Described herein are novel compositions comprising, for example, PDCL3 polypeptides having VEGFR-2 inhibitory activity, inhibitory PDCL3 antibodies and PDCL3-binding fragments thereof, or PDCL3 inhibitory nucleic acid molecules, and methods of their use in anti-angiogenesis and anti-tumor proliferation and invasiveness therapies, such as the treatment of cancer, as well as the treatment of those vascular diseases where pathological angiogenesis plays a role, such as in carotid artery disease, macular degeneration, and plaque neovascularization. Also described herein are novel compositions comprising engineered PDCL3 polypeptides having enhanced chaperone activity, recombinant cells comprising such engineered PDCL3 polypeptides having enhanced chaperone activity, and methods thereof for therapeutic protein production and in vitro protein synthesis.

Products, such as devices, prostheses, and materials, whose surfaces have been modified in order to impart beneficial properties to these products are disclosed. The surface-modified products have improved biocompatibility compared to a corresponding product that lacks the modification. Following implantation in a subject, the surface-modified products induce a lower foreign-body response, compared to a corresponding unmodified product.

Products, such as devices, prostheses, and materials, whose surfaces have been modified in order to impart beneficial properties to these products are disclosed. The surface-modified products have improved biocompatibility compared to a corresponding product that lacks the modification. Following implantation in a subject, the surface-modified products induce a lower foreign-body response, compared to a corresponding unmodified product.

The present invention relates in part to nucleic acids, including nucleic acids encoding proteins, therapeutics and cosmetics comprising nucleic acids, methods for delivering nucleic acids to cells, tissues, organs, and patients, methods for inducing cells to express proteins using nucleic acids, methods, kits and devices for transfecting, gene editing, and reprogramming cells, and cells, organisms, therapeutics, and cosmetics produced using these methods, kits, and devices.

The present invention relates in part to nucleic acids, including nucleic acids encoding proteins, therapeutics and cosmetics comprising nucleic acids, methods for delivering nucleic acids to cells, tissues, organs, and patients, methods for inducing cells to express proteins using nucleic acids, methods, kits and devices for transfecting, gene editing, and reprogramming cells, and cells, organisms, therapeutics, and cosmetics produced using these methods, kits, and devices.

The present invention relates to compounds for use in modulating the toll-like receptor 4 (TLR4) signaling pathway, as well as to a pharmaceutical composition comprising said compounds.

The present invention relates to compounds for use in modulating the toll-like receptor 4 (TLR4) signaling pathway, as well as to a pharmaceutical composition comprising said compounds.

The present invention provides a positively charged co-polymer for use as an antimicrobial agent,wherein said positively charged co-polymer is composed of amino acids and/or derivatives thereof and wherein at least 75 molar percent of said amino acids are selected from the group consisting of alanine, lysine, glutamate, arginine and tyrosine and/or derivatives thereof. The present invention also provides methods for treating, preventing or ameliorating a microbial infection comprising administration of positively charged random co-polymers as well as a pharmaceutical composition comprising said co-polymer. The invention further provides a kit of parts comprising the positively charged random co-polymer.

Stem cell-based therapies can potentially reverse organ dysfunction and diseases but the removal of impaired tissue and reactivation of the program leading to organ regeneration pose major challenges. In mice, a four-day fasting mimicking diet (FMD) induces a step-wise expression of Sox17 and Pdx-1, resembling that observed during pancreatic development and followed by Ngn3-driven generation of insulin-producing β-cells. FMD cycles restore insulin secretion and glucose homeostasis in both a type 2 and type 1 diabetes mouse models. In human type 1 diabetes pancreatic islets, fasting conditions reduce PKA and mTOR activity and induce Sox2 and Ngn3 expression and insulin production. The effects of the FMD are reversed by IGF-1 treatment and recapitulated by PKA and mTOR inhibition. These results indicate that a FMD promotes the reprogramming of pancreatic cells to restore insulin generation in islets from T1D patients and reverse both T1D and T2D phenotypes in mouse models.

Stem cell-based therapies can potentially reverse organ dysfunction and diseases but the removal of impaired tissue and reactivation of the program leading to organ regeneration pose major challenges. In mice, a four-day fasting mimicking diet (FMD) induces a step-wise expression of Sox17 and Pdx-1, resembling that observed during pancreatic development and followed by Ngn3-driven generation of insulin-producing β-cells. FMD cycles restore insulin secretion and glucose homeostasis in both a type 2 and type 1 diabetes mouse models. In human type 1 diabetes pancreatic islets, fasting conditions reduce PKA and mTOR activity and induce Sox2 and Ngn3 expression and insulin production. The effects of the FMD are reversed by IGF-1 treatment and recapitulated by PKA and mTOR inhibition. These results indicate that a FMD promotes the reprogramming of pancreatic cells to restore insulin generation in islets from T1D patients and reverse both T1D and T2D phenotypes in mouse models.