a certain chronic disease were estimated using the Random Forest (RF) algorithm. A training set was created from a general practitioners database of 276 723 cases that included diagnosis and claims data on medication. Model performance for 29 chronic diseases was evaluated using Receiver-Operator Curves, by measuring the Area Under the Curve (AUC). RESULTS:The diseases for which model performance was best were Parkinson's disease (AUC = .89, 95% CI = .77-1.00), diabetes (AUC = .87, 95% CI = .85-.90), osteoporosis (AUC = .87, 95% CI = .81-.92) and heart failure (AUC = .81, 95% CI = .74-.88). Five other diseases had an AUC >.75: asthma, chronic enteritis, COPD, epilepsy and HIV/AIDS. For 16 of 17 diseases tested, the medication categories used in theory-based algorithms were also identified by our method, however the RF models included a broader range of medications as important predictors. CONCLUSION:Data on medication use can be a useful predictor when estimating the prevalence of several chronic diseases. To improve the estimates, for a broader range of chronic diseases, research should use better training data, include more details concerning dosages and duration of prescriptions, and add related predictors like hospitalizations.
| S-EPMC6660107 | biostudies-literature
Project description:Transcriptional enhancers play critical roles in regulation of gene expression, but their identification in the eukaryotic genome has been challenging. Recently, it was shown that enhancers in the mammalian genome are associated with characteristic histone modification patterns, which have been increasingly exploited for enhancer identification. However, only a limited number of cell types or chromatin marks have previously been investigated for this purpose, leaving the question unanswered whether there exists an optimal set of histone modifications for enhancer prediction in different cell types. Here, we address this issue by exploring genome-wide profiles of 24 histone modifications in two distinct human cell types, embryonic stem cells and lung fibroblasts. We developed a Random-Forest based algorithm, RFECS (Random Forest based Enhancer identification from Chromatin States) to integrate histone modification profiles for identification of enhancers, and used it to identify enhancers in a number of cell-types. We show that RFECS not only leads to more accurate and precise prediction of enhancers than previous methods, but also helps identify the most informative and robust set of three chromatin marks for enhancer prediction.
| S-EPMC3597546 | biostudies-literature
Project description:Research on fault detection algorithm was developed with the similarity measure and random forest algorithm. The organized algorithm was applied to unmanned aircraft vehicle (UAV) that was readied by us. Similarity measure was designed by the help of distance information, and its usefulness was also verified by proof. Fault decision was carried out by calculation of weighted similarity measure. Twelve available coefficients among healthy and faulty status data group were used to determine the decision. Similarity measure weighting was done and obtained through random forest algorithm (RFA); RF provides data priority. In order to get a fast response of decision, a limited number of coefficients was also considered. Relation of detection rate and amount of feature data were analyzed and illustrated. By repeated trial of similarity calculation, useful data amount was obtained.
| S-EPMC4098612 | biostudies-other
Project description:Group A Streptococcus (GAS) is an exclusive human pathogen that causes significant disease burden. Global regulator RopB of GAS controls the expression of several major virulence factors including secreted protease SpeB during high cell density. However, the molecular mechanism for RopB-dependent speB expression remains unclear. To understand the mechanism of transcription activation by RopB, we determined the crystal structure of the C-terminal domain of RopB. RopB-CTD has the TPR motif, a signature motif involved in protein-peptide interactions and shares significant structural homology with the quorum sensing RRNPP family regulators. Characterization of the high cell density-specific cell-free growth medium demonstrated the presence of a low molecular weight proteinaceous secreted factor that upregulates RopB-dependent speB expression. Together, these results suggest that RopB and its cognate peptide signals constitute an intercellular signalling machinery that controls the virulence gene expression in concert with population density. Structure-guided mutational analyses of RopB dimer interface demonstrated that single alanine substitutions at this critical interface significantly altered RopB-dependent speB expression and attenuated GAS virulence. Results presented here suggested that a properly aligned RopB dimer interface is important for GAS pathogenesis and highlighted the dimerization interactions as a plausible therapeutic target for the development of novel antimicrobials.
| S-EPMC4794775 | biostudies-literature