Described herein are methods for evaluating a cardiac preparation. The methods involve providing at least one sample comprising one or more cardiac cells, pacing the one or more cardiac cells at two or more fixed rates; and measuring a fixed response of the one or more cardiac cells at each of the two or more fixed rates. Also described herein are methods for evaluating the cardiac effect of a compound. The methods involve providing at least one sample comprising one or more cardiac cells; contacting each sample with the compound; pacing the one or more cardiac cells at two or more fixed rates; and measuring a fixed response of the one or more cardiac cells to the compound at each of the two or more fixed rates.

The present disclosure provides androgen receptor (AR) and phosphodiesterase 5 (PDE-5) inhibitor compounds and compositions including said compounds. The compounds can provide dual functionality for inhibiting AR and inhibiting PDE-5. The present disclosure also provides methods of using said compounds and compositions for inhibiting AR and PDE-5 in a biological system or sample. Also provided are methods of preparing said compounds and compositions, and synthetic precursors of said compounds.

A method for reducing pulmonary hypertension in a mammal that employs FK506 is provided. In certain embodiments, the method comprises administering FK506 to a mammal having pulmonary arterial hypertension associated with defective MBPR2 signaling at a dosage sufficient to reduce blood pressure in the pulmonary artery of the mammal.

The present disclosure relates to a composition for screening an intestinal environment-improving material and a screening method using the composition, and according to the composition and the method of the present disclosure, it is possible to provide an effective analysis method for screening a microbiota-improving candidate material in a personalized manner by providing a method for verifying personalized probiotics, prebiotics, foods, health functional foods and drugs under in vitro conditions based on microbiota and microbiota metabolites.

The present invention relates to compositions and methods for the immunomodulation mediated by the interaction of PD-L2 and RGMb.

A method for identifying an AhR-phospho-RORγt protein complex inhibitor, comprising: (a) providing a cell culture, in which cells in the culture express AhR protein and phospho-RORγt protein; (b) incubating the cell culture in the presence of a test agent; (c) assaying the level of the AhR-phospho-RORγt protein complex in the presence of the test agent; (d) comparing the level of the AhR-phospho-RORγt protein complex in the presence of the test agent with a control; and (e) identifying the test agent as the inhibitor of the AhR-phospho-RORγt protein complex when the comparing step indicates that there is a reduction in the level of the AhR-phospho-RORγt protein complex in the presence of the test agent as compared with the control. A method for identifying a GLK−IQGAP1 protein complex inhibitor is also disclosed. Use of identified inhibitors in the manufacture of a medicament for treating a disease is also disclosed.

Agents that specifically bind to an opioid receptor in a conformationally specific way can be used to induce a conformational change in the receptor. Such agents have therapeutic applications and can be used in X-ray crystallography studies of the receptor. Such agents can also be used to improve drug discovery via compound screening and/or structure-based drug design.

The invention, in some aspects relates to compositions and methods for altering cell activity and function and the introduction and use of light-activated ion channels.

The inventive concept discloses a time series quantification method of supravital dye uptake of a cell using a lens-free imaging system.

In cancers such as prostate cancer, the combination of PTEN loss and activation of Myc activates an adaptive stress response that enables tumor cells to escape the stress of massively upregulated protein synthesis. This pro-survival response is mediated by the PERK-phosphorylated eIF2α axis of the UPR adaptive response. Agents that disrupt PERK-eIF2α pathways disrupt the adaptive response and lead to cancer cell death from uncontrolled growth. For example, ISRIB and derivatives may be employed as therapeutic agents to disrupt PERK-mediated adaptive mechanisms. Additionally PTEN loss and activation of Myc provides a diagnostic marker that enables better prognosis and the selection of amenable treatments.