Patents by Inventor Kersti K. Linask

Kersti K. Linask 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).

  • Patent number: 9308210
    Abstract: The canonical Wnt signaling pathway is implicated in wound healing. Administration of a composition having myo-inositol and folic acid upregulates fibronectin and provides the greatest protection in an additive/synergistic manner against adverse Wnt/?-catenin-mediated effects on cell processes relating to cell differentiation, proliferation, and migration that relate to wound healing.
    Type: Grant
    Filed: November 10, 2014
    Date of Patent: April 12, 2016
    Assignee: University of South Florida
    Inventor: Kersti K. Linask
  • Publication number: 20150141430
    Abstract: The canonical Wnt signaling pathway is implicated in wound healing. Administration of a composition having myo-inositol and folic acid upregulates fibronectin and provides the greatest protection in an additive/synergistic manner against adverse Wnt/?-catenin-mediated effects on cell processes relating to cell differentiation, proliferation, and migration that relate to wound healing.
    Type: Application
    Filed: November 10, 2014
    Publication date: May 21, 2015
    Applicant: University of South Florida
    Inventor: Kersti K. Linask
  • Patent number: 8883744
    Abstract: The canonical Wnt signaling pathway is implicated in many disorders including neural tube defects, limb malformations, and heart defects, developmental disorders associated with alcohol exposure (fetal alcohol syndrome) or exposure to bipolar medications (i.e. lithium), wound healing, and Alzheimer's disease. Elevated plasma homocysteine (HCy), which results from folate (folic acid, FA) deficiency, the mood-stabilizing drug lithium (Li), and alcohol (ethanol) are linked to the induction of human congenital heart and neural tube defects. FA supplementation ameliorates the observed developmental errors in the Li-HCy, or alcohol-exposed mouse embryos and normalized heart function. Li, HCy or Wnt3A suppress Wnt-modulated Hex and Islet-1 expression. FA protects from the gene misexpression that is induced by all three factors. Administration of myo-inositol with FA synergistically enhances the protective effect.
    Type: Grant
    Filed: October 8, 2013
    Date of Patent: November 11, 2014
    Assignee: University of South Florida
    Inventor: Kersti K. Linask
  • Publication number: 20140094467
    Abstract: The canonical Wnt signaling pathway is implicated in many disorders including neural tube defects, limb malformations, and heart defects, developmental disorders associated with alcohol exposure (fetal alcohol syndrome) or exposure to bipolar medications (i.e. lithium), wound healing, and Alzheimer's disease. Elevated plasma homocysteine (HCy), which results from folate (folic acid, FA) deficiency, the mood-stabilizing drug lithium (Li), and alcohol (ethanol) are linked to the induction of human congenital heart and neural tube defects. FA supplementation ameliorates the observed developmental errors in the Li-HCy, or alcohol-exposed mouse embryos and normalized heart function. Li, HCy or Wnt3A suppress Wnt-modulated Hex and Islet-1 expression. FA protects from the gene misexpression that is induced by all three factors. Administration of myo-inositol with FA synergistically enhances the protective effect.
    Type: Application
    Filed: October 8, 2013
    Publication date: April 3, 2014
    Applicant: UNIVERSITY OF SOUTH FLORIDA
    Inventor: Kersti K. Linask
  • Publication number: 20120022007
    Abstract: The canonical Wnt signaling pathway is implicated in many disorders including neural tube defects, limb malformations, and heart defects, developmental disorders associated with alcohol exposure (fetal alcohol syndrome) or exposure to bipolar medications (i.e. lithium), wound healing, and Alzheimer's disease. Elevated plasma homocysteine (HCy), which results from folate (folic acid, FA) deficiency, the mood-stabilizing drug lithium (Li), and alcohol (ethanol) are linked to the induction of human congenital heart and neural tube defects. FA supplementation ameliorates the observed developmental errors in the Li-HCy, or alcohol-exposed mouse embryos and normalized heart function. Li, HCy or Wnt3A suppress Wnt-modulated Hex and Islet-1 expression. FA protects from the gene misexpression that is induced by all three factors. Administration of myo-inositol with FA synergistically enhances the protective effect.
    Type: Application
    Filed: September 6, 2011
    Publication date: January 26, 2012
    Applicant: UNIVERSITY OF SOUTH FLORIDA
    Inventor: Kersti K. Linask