Patents by Inventor Marjana Tomic
Marjana Tomic has filed for patents to protect the following inventions. This listing includes patent applications that are pending as well as patents that have already been granted by the United States Patent and Trademark Office (USPTO).
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Patent number: 9168214Abstract: It has been discovered that vascular endothelial growth factor (“VEGF”) promotes migration of activated (but not differentiating) keratinocytes to skin. This growth factor specifically increases migration of keratinocytes of the “wounded skin” phenotype but does not have significant effects upon differentiated keratinocytes. It also increases collagen deposition and reduces wrinkles, enhances skin quality, and increases skin thickness to normal levels in individuals where skin has thinned due to age or disorder such as diabetes. It is particularly well suited for use as cosmeceuticals when applied in purified form and in known amounts. The data presented in the examples demonstrate efficacy and specificity of VEGF in enhancing migration of normal human keratinocytes as well as formation of new granulation tissue including collagen formation. VEGF induces keratinocyte and fibroblast migration, formation of new tissue, and not only induces deposition of collagen but improves alignment of the collagen fibers.Type: GrantFiled: August 18, 2010Date of Patent: October 27, 2015Assignee: New York UniversityInventors: Harold Brem, Marjana Tomic-Canic
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Patent number: 8889615Abstract: Compositions for antagonizing phosphorylation and subsequent degradation of glycogen synthase kinase 3 beta (GSK3?) in epidermal cells are disclosed. GSK3? phosphorylation antagonists include molecules that function to inhibit or reduce the binding activity or enzymatic activity of an upstream signaling molecule leading to GSK3? phosphorylation, or by downregulating the expression of one or more upstream signaling molecules involved in regulating GSK3? phosphorylation. Methods of using the GSK3? phosphorylation antagonists to inhibit or reduce the phosphorylation and degradation of GSK3? in epidermal cells are provided. The methods are useful to promote epithelialization and closure of wounds, such as chronic non-healing wounds.Type: GrantFiled: December 29, 2010Date of Patent: November 18, 2014Assignee: New York UniversityInventors: Marjana Tomic-Canic, Harold Brem
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Patent number: 8802660Abstract: The present invention relates to methods and compositions that control, i.e., antagonize/inhibit or agonize/stimulate, de novo glucocorticoid production in the skin. Such methods and compositions can be used for the prevention and/or treatment of a variety of skin conditions, including inflammation, acute wounds, chronic non-healing wounds, keloid, fibrotic or hypertrophic scars, and epithelial-derived cancer.Type: GrantFiled: March 12, 2008Date of Patent: August 12, 2014Assignee: New York UniversityInventors: Marjana Tomic-Canic, Harold Brem, Herbert H. Samuels
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Patent number: 8673859Abstract: It has been discovered that granulocyte macrophage colony stimulating factor (“GM-CSF”) promotes migration of activated (but not differentiating) keratinocytes to wound sites. It was also discovered that GM-CSF increases the quantity and improves the quality of collagen. This growth factor specifically increases migration of keratinocytes of the “wound” phenotype but does not have significant effects upon differentiated keratinocytes. Examples demonstrate reversal of skin impairment in multiple animal models of diabetic skin imparment when provided in an effective amount over an effective time period. The examples also demonstrate the efficacy of the formulations in cosmetic applications.Type: GrantFiled: March 20, 2008Date of Patent: March 18, 2014Assignee: New York UniversityInventors: Harold Brem, Marjana Tomic
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Publication number: 20120289463Abstract: Compositions for antagonizing phosphorylation and subsequent degradation of glycogen synthase kinase 3 beta (GSK3?) in epidermal cells are disclosed. GSK3? phosphorylation antagonists include molecules that function to inhibit or reduce the binding activity or enzymatic activity of an upstream signaling molecule leading to GSK3? phosphorylation, or by downregulating the expression of one or more upstream signaling molecules involved in regulating GSK3? phosphorylation. Methods of using the GSK3? phosphorylation antagonists to inhibit or reduce the phosphorylation and degradation of GSK3? in epidermal cells are provided. The methods are useful to promote epithelialization and closure of wounds, such as chronic non-healing wounds.Type: ApplicationFiled: December 29, 2010Publication date: November 15, 2012Applicant: New York UniversityInventors: Marjana Tomic-Canic, Harold Brem
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Publication number: 20120052110Abstract: Provided herein are compositions and methods that inhibit expression of Adam12 gene products, such as ADAM12 mRNA and/or ADAM12 polypeptides, as a therapeutic approach for the treatment of, or promotion of healing of, wounds.Type: ApplicationFiled: August 4, 2011Publication date: March 1, 2012Applicant: Hospital for Special SurgeryInventors: Marjana TOMIC, Carl Peter Blobel, Asheesh Harsha
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Patent number: 8012947Abstract: Provided herein are compositions and methods that inhibit expression of Adam12 gene products, such as ADAM12 mRNA and/or ADAM12 polypeptides, as a therapeutic approach for the treatment of, or promotion of healing of, wounds.Type: GrantFiled: March 12, 2008Date of Patent: September 6, 2011Assignee: Hospital for Special SurgeryInventors: Marjana Tomic, Carl Peter Blobel, Asheesh Harsha
