Vision‐based autonomous inspection of concrete surface defects is crucial for efficient maintenance and rehabilitation of infrastructures and has become a research hot spot. However, most existing vision‐based inspection methods mainly focus on detecting one kind of defect in nearly uniform testing background where defects are relatively large and easily recognizable. But in the real‐world scenarios, multiple types of defects often occur simultaneously. And most of them occupy only small fractions of inspection images and are swamped in cluttered background, which easily leads to missed and false detections. In addition, the majority of the previous researches only focus on detecting defects but few of them pay attention to the geolocalization problem, which is indispensable for timely performing repair, protection, or reinforcement works. And most of them rely heavily on GPS for tracking the locations of the defects. However, this method is sometimes unreliable within infrastructures where the GPS signals are easily blocked, which causes a dramatic increase in searching costs. To address these limitations, we present a unified and purely vision‐based method denoted as defects detection and localization network, which can detect and classify various typical types of defects under challenging conditions while simultaneously geolocating the defects without requiring external localization sensors. We design a supervised deep convolutional neural network and propose novel training methods to optimize its performance on specific tasks. Extensive experiments show that the proposed method is effective with a detection accuracy of 80.7% and a localization accuracy of 86% at 0.41 s per image (at a scale of 1,200 pixels in the field test experiment), which is ideal for integration within intelligent autonomous inspection systems to provide support for practical applications.
Failure of resolution pathways in periodontitis is reflected in levels of specialized pro-resolving lipid mediators (SPMs) and SPM pathway markers but their relationship with the subgingival microbiome is unclear. This study aimed to analyze and integrate lipid mediator level, SPM receptor gene expression and subgingival microbiome data in subjects with periodontitis vs. healthy controls. The study included 13 periodontally healthy and 15 periodontitis subjects that were evaluated prior to or after non-surgical periodontal therapy. Samples of gingival tissue and subgingival plaque were collected prior to and 8 weeks after non-surgical treatment; only once in the healthy group. Metabololipidomic analysis was performed to measure levels of SPMs and other relevant lipid mediators in gingiva. qRT-PCR assessed relative gene expression (2-ΔΔCT) of known SPM receptors. 16S rRNA sequencing evaluated the relative abundance of bacterial species in subgingival plaque. Correlations between lipid mediator levels, receptor gene expression and bacterial abundance were analyzed using the Data Integration Analysis for Biomarker discovery using Latent cOmponents (DIABLO) and Sparse Partial Least Squares (SPLS) methods. Profiles of lipid mediators, receptor genes and the subgingival microbiome were distinct in the three groups. The strongest correlation existed between lipid mediator profile and subgingival microbiome profile. Multiple lipid mediators and bacterial species were highly correlated (correlation coefficient ≥0.6) in different periodontal conditions. Comparing individual correlated lipid mediators and bacterial species in periodontitis before treatment to healthy controls revealed that one bacterial species, Corynebacterium durum, and five lipid mediators, 5(S)6(R)-DiHETE, 15(S)-HEPE, 7-HDHA, 13-HDHA and 14-HDHA, were identified in both conditions. Comparing individual correlated lipid mediators and bacterial species in periodontitis before treatment to after treatment revealed that one bacterial species, Anaeroglobus geminatus, and four lipid mediators, 5(S)12(S)-DiHETE, RvD1, Maresin 1 and LTB4, were identified in both conditions. Four Selenomonas species were highly correlated with RvD1, RvE3, 5(S)12(S)-DiHETE and proinflammatory mediators in the periodontitis after treatment group. Profiles of lipid mediators, receptor gene and subgingival microbiome are associated with periodontal inflammation and correlated with each other, suggesting inflammation mediated by lipid mediators influences microbial composition in periodontitis. The role of correlated individual lipid mediators and bacterial species in periodontal inflammation have to be further studied.
Motivation Cell label annotation is a challenging step in the analysis of scRNA-seq data, especially for tissue types that are less commonly studied. The accumulation of scRNA-seq studies and biological knowledge leads to several well-maintained cell marker databases. Manually examining the cell marker lists against these databases can be difficult due to the large amount of available information. Additionally, simply overlapping the two lists without considering gene ranking might lead to unreliable results. Thus, an automated method with careful statistical testing is needed to facilitate the usage of these databases. Results We develop a user-friendly computational tool, EasyCellType, that automatically checks an input marker list obtained by differential expression analysis against the databases and provides annotation recommendations in graphical outcomes. The package provides two statistical tests, gene set enrichment analysis (GSEA) and a modified version of Fisher’s exact test, as well as customized database and tissue type choices. We also provide an interactive shiny application to annotate cells in a user-friendly friendly Graphical User Interface (GUI). The simulation study and real data applications demonstrate favorable results by the proposed method. Availability https://biostatistics.mdanderson.org/shinyapps/EasyCellType/ https://bioconductor.org/packages/devel/bioc/html/EasyCellType.html Supplementary information Supplementary data are available at Bioinformatics online.
The T-cell receptor (TCR) repertoire is highly diverse among the population and plays an essential role in initiating multiple immune processes. TCR sequencing (TCR-seq) has been developed to profile the T cell repertoire. Similar to other high-throughput experiments, contamination can happen during several steps of TCR-seq, including sample collection, preparation and sequencing. Such contamination creates artifacts in the data, leading to inaccurate or even biased results. Most existing methods assume ‘clean’ TCR-seq data as the starting point with no ability to handle data contamination. Here, we develop a novel statistical model to systematically detect and remove contamination in TCR-seq data. We summarize the observed contamination into two sources, pairwise and cross-cohort. For both sources, we provide visualizations and summary statistics to help users assess the severity of the contamination. Incorporating prior information from 14 existing TCR-seq datasets with minimum contamination, we develop a straightforward Bayesian model to statistically identify contaminated samples. We further provide strategies for removing the impacted sequences to allow for downstream analysis, thus avoiding any need to repeat experiments. Our proposed model shows robustness in contamination detection compared with a few off-the-shelf detection methods in simulation studies. We illustrate the use of our proposed method on two TCR-seq datasets generated locally.
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