The present invention relates to compounds of formula I: in which A.sup.1-A.sup.7 and R.sup.1 to R.sup.5 are defined herein, for use in the treatment of a condition or disease which is alleviated by the activation of retinoic acid receptors (RAR). The invention also relates to pharmaceutical compounds comprising such compounds, and related methods of treatment. In an aspect, the invention relates to a method of screening compounds for therapeutic potential in the treatment of a condition or disease which is alleviated by the activation of retinoic acid receptors (RAR). Aspects of the invention relate to novel compounds of formula I in which at least one of A.sup.1 to A.sup.3 is or at least one of A.sup.4 is CR.sup.12 or A.sup.5 is CR.sup.13 in which R.sup.12/R.sup.13 is halogen.

A novel omega-3 fatty acid/lipid-based nutraceutical composition and a method of optimizing said omega-3 fatty acid/lipid-based nutraceutical composition. The nutraceutical composition and method is based on the insight that different forms of high omega-3 fatty acid lipids (e.g. triglyceride form, ethyl ester form, free fatty acid form, phospholipid form) have different molecular modes and levels of action. Specifically, the phospholipid form is likely more effective at promoting membrane fluidity and permeability, while the free fatty acid form is likely more effective at regulating cell receptors, such as the PPARa receptors, that are responsible for various metabolic effects including lipid metabolism. The desirability of producing omega-3 compositions that may act synergistically and thus more robustly to improve health and to some extent mimic markers of life extension such as shown by caloric restriction, along with specific optimization methods, markers, and compositions are taught.

The present disclosure provides a micro-organismal product and a method for treating a patient with sickle cell disease. In one aspect, the method comprises determining a concentration of one or more biological markers in serum of the patient indicative of breach of an intestinal barrier in sickle cell disease; and administering a micro-organismal product to the patient that restores intestinal permeability of the patient by, for example, upregulating tight-junctions of the patient's intestine.

Methods for using gene expression changes in response to drugs of abuse in human neural organoids to identify and predict susceptibility to drug abuse and develop therapeutic countermeasures are disclosed.

A method for determining predisposition of a subject to developing renal dysfunction (AKI), and to a kit for use in making such a determination is provided. Suitably at least one marker selected from Midkine (MK) or H-FABP present in a blood or urine sample is used in the method.

The present invention relates to compositions and methods comprising a retinoic acid receptor inhibitor, a retinoic X receptor inhibitor or an inhibitor of an enzyme in the retinoic acid biosynthesis pathway for treatment of a patient having a solid tumor. In some embodiments, the solid tumor is a sarcoma.

The current disclosure provides specific peptides, and derived ionization characteristics of the peptides from the estrogen receptor (ER), progesterone receptor (PR), and/or antigen Ki67 (Ki67) proteins that are particularly advantageous for quantifying the ER, PR, and/or Ki67 proteins directly in biological samples that have been fixed in formalin by the method of Selected Reaction Monitoring/Multiple Reaction Monitoring (SRM/MRM) mass spectrometry. Such biological samples are chemically preserved and fixed wherein the biological sample is selected from tissues and cells treated with formaldehyde containing agents/fixatives including formalin-fixed tissue/cells, formalin-fixed/paraffin embedded (FFPE) tissue/cells, FFPE tissue blocks and cells from those blocks, and tissue culture cells that have been formalin fixed and or paraffin embedded. A protein sample is prepared from a biological sample using the Liquid Tissue reagents and protocol, and the ER, PR, and/or Ki67 proteins are quantitated in the Liquid Tissue sample by the method of SRM/MRM mass spectrometry by quantitating in the protein sample at least one or more of the peptides described for one or more of the ER, PR, and/or Ki67 proteins. These peptides can be quantitated if they reside in a modified or in an unmodified form. An example of a modified form of an ER, PR, and/or Ki67 peptide is phosphorylation of a tyrosine, threonine, serine, and/or other amino acid residues within the peptide sequence.

The present disclosure provides compositions and methods for the treatment of PPARG activated cancer. For example, the present disclosure provides PPARG signaling modulators for the treatment of bladder cancer. In particular, therapeutic and/or prophylactic compositions and uses of PPARG inverse-agonists are described.

Disclosed are a kit for testing myocardial infarction rapidly and a preparation method and use thereof. The kit comprises a strip capable of detecting three markers, namely, human myeloperoxidase (MPO), heart-fatty acid binding protein (FABP3) and cardiac troponin I (cTnI) simultaneously. The strip comprises a sample pad, a conjugate pad, a chromatographic membrane coated with three test lines and a quality control line, and a sample absorption pad. Antibodies of the three markers are all marked on the conjugate pad. The chromatographic membrane has three test lines formed by coating paired antibodies of the three markers respectively, the paired antibodies of the three markers being able to specifically combine with the three markers, respectively. The kit has advantages such as convenient operation, rapid response, high sensitivity and high specificity, point of care test, and economical and practical etc.

A method for identifying an AhR-phospho-RORt protein complex inhibitor, comprising: (a) providing a cell culture, in which cells in the culture express AhR protein and phospho-RORt protein; (b) incubating the cell culture in the presence of a test agent; (c) assaying the level of the AhR-phospho-RORt protein complex in the presence of the test agent; (d) comparing the level of the AhR-phospho-RORt 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-RORt protein complex when the comparing step indicates that there is a reduction in the level of the AhR-phospho-RORt protein complex in the presence of the test agent as compared with the control. A method for identifying a GLKIQGAP1 protein complex inhibitor is also disclosed. Use of identified inhibitors in the manufacture of a medicament for treating a disease is also disclosed.