Abstract: The present invention provides methods for treating glaucoma by administering compounds capable of stabilizing misprocessed or misfolded proteins that are responsible for the condition.

Abstract: The present invention provides a method for lowering intraocular pressure and providing neuroprotection to a patient in need thereof by administering a therapeutically effective amount of at least one non-nucleotide or non-protein agent that inhibits expression and/or signaling of connective tissue growth factor (CTGF).

Abstract: The present invention provides a method for lowering intraocular pressure and providing neuroprotection to a patient in need thereof by administering a therapeutically effective amount of at least one non-nucleotide or non-protein agent that inhibits expression and/or signaling of connective tissue growth factor (CTGF).

Abstract: The present invention provides a method for lowering intraocular pressure and providing neuroprotection to a patient in need thereof by administering a therapeutically effective amount of at least one non-nucleotide or non-protein agent that inhibits expression and/or signaling of connective tissue growth factor (CTGF).

Abstract: The invention concerns in one embodiment a method of treating glaucoma or elevated intraocular pressure comprising administering a pharmaceutically effective amount of a composition comprising at least one prenyltransferase inhibitor. In another embodiment, the invention concerns a composition for the treatment of elevated intraocular pressure and glaucoma comprising a pharmaceutically effective amount of a prenyltransferase inhibitor.

Abstract: The present invention provides methods for identifying a patient at risk for developing AMD by identifying the presence of the Y402H polymorphism or other at risk variants in the complement factor H gene. The present invention further provides methods for treating persons having AMD or at risk for developing AMD as a result of having the Y402H polymorphism or other at risk variants in the complement factor H gene.

Abstract: An ophthalmic pharmaceutical composition useful in the treatment of glaucoma and control of intraocular pressure comprising an effective amount of a selective modulator of ALK5 receptor activity is disclosed. Also disclosed is a method of treating glaucoma and controlling intraocular pressure comprising applying a therapeutically effective amount of a pharmaceutical composition comprising a selective modulator of ALK5 receptor activity to an affected eye of a patient.

Abstract: The present invention provides a method for lowering intraocular pressure and providing neuroprotection to a patient in need thereof by administering a therapeutically effective amount of at least one agent that inhibits binding and/or signaling of connective tissue growth factor (CTGF) via the TrkA/p75NTR receptor complex.

Abstract: RNA interference is provided for inhibition of ocular hypertension target mRNA expression for lowering elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension. Ocular hypertension targets include carbonic anhydrase II, IV, and XII; ?1- and ?2 adrenergic receptors; acetylcholinesterase; Na+/K+-ATPase; and Na—K-2Cl cotransporter. Ocular hypertension is treated by administering interfering RNAs of the present invention.

Abstract: RNA interference is provided for inhibition of ocular hypertension target mRNA expression for lowering elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension. Ocular hypertension targets include carbonic anhydrase II, IV, and XII; ?1- and ?2 adrenergic receptors; acetylcholinesterase; Na+/K+-ATPase; and Na—K-2Cl cotransporter. Ocular hypertension is treated by administering interfering RNAs of the present invention.

Abstract: RNA interference is provided for inhibition of connective tissue growth factor mRNA expression in ocular disorders involving CTGF expression. Ocular disorders involving aberrant CTGF expression include glaucoma, macular degeneration, diabetic retinopathy, choroidal neovascularization, proliferative vitreoretinopathy and wound healing. Such disorders are treated by administering interfering RNAs of the present invention.

Abstract: The present invention provides a method for lowering intraocular pressure and providing neuroprotection to a patient in need thereof by administering a therapeutically effective amount of at least one non-nucleotide or non-protein agent that inhibits expression and/or signaling of lysyl oxidase (LOX) or a lysyl oxidase-like protease (LOXL).

Abstract: Compositions containing inhibitors of cathepsin K (CTSK) expression and/or activity are provided. Methods for the treatment of glaucoma using the compositions of the invention are further provided.

Abstract: The use of HMG-CoA reductase inhibitors (e.g., statins) to treat glaucoma, control intraocular pressure, preserve the trabecular meshwork, protect against ocular neurodegeneration and/or protect against glaucomatous retinopathy is described. The preferred HMG-CoA reductase inhibitors, which are statins having an RI value of 0.2 to 0.7 (e.g., pravastatin), are administered via topical application to the affected eye(s) of the patient.

Abstract: The present invention provides a method for lowering intraocular pressure and providing neuroprotection to a patient in need thereof by administering a therapeutically effective amount of at least one non-nucleotide or non-protein agent that inhibits expression and/or signaling of connective tissue growth factor (CTGF).

Abstract: The short form version of c-Maf transcription factor is up-regulated in steroid-treated and transforming growth factor beta2-treated trabecular meshwork cells, and is present at elevated levels in glaucomatous versus normal trabecular meshwork cells and in glaucomatous versus normal optic nerve head tissue. Expression of short form c-Maf transcription factor under these conditions indicates a causal or effector role for the factor in primary open-angle and steroid-induced glaucoma pathogenesis. Antagonism of short form c-Maf transcription factor expression and/or activity in the trabecular meshwork or other ocular tissue is provided for inhibiting or alleviating glaucoma pathogenesis. Antagonists include cyclin-dependent kinase 2 inhibitors.

Abstract: A process for producing animal drinking water is provided. The process comprises flowing water through a fluid proportioning device, which comprises three or more fluid transferring devices, to create a downstream water and to actuate the fluid transferring devices; drawing three or more compounds each from a separate source and flowing each compound separately through one of the fluid transferring devices; and injecting the compounds into the downstream water. The fluid proportioning device further comprises a conduit to the inlet of each fluid transferring device, a conduit to the outlet of each fluid transferring device, a water inlet to the device, and a water outlet from the device in which the fluid transferring device is proportionally actuated by the flow of water through the device.