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Ambati, US

Anilkumar Ambati, Morrisville, NC US

Patent application numberDescriptionPublished
20090094329SOLUTION FOR MANAGING MULTIPLE RELATED DISCUSSION THREADS IN AN ONLINE COLLABORATION ENVIRONMENT - The present invention discloses a server-side collaboration system that includes a set of discussion threads, a server-side software component, and a server-side data store. The discussion threads can be managed by a collaboration session leader. The collaboration session leader can be a user authorized to define the topic, to create the plurality of discussion threads for the topic, and to assign a set of participants to each created discussion thread. The server-side software component can permit remotely located clients to post and view content by discussion thread during a real-time collaboration, which includes a text exchange capability. Client using participants can be restricted to posting content to discussion threads as authorized by the collaboration session leader. The server-side data store can maintain a viewable history of posted content organized by discussion thread.04-09-2009

Balamurali Ambati, Augusta, GA US

Patent application numberDescriptionPublished
20080318857Compositions and Methods for the Intracellular Disruption of Vegf and Vegfr-2 By Intraceptors - The present invention provides an intraceptor that interacts with and decreases activity of with VEGF and/or a VEGFR for the treatment of angiogenesis-related conditions. The present invention further provides pharmaceutical compositions, and methods of use thereof, for the treatment and prevention of an angiogenesis-related condition using said intraceptors. The invention further provides for nucleic acids encoding said intraceptors.12-25-2008

Balamurali K. Ambati, Sandy, UT US

Patent application numberDescriptionPublished
20110282328Intraocular Drug Delivery Device and Associated Methods - The present invention provides devices, systems, and methods for delivery of an active agent into the eye of a subject. In one aspect, for example, an ocular active agent delivery device (11-17-2011

Balamurali K. Ambati, Taylorsville, UT US

Patent application numberDescriptionPublished
20120089113INTRAOCULAR DRUG DELIVERY DEVICE AND ASSOCIATED METHODS - Devices, systems, and methods for delivery of an active agent into the eye of a subject can include an ocular active agent delivery device (04-12-2012

Jayakrishina Ambati, Lexington, KY US

Patent application numberDescriptionPublished
20090238793TOLL LIKE RECEPTOR (TLR) STIMULATION FOR OCULAR ANGIOGENESIS AND MACULAR DEGENERATION - Provided are methods and compositions for the treatment or prevention of ocular angiogenesis and neovascularization. Administration of stimulators of the TLR3 and TLR7 receptors, Trif or of IL-10 and IL-12 inhibits ocular angiogenesis. Furthermore, all siRNAs (both targeted and non-targeted) can inhibit ocular angiogenesis.09-24-2009

Jayakrishna Ambati, Lexington, KY US

Patent application numberDescriptionPublished
20080299130Methods And Compositions For The Treatment Of Ocular Neovascularization - The invention relates to compositions and methods for the treatment or prevention of ocular neovascularization by reducing macrophage infiltration into the eye. The compositions of the invention include an antagonist of MCP-1 and/or CCR2 that blocks MCP-1 binding to or activation of CCR2y.12-04-2008
20090123375CCR3 Inhibition for Ocular Angiogenesis and Macular Degeneration - Provided are methods and compositions for the treatment or prevention of ocular angiogenesis and neovascularization. Administration of inhibitors of the CCR3 receptor or its ligands eotaxin (CCL11), eotaxin-2 (CCL24) or eotaxin-3 (CCL26) inhibits ocular angiogenesis.05-14-2009
20090186376sVEGFR-2 AND ITS ROLE IN LYMPHANGIOGENESIS MODULATION - Disclosed herein are nucleic acid molecules comprising a nucleotide sequence of sVEGF-2, proteins encoded by those sequences and antibodies that bind to the protein. Also disclosed are methods for inhibiting or enhancing expression or activity of sVEGFR-2 and methods for inhibiting graft rejection, particularly cornea graph rejection. Also described are methods for inhibiting lymphangiogenesis and lymphatic endothelial cell proliferation by administering an effective amount of sVEGFR-2 and methods for treating lymphedema by inhibiting the activity of sVEGFR-2.07-23-2009
20090260091Methods and animal model for analyzing age-related macular degeneration - Methods for testing candidate drugs for treatment of age-related macular degeneration are provided. Ccl2-deficient, and Ccr2-deficient mice are used to determine the effect of candidate drugs and treatments on development of age-related macular degeneration. Also provided is a Ccl2-deficient, Ccr2-deficient dual knockout mouse, which is a useful animal model for age-related macular degeneration.10-15-2009
20110097390Ultra-Small RNAs as Toll-Like Receptor-3 Antagonists - Provided are methods and compositions for the treatment or prevention of macular degeneration or other diseases or disorders associated with activation of TLR04-28-2011
20110268723CCR3 Inhibition for Ocular Angiogenesis and Macular Degeneration - Provided are methods and compositions for the treatment or prevention of ocular angiogenesis and neovascularization. Administration of inhibitors of the CCR3 receptor or its ligands eotaxin (CCL11), eotaxin-2 (CCL24) or eotaxin-3 (CCL26) inhibits ocular angiogenesis.11-03-2011
20120064010CCR3 and its Ligands Are Therapeutic and Diagnostic Targets for Neovascular Age-Related Macular Degeneration - The results presented herein demonstrate the specific expression of CCR3 in CNV endothelial cells in humans with AMD, and despite the expression of its ligands, eotaxin-1, -2, and -3, neither eosinophils nor mast cells are present in human CNV. The genetic or pharmacological targeting of CCR3 or eotaxins as disclosed herein inhibited injury-induced CNV in mice. CNV suppression by CCR3 blockade was due to direct inhibition of endothelial cell proliferation, and was uncoupled from inflammation as it occurred in mice lacking eosinophils or mast cells and was independent of macrophage and neutrophil recruitment. CCR3 blockade was more effective at reducing CNV than vascular endothelial growth factor-A (VEGF-A) neutralization, which is currently in clinical use, and, unlike VEGF-A blockade, not toxic to the mouse retina. In vivo imaging with CCR3-targeting quantum dots located spontaneous CNV invisible to standard fluorescein angiography in mice before retinal invasion. CCR3 targeting is useful in reducing vision loss due to AMD through early detection and therapeutic angioinhibition.03-15-2012

Patent applications by Jayakrishna Ambati, Lexington, KY US