The present disclosure relates to assays and methods for the detection of renal inflammation by measuring the level of P2Y14 and/or UDP-glucose in a sample from a subject, such as a urine sample. The present disclosure also relates to methods for the treatment of renal inflammation by administering a P2Y14 inhibitor.

The presently disclosed subject matter relates to methods of screening raw materials and pet food products to manufacture a palatable pet food product. The presently disclosed subject matter also relates to methods for identifying compounds that modulate the activity and/or expression of a bitter taste receptor.

This invention provides test methods and test kits for determination of T2R phenotype.

A modality for preventing or treating fibrotic diseases by identifying a marker protein for myofibroblasts is provided.

The present invention relates to prophylactic or therapeutic agents for fibrotic diseases, which contain an inhibitor of GPR176 as an active ingredient.

Provided herein are methods of determining binding kinetics of a ligand. In some embodiments, the methods include contacting the ligand with a first surface of a substrate, which first surface comprises an electrically conductive coating and a population of virions connected to the first surface via one or more linker moieties, wherein viral envelopes of the virions display one or more proteins that bind, or are capable of binding, to the ligand, applying an alternating current electric field to the substrate to induce the virions to oscillate proximal to the first surface of the substrate, and detecting changes in oscillation amplitudes of the virions over a duration. Related virion oscillator array devices, systems and computer readable media are also provided.

It is therefore the objective of the present invention to provide minigastrin derivates which further improve the accumulation in CCK-2 receptor positive tumours by simultaneously very low accumulation in other organs, e.g. the kidneys. This objective is achieved according to the present invention by a minigastrin derivate having the formula: X-Z-Ala-Tyr-Gly-Trp-Met-Asp-Phe-NH.sub.2 (Y), wherein at least one of the connecting or terminal amide bonds between, before or after the amino acids of the sequence Z, Ala, Tyr, Gly, Trp, Met, Asp, Phe and NH.sub.2 or Y (C-terminal) is replaced by a 1,4-disubstituted or a 1,5-disubstituted 1,2,3-triazole, while X stands for a chemical group attached to the peptide for the purpose of diagnostic and/or therapeutic intervention at CCK-2 receptor relevant diseases, Y stands for C-terminal modifications of the peptide, such as amide, primary and secondary amides, free carboxylic acids and carboxylic ester derivatives including but not limited to amides and esters derived from linear or branched alkyl-,alkenyl-, alkynyl- aromatic-, and heterocyclic alcohols, and Z stands for a linker or DGlu* wherein DGlu* stands for a chain of DGlu having 1 to 6 repetitions (-DGlu-to-DGlu-DGlu-DGlu-DGlu-DGlu-DGlu-). These minigastrin derivates have a high specific internalization, excellent IC.sub.50 values and sufficient plasma stability.

The present invention pertains to a method for identifying a compound that can be used in mitigating and/or the treatment of a disease associated with abnormal astrocytic function, said method comprising: (i) providing a compound; (ii) determining whether said compound is a ligand for the GPR81 receptor by determining said compound's binding energy with the GPR81 receptor using molecular dynamics (MD) simulations and comparing said binding energy to the binding energy determined for a reference compound (such as L-lactate) with the GPR81 receptor; and (iii) if said compound is determined to be a ligand for the GPR81 receptor, bringing said compound in contact with a living astrocyte and determining the cAMP level in said astrocyte contacted with said compound. The present invention further pertains to an agent elevating the cAMP level in astrocytes for use in mitigating and/or in the treatment of a disease associated with abnormal astrocytic function.

The present disclosure provides a newly conceived of platform for identifying novel pain and/or pruritus-inhibiting agents (e.g., small molecule compounds, peptides, antigen binding proteins (e.g., antibodies or antibody fragments) that are efficacious, safe, and non-addictive alternatives for pain and pruritus management in place of (or in some embodiments, in combination with) “first line” treatments, such as gabapentin, pregabalin, and opioids. The present disclosure also provides for a method of treating pain and/or a pruritus comprising administering a therapeutically effective amount of an agent that activates a G.sub.ai/o-coupled G-Protein Coupled Receptor (GPCR) that is selectively expressed in the nociceptor and/or pruriceptor neuron subtypes of the somatosensory neurons. The disclosure also provides a method of inhibiting a nociceptor and/or pruriceptor somatosensory neurons, comprising contacting the nociceptor and/or pruriceptor somatosensory neuron with an agonist of a G-Protein Coupled Receptor (GPCR) expressed on the nociceptor and/or pruriceptor somatosensory neuron.

Disclosed herein is a G protein-coupled receptor (GPCR) assay platform comprised of two complementary systems that equate dynamic intermolecular interactions between a receptor and transducer with more complex stimulus-response cascades in living cells. In the disclosed in vitro ADSoRB method, the forced dissociation of transducers like G protein heterotrimers from receptors alters receptor conformations and ligand interactions to simulate pathway activation in a cell. In the disclosed TRUPATH method, measuring the extent of engineered G protein heterotrimer complex dissociation provides single transducer resolution in a cell.

The present disclosure relates generally to compositions and methods for diagnosing or predicting autism spectrum disorder (ASD). The methods are based on the discovery that certain genes, such as SOD2, OXT, GPER, and ERRα, have different expression levels in CD34+ cells or MNCs in ASD patients as compared to individuals not having ASD. Once the ASD patient is identified or predicted, compositions and methods are also provided for preventing or treating the ASD.