Abstract: Methods, agents and compositions thereof for treating psoriatic arthritis (PsA) are encompassed herein.

Abstract: Methods, reagents and compositions thereof for predicting RA onset in susceptible individuals, diagnosing RA onset, and/or evaluating efficacy of a therapeutic regimen for treating RA are described herein. Determining the amount of a particular bacterial species comprising SEQ ID NO: 1, SEQ ID NO: 2, or SEQ ID NO: 3 (SEQ ID NO: 1+ bacteria) serves as a biomarker for the above indications.

Abstract: This disclosure relates to methods and kits for diagnosing osteoarthritis and for determining the progression of osteoarthritis in a subject.

Abstract: This application relates to methods and kits for detecting predisposition to increased risk for osteoarthritis associated conditions.

Abstract: Methods, reagents and compositions thereof for predicting RA onset in susceptible individuals, diagnosing RA onset, and/or evaluating efficacy of a therapeutic regimen for treating RA are described herein. Determining the amount of a particular bacterial species comprising SEQ ID NO: 1, SEQ ID NO: 2, or SEQ ID NO: 3 (SEQ ID NO: 1+bacteria) serves as a biomarker for the above indications.

Abstract: Methods, reagents and compositions thereof for predicting risk for NORA onset in susceptible individuals, diagnosing NORA onset, and/or evaluating efficacy of a therapeutic regimen for treating RA are described herein. Determining the amount of at least one of SEQ ID NOs: 1-19 and/or at least one of a KO presented in either of Tables S4 or S5 serves as a biomarker for the above indications.

Abstract: Methods, agents and compositions thereof for treating psoriatic arthritis (PsA) are encompassed herein.

Abstract: Methods, agents and compositions thereof for treating psoriatic arthritis (PsA) and psoriasis (Ps) are encompassed herein, as are methods for identifying pathogenic dysbiosis in a subject, the presence of which is a positive indicator of risk for developing PsA or of the presence of PsA in a subject with arthritic symptoms.

Abstract: This disclosure relates to methods and kits for diagnosing osteoarthritis and for determining the progression of osteoarthritis in a subject.

Abstract: This disclosure relates to methods and kits for diagnosing osteoarthritis and for determining the progression of osteoarthritis in a subject.

Abstract: Methods for identifying subjects having, or at risk for developing, osteoarthritis or other cartilage degenerative conditions by measuring levels of expression of F-spondin are provided. Assays, kits and methods for determining and assaying the presence of F-spondin in individual patients are disclosed. Oligonucleotide probes and primers for use in the assays, kits and methods are described. Assays and methods are disclosed for identifying candidate compounds that modulate F-spondin levels of expression and/or function or for determining and evaluating an individual's response to drugs and therapeutic agents, are provided. The invention further relates to the modulation of F-spondin, particularly the inhibition of F-spondin, for increasing or stimulating bone formation and/or growth and mediating the alleviation of bone disease, disorders or conditions.

Abstract: This disclosure relates to methods and kits for diagnosing osteoarthritis and for determining the progression of osteoarthritis in a subject.

Abstract: This application relates to methods and kits for detecting predisposition to increased risk for osteoarthritis associated conditions.

Abstract: Methods for identifying subjects having, or at risk for developing, osteoarthritis or other cartilage degenerative conditions by measuring levels of expression of F-spondin are provided. Assays, kits and methods for determining and assaying the presence of F-spondin in individual patients are disclosed. Oligonucleotide probes and primers for use in the assays, kits and methods are described. Assays and methods are disclosed for identifying candidate compounds that modulate F-spondin levels of expression and/or function or for determining and evaluating an individual's response to drugs and therapeutic agents, are provided. The invention further relates to the modulation of F-spondin, particularly the inhibition of F-spondin, for increasing or stimulating bone formation and/or growth and mediating the alleviation of bone disease, disorders or conditions.

Abstract: The invention is a method of inhibiting the production of nitric oxide (NO) in an in vivo, in vitro, or ex vivo biological system. The method employs a tetracycline compound to inhibit the production of NO and/or to inhibit the expression or activity of an inducible isoform of nitric oxide synthase (iNOS). Preferably, the tetracycline compound has inhibitory activity for metalloproteinases. Also it is preferred that the tetracycline compound is provided to the biological system in an amount which has little or no antibacterial activity in the system. Accordingly, preferred tetracycline compounds are tetracycline compounds which have be modified to reduce or eliminate their antimicrobial activity. The method can be used to treat medical conditions in mammals characterized by NO production mediated by iNOS, including, for example, inflammatory conditions.

Abstract: A method is disclosed for inhibiting endogenous production of nitric oxide (NO) in an in vivo, in vitro, or ex vivo mammalian system. The method employs a tetracycline compound to inhibit production of NO and/or to inhibit the expression or activity of an inducible isoform of nitric oxide synthase (iNOS). Preferably, the tetracycline compound has inhibitory activity for metalloproteinases. Also it is preferred that the tetracycline compound is provided to the mammalian system in an amount which has little or no antibacterial activity in the system. Accordingly, preferred tetracycline compounds are tetracycline compounds which have be modified to reduce or eliminate their antimicrobial activity. The method can be used to treat medical conditions in mammals characterized by NO production mediated by iNOS, including, for example, inflammatory conditions.

Abstract: An novel isoform of inducible nitric oxide synthase (OA-NOS) has been identified in osteoarthritis-affected articular cartilage. Some properties, including molecular weight, are similar to the constitutive isoform of neuronal nitric oxide synthase (ncnos) while other properties share similarity with the previously identified inducible nitric oxide (iNOS). Acetylating agents, such as aspirin and N-acetylimidazole act on both iNOS and OA-NOS by inhibiting their catalytic activities. A method is provided to screen for acetylating agents that inhibit OA-NOS, and the selective inhibition of OA-NOS by inhibitory agents is determined by comparison to a panel of different isoforms of nitric oxide synthase.