Disclosed herein are methods and compositions for the diagnosis and treatment of Vascular Associated Maculopathy, or a symptom thereof, in a subject. Disclosed herein are methods and compositions for the diagnosis and treatment of one or more symptoms associated with Vascular Associated Maculopathy Disclosed in a subject. Disclosed herein are methods and compositions for the diagnosis and treatment of severe maculopathy or late stage maculopathy in a subject. Disclosed herein are methods and compositions for the diagnosis and treatment of resolving aberrant choriocapillaris lobules in a subject.

Provides are approaches for anticancer and antiaging treatments by administration of reverse transcriptase (RT) activity inhibitors that function to inhibit RT encoded by ORF2 of LINE1, or any RT that can participate in transcriptional activation of retroelements. Also provided are approaches to discovery of new compounds that can inhibit RTs, and identifying individuals who would benefit from treatment with such RT inhibitors, and treating such individuals. The methods are applicable for use in populations of cancer cells, pre-cancerous cells, somatic cells, and combinations thereof. Also provided are methods for monitoring the efficacy of a treatment that inhibits development of resistance to pharmaceutical agents, methods for prophylaxis and/or therapy for a pathology correlated with accumulation of somatic cells capable of spontaneously generating genetic alterations independently of cell divisions, wherein such cells express functional LINE1 elements. Also provides are methods for treating and/or preventing age-related conditions in an individual by administering an agent capable of selectively killing the cells that exhibit genetic instability as evidenced by expression of functional LINE 1. Also provided are methods for sensitizing cancer cells to a chemotherapeutic agent by administering an RT inhibitor.

The present disclosure relates to a method of treating arthritis by targeting Tankyrase. The methods according to the present disclosure can be advantageously used for regeneration of cartilage tissue and for treating osteoarthritis by maximizing the matrix synthesis in cartilage by inhibition of Tankyrase and regulation of other proteins related therewith.

A method of treating a disease, condition or state characterized by an exacerbated immune response is disclosed. The method of treatment can include topoisomerase I inhibitors and pharmaceutical compositions comprising topoisomerase I inhibitors, which can be administered alone or in combination with another therapeutic agent. The method can be used to treat a range of diseases, disorders, conditions and states, including but not limited to sepsis, acute liver failure, and endotoxic and/or exotoxic shock. These diseases, disorders, conditions and states can be caused by a variety of microorganisms and/or portions of microorganisms including but not limited to Ebola virus, Lassa virus, Influenza virus, Legionella, lipopolysaccharide (LPS), and bacterial endotoxins/exotoxins.

The disclosure relates to treating and diagnosing telomere diseases, and methods of screening agents for treating and diagnosing telomere diseases.

The present invention refers to the use of protein kinase inhibitors and more specifically to the use of inhibitors of the protein kinase c-Jun amino terminal kinase, JNK inhibitor sequences, chimeric peptides, or of nucleic acids encoding same as well as pharmaceutical compositions containing same, for the treatment of various diseases or disorders strongly related to JNK signaling.

A method of treating systemic lupus erythematosus in a subject is provided in which a therapeutically effective amount of PIC1 is administered to the subject. A method of treating transfusion-related acute lung injury is also provided where a therapeutically effective amount of PIC1 is administered to the subject. PIC1 can modulate immune complex activation of the complement system and NET formation in the subject. PIC1 can also inhibit myeloperoxidase (MPO) activity in the subject.

This disclosure provides methods and pharmaceutical compositions for reducing or eliminating cardiotoxicity, particularly cardiotoxicity induced by a cancer treatment or other therapy. In some cases, the methods and compositions prevent or reduce cardiotoxicity caused by anthracycline treatment. The methods provided herein often comprise administering a protective agent such as myricetin, tricetin, robinetin, ficetin, vitexin, quercetin, dihydrorobinetin, kaempferol, 7,3′,4′,5′-tetrahydroxyflavone, and myricitrin in conjunction with the administration of a cancer drug or other treatment. They may comprise administering a protective agent in combination with dexrazoxane. The compositions provided herein include co-formulations of a protective agent with a different protective agent or with a cancer treatment (e.g., anthracycline drug).

Nucleic acids and proteins having a mutant MEK sequence, and methods concerning identification of patients having resistance to treatment with anti-cancer agents, specifically inhibitors of RAF or MEK are provided. Methods of treatment and for optimizing treatment for patients having a mutation in a MEK1 sequence are also provided.

A method comprising administering, to a subject in need thereof, an effective amount of a nucleotide effective to disrupt one or more pathways leading to sepsis. The nucleotide may be a nitric oxide disruptor effective to decrease the expression of inducible nitric oxide synthase. The nitric oxide disrupter may comprise a polynucleotide strand exhibiting at least 70% sequence identity to one of Sequence ID No. 1 through Sequence ID No. 47. Additionally or alternatively, the nucleotide may be an α disintegrin and metalloproteinase (ADAM) enzyme inhibitor effective to decrease the expression of ADAM enzyme. The ADAM enzyme inhibitor may comprise a polynucleotide strand exhibiting at least 70% sequence identity to one of Sequence ID No. 48 through Sequence ID No. 56.