A Novel Secretome Biotherapeutic Influences Regeneration in Critical Size Bone Defects.

Severe traumatic injuries often result in critical size bone defects, which are unable to heal without treatment. Autologous grafting is the standard of care but requires additional surgeries for graft procurement. Amnion-derived multipotent progenitor cells release a secretome of biomolecules identified as integral to the process of bone regeneration and angiogenesis.

Amnion-derived multipotent progenitor cells inhibit blood monocyte differentiation into mature dendritic cells.

Cells derived from the placenta have become the focus of extensive research concerning their ability to be used for regenerative medicine or cellular therapies. In a previous study, we characterized amnion-derived multipotent progenitor cells, or AMP cells, by in vitro methods and showed they were able to inhibit antigen-specific T-cell proliferation in a cell-to-cell contact-dependent fashion. Here we examine specific mechanisms involved in immunomodulation by AMP cells.

Immunogenicity and immunomodulatory effects of amnion-derived multipotent progenitor cells.

This is the first study on the immunologic properties of a clinically relevant population of cells derived from the amnion of human placenta. Unlike other cells from the amnion, these amnion-derived multipotent progenitor cells (AMP cells), from human amnion, grow in serum-free conditions and have never been cultured in the presence of medium containing animal-derived components. This study reports the immunologic characteristics of AMP cells and their roles as immunomodulators.

Real time PCR assays to detect common mutations in the biotinidase gene and application of mutational analysis to newborn screening for biotinidase deficiency.

Biotinidase deficiency is an autosomal recessive disorder of biotin metabolism caused by defects in the biotinidase gene. Symptoms of biotinidase deficiency are resolved or prevented with oral biotin supplementation and as such newborn screening is performed to prospectively identify affected individuals prior to the onset of symptoms. Biotinidase deficiency is detected by determining the activity of the biotinidase enzyme utilizing the newborn dried blood spot and colorimetric end point analysis.

Analysis of common mutations in the galactose-1-phosphate uridyl transferase gene: new assays to increase the sensitivity and specificity of newborn screening for galactosemia.

Classical galactosemia is a genetic disease caused by mutations in the galactose-1-phosphate uridyl transferase (GALT) gene. Prospective newborn screening for galactosemia is routine and utilizes the universally collected newborn dried blood specimen on filter paper. Screening for galactosemia is achieved through analysis of total galactose (galactose and galactose-1-phosphate) and/or determining the activity of the GALT enzyme.