The present invention provides a method of quantifying miR-185 as a potential biomarker in lipid disorder or cardiovascular diseases in human. The present invention also provides a method of modulating miR-185 in regulating LDL and cholesterol metabolism in cells. The present invention has therapeutic potential in the treatment of cholesterol/LDL related cardiovascular diseases in humans.

In certain embodiments, the present disclosure provides compounds and methods of increasing the amount or activity of a target protein in a cell. In certain embodiments, the compounds comprise a translation suppression element inhibitor. In certain embodiments, the translation suppression element inhibitor is a uORF inhibitor. In certain embodiments, the uORF inhibitor is an antisense compound.

A method of producing induced exosomes, the method comprising: contacting an isolated population of stem cells with an amount of a prostaglandin E receptor 4 (EP4) antagonist effective for inducing release of exosomes, whereby induced exosomes are released from the stem cells, and isolating the induced exosomes.

Various aspects of the present invention relate to a method of treating cancer in a subject having cancer cells, wherein the cancer cells possess at least one growth hormone receptor, and wherein the method includes controlling an action of the growth hormone receptor. In various non-limiting embodiments, controlling an action of the growth hormone receptor may occur via knock down of the growth hormone receptor, or may be caused by inhibiting growth hormone action, such as via the use of antibodies directed against growth hormone or the growth hormone receptor. Methods may also relate to administering an antagonist of the growth hormone receptor, and administering at least one anti-tumor drug in concert with administration of the antagonist. Another aspect may include a method of maintaining an anti-tumor drug in cancer cells of a subject by controlling an action of at least one growth hormone receptor in the cancer cells.

As described below, the present invention features genetically modified immune cells having enhanced anti-neoplasia activity, resistance to immune suppression, and decreased risk of eliciting a graft versus host reaction, or a combination thereof. The present invention also features methods for producing and using these modified immune effector cells.

The present disclosure provides methods of identifying non-productive splice sites in target RNA transcripts and antisense oligonucleotides that increase the expression of said target RNA transcripts. In an embodiment, the target RNA transcript comprises ADAR, ARSA, ATPIA2, CACNAIA, DNMI, EIF2BI, EIF2B2, EIF2B5, IDUA, MFSD8, NF2, NPC1L PEXI, PRICKLE2, PRRT2, RAM, SETD5, SHANKS, SLC6A1, STXBPI, STX1B, and TCF4.

Embodiments of the present invention relate to use of a GP73 inhibitor in preparation of a drug for treating diabetes. In the embodiments of the present invention, the inventor finds that GP73 plays a key role in blood glucose regulation, and in particular, finds that soluble GP73 can specifically bind to glucagon to form a complex, enhances the blood glucose-rising function and gluconeogenesis function of glucagon and prolongs the half-life of glucagon; and finds soluble GP73 can activate the glucose production in liver and/or kidney and a gluconeogenesis signaling pathway in a glucagon-independent manner. Based on the blood glucose regulation effect of the GP73 described above, the inventor also proves through animal experiments: the GP73 inhibitor can reduce the blood glucose level and glycated hemoglobin level of diabetic mice and have a protective effect on islet β cells, and thereby having the effect of treating diabetes.

This disclosure relates to novel SARS-CoV-2 targeting sequences. Novel SARS-CoV-2 targeting oligonucleotides for the treatment of SARS-CoV-2 infection are also provided.

The present invention relates to a technique capable of treating a retinal neurodegenerative disease through regeneration of a retinal nerve by targeting Prox1 in the mammalian retina using an inhibitor which inhibits Prox1 expression or migration. According to the present invention, inducing the regeneration of the damaged retina in mammals, and thus can be commonly applied to the treatment of various retinal neurodegenerative diseases causing vision loss, and furthermore, when combining with a selective retinal nerve differentiation method or the like, it is expected that the method can be used for the development of an innovative retinal regeneration method capable of selectively regenerating only specific degenerating retinal neurons.

The present disclosure provides methods of treating a subject having decreased bone mineral density or at risk of developing decreased bone mineral density, and methods of identifying subjects having an increased risk of developing decreased bone mineral density.