The invention relates to methods for predicting the in vivo nephrotoxicity of a drug substance, in particular a nucleic acid molecule such as a siRNA or an antisense oligonucleotide using an in vitro cell based assay measuring the levels of extracellular EGF as toxicity biomarker, potentially in combination with other biomarkers like ATP and KIM-1.

Provided herein are fragment length profiles of nucleic acid libraries, methods of generating fragment length profiles of nucleic acid libraries and methods of using fragment length profiles for diagnostics and/or prognostics. The application further provides methods, compositions and kits for determining the infection stage or the site of localization in a subject.

The present disclosure relates to the generation and uses of an improved set of biomarkers that are aryl hydrocarbon receptor (AHR) target genes, designated as “AHR biomarkers.” The AHR biomarkers described herein allow one to efficiently determine AHR activation groups and sub-groups, in particular for an improved classification of tumors. As used herein, AHR activation groups are called “AHR activation signatures”. The AHR biomarkers comprise markers that are important in diagnosis and therapy, for example for selecting patients for treatment with AHR activation modulating interventions, and monitoring of therapy response.

Disclosed are methods and articles (e.g., gene arrays or antibodies) for determining the progression or regression of liver fibrosis, for the diagnosis of liver disease, and for screening compounds for hepatotoxicity and efficacy against liver fibrosis. Related therapeutic methods also are disclosed.

A method and system for predicting liver injury in vivo due to hepatocyte damage by a test compound are provided. The method includes acquiring images of fluorescently stained cells obtained from a cell culture in which the cells have been treated with a dose-range of at least the test compound and its vehicle. The cells may be hepatic cells including primary or immortalized hepatocytes, hepatoma cells or induced pluripotent stem cell-derived hepatocyte-like cells. The acquired images are segmented. The method further includes extracting and analyzing one or more phenotypic features from the segmented images, wherein the one or more phenotypic features are selected from the group of intensity, textural, morphological, or ratiometric features consisting of (a) features of DNA, (b) features of RELA (NF-KB p65), and (c) features of actin filaments at different subcellular regions and d) features of cellular organelles and their substructures in the segmented images. Finally, the method includes normalizing results from the treated samples to vehicle controls and predicting the probability of liver injury by the test compound based on test compound-induced normalized changes of the extracted and selected phenotypic features using machine learning methods.

The present invention relates to a method for identifying agents which are capable of inducing respiratory sensitization in a mammal, and arrays and analytical kits for use in such methods.

An apoptosis regulatory gene is detected in an irradiated-thymic lymphoma cell by a method for detecting such an apoptosis regulatory gene in a low-dose-rate and low-level-irradiated thymic lymphoma cell of a mouse. This has an effect of revealing the function of an apoptosis regulatory gene by means of irradiation and providing a gene profile, by detecting an apoptosis regulatory gene detected in an irradiated-thymic lymphoma cell. The detected apoptosis regulatory gene is used to construct a gene profile that can assess the dose-response relationship of industrial and healthcare workers living in a low level-radiation environment. The detected apoptosis regulatory gene can be used as an index for evaluating the extent of cancer progression and the degree of treatment in patients with thymic lymphoma. The method for detecting such an apoptosis regulatory gene is used to prepare a composition for diagnosing thymic lymphoma and a diagnostic kit.

The present invention relates to three-dimensional (3D) tissue constructs and methods of using such 3D tissue constructs to screen for neurotoxic agents. In particular, provided herein are methods of producing and using complex, highly uniform human tissue models comprising physiologically relevant human cells, where the tissue models have the degree of sample uniformity and reproducibility required for use in quantitative high-throughput screening applications.

Disclosed are a CRISPR-Cas14a responsive photoelectrochemical sensing detection method and a kit for detecting T2 toxin, relating to the technical field of small molecule toxin detection; the detection method includes: (1) preparation of a magnetic probe; (2) electrode modification; (3) identification of magnetic beads; (4) SDA isothermal amplification; (5) cutting; (6) photoelectrochemical detection; and (7) standard curve plotting. According to the present application, using SDA to enlarge and amplify the signal isothermally, target is detected by Cas14a trans cleavage property and photoelectric signal with good stability, high specificity of reaction, high sensitivity.

Methods, systems, and kits with reagents for assessing genotoxicity, are disclosed herein. Genotoxicity and their mechanisms of action can be determined within a few days of a subjects exposure. Some embodiments of the technology are directed to utilizing Duplex Sequencing for assessing a genotoxic potential of a compound (e.g., a chemical compound) in an exposed subject. Other embodiments of the technology are directed to utilizing Duplex Sequencing for determining a mutation signature associated with a genotoxic agent; and/or a safe threshold level of genotoxin exposure. Additional embodiments of the technology are directed to identifying one or more genotoxic agents a subject may have been exposed to by comparing the subjects DNA mutation spectrum to the mutation spectra of known mutagenic compounds. Once a genotoxin exposure in a subject is identified, or confirmed, then a prophylactic, and/or inhibitory therapeutic course of treatment is provided.