Tao Chen

N -Nitroso-methylphenylamine (NMPA) is a rat esophageal carcinogen that has been found in food, tobacco and drugs. In this study, NMPA was administered via drinking water to Big Blue transgenic rats over 28 days following methods recommended in OECD TG 488; benzo[ a ]pyrene (B[a]P) was administered as the positive control. The esophagus, liver, and bone marrow were collected and analyzed for mutation using both the cII mutation assay and Duplex Sequencing (DS). NMPA treatment induced tissue-specific mutations, with the esophagus exhibiting the highest mutagenic response in both the cII and DS assays, followed by the liver; bone marrow remained relatively unaffected, showing no increase in the cII assay and only a slight elevation when analyzed by DS. The DS mutational spectrum for NMPA was characterized by a broadly distributed elevation across all base substitution types and in all trinucleotide contexts, distinguishing it from other small-molecule nitrosamines. Notably, DS detected fold-increases in NMPA mutagenesis greater than those detected by the transgenic rodent (TGR) assay, with a maximum 7.5-fold increase in genomic mutation frequency in the esophagus compared to the 5.6-fold increase in the cII gene. These data suggest that NMPA is an organ-specific mutagen, and that its mutagenic potency corresponds with its carcinogenicity in the primary target tissue and other tissues.

Environmental pollution has become a global public health crisis, posing profound threats to human reproductive stability and fetal developmental homeostasis

Software engineers must make decisions that trade off competing goals (faster vs. cheaper, secure vs. usable, accurate vs. interpretable, etc.). Despite MSR’s proven techniques for exploring such goals, researchers still struggle with these trade-offs. Similarly, industrial practitioners deliver sub-optimal products since they lack the tools needed to explore these trade-offs. To address this, MOOT (http://tiny.cc/moot) is a repository of many SE multi-objective optimization tasks. MOOT’s 120+ tasks cover software configuration, cloud tuning, project health, process modeling, hyperparameter optimization, and more. Sample scripts for reading MOOT and generating baseline results are available– just clone the repository and run the sample rqx.sh files (from tiny.cc/moot0). To the best of our knowledge, MOOT is the largest and most varied collection of real multi-objective optimization tasks in SE. We note that MOOT’s novelty is infrastructural, not algorithmic—we contribute curated data and research enablement, not new optimization methods. MOOT enables harder and more credible research. MOOT lets us replace studies on toy problems (or just half a dozen hand-picked examples) with case studies on 120+ examples. Such studies could focus on stability, sample efficiency, failure modes, cross-domain generality, or many other questions (see list in this document).

DNA methylation is one of the most extensively studied epigenetic modifications and plays an essential role in cardiac development. The zebrafish is a popular model for studying heart development due to its genetic similarity to mammals and transparent embryos. However, its small size presents challenges in obtaining sufficient DNA for methylation analysis. In this study, zebrafish embryos were exposed to 5-Azacytidine (5-AzaC) at concentrations of 0 µM, 25 µM, and 50 µM from 2-72 hours post-fertilization (2-72 hpf). Hearts were isolated from whole embryos, fixed, and permeabilized. The samples were then treated with proteinase K and HCl to facilitate access to DNA, followed by probing with an anti-5-methylcytosine (anti-5 mC) antibody. After incubation with a secondary antibody, the hearts were co-stained with DAPI. Fluorescence images were captured using a microscope and analyzed with ImageJ. Results demonstrated that 5-AzaC treatment significantly reduced global DNA methylation levels in zebrafish embryonic hearts. In conclusion, we present a sensitive immunofluorescence method to detect global DNA methylation levels within a single zebrafish larvae heart. This technique can be used to evaluate DNA methylation changes induced by environmental pollutants and to explore their impacts on heart development.

Multimodal emotion recognition (MER) has gained significant attention inrecent years. While most current methods focus on exploring inter-modalcorrelations through complex fusion strategies, they often overlook potentialcausal relationships, which may lead models to learn spurious correlationsand ultimately limit recognition performance. To address this issue, thispaper proposes a causality-inspired multimodal emotion recognition model(MERCI). Grounded in the causal structure of the emotion elicitation process,the model introduces a novel dual-channel architecture. It establishestwo distinct causal pathways: a predictive support channel that extracts featuresfrom video content responsible for eliciting emotional responses, and adiagnostic support channel that utilizes eye movement features to infer emotionalstates. Guided by statistical priors derived from participant data, themodel learns more discriminative and robust feature representations. Subsequently,Bayesian rule is employed to integrate the prediction probabilitiesfrom both channels with the prior probabilities for final emotion classification.Extensive experiments—including cross-subject, cross-video-type, and5-fold cross-validation evaluations— on the public Mahnob-HCI, VLMED,and SEED-IV datasets demonstrate that the proposed method outperformsexisting approaches.

Trichloroethylene (TCE) is an organic solvent with various industrial applications. Therefore, the study aimed to determine the effects of TCE on cytotoxicity, apoptosis, reactive oxygen species (ROS) production, global histone modifications, and regulation in microRNAs (miRNAs) related to cancer pathways in human embryonic kidney cells (HEK‐293) after exposure to TCE at concentrations of 0.03, 0.1, and 0.3 mM for 24 h. Results indicated that TCE caused dose‐ dependent cytotoxicity without induction of significant apoptosis or ROS production at concentrations of ≤ 0.3 mM. Upregulation in myc , pten , and mgmt and downregulation in ctnb1 , cd44 , and cdkn2a genes involved in cell cycle regulation and proliferation were detected. TCE decreased the expression of the ezh2 gene and increased the expression of riz1 and hat1 genes, which are associated with chromatin‐modifying enzymes. Additionally, the levels of H3K27me3, H3K4me3, and H3K9me3 changed significantly. However, the alterations in global levels of H3K9ac were insignificant. TCE significantly altered the expression of approximately 25% of miRNAs related to cancer pathway in the miRNA array panel, as it upregulated 19 miRNAs and downregulated 4 miRNAs of the tested 84 miRNAs. Considering the effects on chromatin modification, proliferation rate, and miRNAs, it can be concluded that these mechanisms may be involved in TCE‐induced nephrotoxicity.