A medium composition, containing a basic fibroblast growth factor (bFGF) at not less than 150 ng/mL is useful for culturing cells.

The disclosure generally relates to methods for generating cardiac fibroblast cells from epicardial cardiac progenitor cells, populations of cardiac fibroblast cells and uses thereof.

The invention generally relates to collagen-binding agent compositions and methods of using the same. More specifically, the invention relates in part to new collagen-binding agent compositions and methods that may be used to treat damaged collagen within tissues or used to specifically target therapeutics to tissues containing undamaged or damaged collagen.

The present disclosure provides FGF1 mutant proteins having one or more mutations in the heparin binding domain. Such mutants may also have an N-terminal deletion, point mutation(s), or combinations thereof. In some examples, the mutant FGF1 proteins have reduced mitogenic activity. Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. The disclosed FGF1 mutants can reduce blood glucose in a mammal, and in some examples are used to treat a metabolic disorder.

Provided are a mutated nucleic acid molecule of a recombinant human-basic fibroblast growth factor (rh-bFGF), a pharmaceutical composition of the rh-bFGF, and a use thereof.

The present disclosure provides FGF2 mutant proteins, such as those having an N-terminal deletion, point mutation(s), or combinations thereof, which can reduce blood glucose in a mammal. Thus, the disclosed mutant FGF2 proteins can be used to treat one or more metabolic diseases. In some examples, mutant FGF2 proteins have reduced mitogenic activity. Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. Methods of using the disclosed molecules to reduce blood glucose levels, for example to treat a metabolic disorder are also provided.

The present invention relates to the development of stable mutants of FGF-1 and FGF-2. In particular, it relates to novel engineered FGF-1 and FGF-2 polypeptides as well as polynucleotides, DNA constructs, and vectors encoding such polypeptides. In another aspect, pharmaceutical compositions and hydrogels including the disclosed polypeptides, polynucleotides, DNA constructs, and vectors are provided. In a still further aspect, methods of treating conditions using the compositions disclosed herein are provided.

The present disclosure relates to nucleic acid vaccine compositions and methods for preventing or treating pathological conditions, such as cancer or infectious disease. Further, the disclosure provides methods for more efficient production of antigens via mRNA containing one or more non-conventional start codons to promote multiplex initiation of translation in eukaryotic cells.

[Object] To provide a gene transfer carrier that specifically accumulates only at a disease site even with systemic administration, has a high protein expression rate, and disappears from the disease site accompanying a cure, and a method for the treatment of an ischemic disease using same. [Solution means] The above-mentioned object has been accomplished by providing a gene transfer carrier formed from an anaerobic bacterium that can grow specifically at the site of an ischemic disease and can express at least one type of protein that is useful for the diagnosis or treatment of an ischemic disease, a pharmaceutical composition containing the gene transfer carrier, and a treatment method for an ischemic disease utilizing same.

The present invention provides methods for antigen and/or bioactive molecule delivery to antigen presenting cells utilizing ASC specks as vehicles; 1) the ASC speck composition is made of ASC protein(s) and the antigen and/or bioactive molecule(s) purified from cells as a compact micro-spherical structure; 2) purified micro-spherical ASC speck delivery vehicles are stable at 37° C. for more than 30 days; and 3) antigen and/or bioactive molecules carried by ASC specks can be efficiently phagocytosed by antigen presenting cells and their degradation in the lysosome allows antigen processing and presentation.