Abstract: The present invention provides compositions and methods for inhibiting Dkk-1 for treating or preventing an inflammatory or inflammatory-related disease or disorder.

Abstract: The present invention provides compositions and methods for inhibiting Dkk-1 for treating or preventing an inflammatory or inflammatory-related disease or disorder.

Abstract: Antimicrobial compositions including a cell penetrating peptide (CPP) having the amino acid sequence Tyr-Ala-Arg-Val-Arg-Arg-Arg-Gly-Pro-Arg-Gly-Tyr-Ala-Arg-Val-Arg-Arg-Arg-Gly-Pro-Arg-Arg (SEQ ID NO:1) or variant thereof are disclosed. The CPP, which itself has antimicrobial properties, can be advantageously combined with or conjugated to a cargo to increase the delivery, efficacy, or combinations thereof, of the cargo into cells. In preferred embodiments, the CPP is combined with or conjugated to a functional nucleic acid, such as an external guide sequence (EGS) which can target and reduce expression of essential microbial genes or genes than impart resistance to antimicrobial drugs. Methods of using the compositions alone or in combination with traditional antimicrobial drugs to treat infections are also disclosed.

Abstract: Antimicrobial compositions including a cell penetrating peptide (CPP) having the amino acid sequence Tyr-Ala-Arg-Val-Arg-Arg-Arg-Gly-Pro-Arg-Gly-Tyr-Ala-Arg-Val-Arg-Arg-Arg-Gly-Pro-Arg-Arg (SEQ ID NO:1) or variant thereof are disclosed. The CPP, which itself has antimicrobial properties, can be advantageously combined with or conjugated to a cargo to increase the delivery, efficacy, or combinations thereof, of the cargo into cells. In preferred embodiments, the CPP is combined with or conjugated to a functional nucleic acid, such as an external guide sequence (EGS) which can target and reduce expression of essential microbial genes or genes than impart resistance to antimicrobial drugs. Methods of using the compositions alone or in combination with traditional antimicrobial drugs to treat infections are also disclosed.

Abstract: Clinical performance of currently available human skin equivalents is limited by failure to develop perfusion. To address this problem we have developed a method of endothelial cell transplantation that promotes vascularization of human skin equivalents in vivo. Living skin equivalents were constructed by sequentially seeding the apical and basal surfaces of acellular dermis with cultured human keratinocytes and Bcl-2 transduced HUVEC or umbilical cord cells sequentially. After orthotopic implantation of grafts comprising cultured human keratinocytes and Bcl-2 transduced HUVEC cells onto mice, the grafts displayed both a differentiated human epidermis and perfusion through the HUVEC-lined microvessels. These vessels, which showed evidence of progressive maturation, accelerated the rate of graft vascularization. Successful transplantation of such vascularized human skin equivalents should enhance clinical utility, especially in recipients with impaired angiogenesis.