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Publication number: 20110190372Abstract: Compositions and methods for antagonizing miRNAs that are overexpressed in chronic, non-healing wounds, as compared to healthy tissue, are disclosed. The miRNA antagonists are oligonucleotides that hybridize to selected pre-miRNA or mature miRNAs and prevent the miRNAs from binding to and downregulating their target mRNAs. Methods of using the miRNA antagonists to treat inflammatory disorders, including to promote healing of chronic, non-healing wounds and acute wounds are provided.Type: ApplicationFiled: August 9, 2010Publication date: August 4, 2011Applicant: NEW YORK UNIVERSITYInventors: Marjana Tomic-Canic, Harold Brem
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Publication number: 20100310517Abstract: It has been discovered that vascular endothelial growth factor (“VEGF”) promotes migration of activated (but not differentiating) keratinocytes to skin. This growth factor specifically increases migration of keratinocytes of the “wounded skin” phenotype but does not have significant effects upon differentiated keratinocytes. It also increases collagen deposition and reduces wrinkles, enhances skin quality, and increases skin thickness to normal levels in individuals where skin has thinned due to age or disorder such as diabetes. It is particularly well suited for use as cosmeceuticals when applied in purified form and in known amounts. The data presented in the examples demonstrate efficacy and specificity of VEGF in enhancing migration of normal human keratinocytes as well as formation of new granulation tissue including collagen formation. VEGF induces keratinocyte and fibroblast migration, formation of new tissue, and not only induces deposition of collagen but improves alignment of the collagen fibers.Type: ApplicationFiled: August 18, 2010Publication date: December 9, 2010Inventors: Harold Brem, Marjana Tomic-Canic
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BIOLOGICAL MARKERS OF CHRONIC WOUND TISSUE AND METHODS OF USING FOR CRITERIA IN SURGICAL DEBRIDEMENT
Publication number: 20090203006Abstract: The present invention relates to methods for identifying tissue sites in a chronic wound that are suitable for debridement and whether debridement procedure has been successful using particular biological markers of the cells within the tissue sites of the chronic wounds.Type: ApplicationFiled: May 1, 2007Publication date: August 13, 2009Applicant: New York Society for the Ruptured and Crippled Maintaining the Hospital for Special SurgeryInventors: Harold Brem, Marjana Tomic-Canic -
Publication number: 20090191156Abstract: It has been discovered that granulocyte macrophage colony stimulating factor (“GM-CSF”) promotes migration of activated (but not differentiating) keratinocytes to wound sites. It was also discovered that GM-CSF increases the quantity and improves the quality of collagen. This growth factor specifically increases migration of keratinocytes of the “wound” phenotype but does not have significant effects upon differentiated keratinocytes. Examples demonstrate reversal of skin impairment in multiple animal models of diabetic skin imparment when provided in an effective amount over an effective time period. The examples also demonstrate the efficacy of the formulations in cosmetic applications.Type: ApplicationFiled: March 20, 2008Publication date: July 30, 2009Inventors: Harold Brem, Marjana Tomic
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Publication number: 20090068251Abstract: Provided herein are compositions and methods that inhibit expression of Adam12 gene products, such as ADAM12 mRNA and/or ADAM12 polypeptides, as a therapeutic approach for the treatment of, or promotion of healing of, wounds.Type: ApplicationFiled: March 12, 2008Publication date: March 12, 2009Applicant: Hospital for Special SurgeryInventors: Marjana TOMIC, Carl Peter Blobel, Asheesh Harsha
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Publication number: 20080274079Abstract: The present invention relates to methods and compositions that control, i.e., antagonize/inhibit or agonize/stimulate, de novo glucocorticoid production in the skin. Such methods and compositions can be used for the prevention and/or treatment of a variety of skin conditions, including inflammation, acute wounds, chronic non-healing wounds, keloid, fibrotic or hypertrophic scars, and epithelial-derived cancer.Type: ApplicationFiled: March 12, 2008Publication date: November 6, 2008Applicant: New York Society for the Ruptured and Crippled Maintaining the Hospital for Special SurgeryInventors: Marjana Tomic-Canic, Harold Brem
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Publication number: 20080234194Abstract: It has been discovered that vascular endothelial growth factor (“VEGF”) promotes migration of activated (but not differentiating) keratinocytes to skin. This growth factor specifically increases migration of keratinocytes of the “wounded skin” phenotype but does not have significant effects upon differentiated keratinocytes. It also increases collagen deposition and reduces wrinkles, enhances skin quality, and increases skin thickness to normal levels in individuals where skin has thinned due to age or disorder such as diabetes. It is particularly well suited for use as cosmeceuticals when applied in purified form and in known amounts. The data presented in the examples demonstrate efficacy and specificity of VEGF in enhancing migration of normal human keratinocytes as well as formation of new granulation tissue including collagen formation. VEGF induces keratinocyte and fibroblast migration, formation of new tissue, and not only induces deposition of collagen but improves alignment of the collagen fibers.Type: ApplicationFiled: March 20, 2008Publication date: September 25, 2008Inventors: Harold Brem, Marjana Tomic