Abstract: The invention is directed to novel methods for reducing the number of apoptotic cell deaths in a population of cells undergoing excessive cellular apoptosis. The invention is also directed to novel methods for preventing apoptotic cell death in a population of cells at risk for developing excessive cellular apoptosis. In particular, the invention is directed to novel methods for reducing or preventing excessive cellular apoptosis comprising exposing cells exhibiting or at risk for developing excessive cellular apoptosis to a novel cellular factor-containing composition called Amnion-derived Cellular Cytokine Solution (referred to herein as ACCS), which is obtained from the culturing of Amnion-derived Multipotent Progenitor (AMP) cells, or AMP cells.

Abstract: The invention is directed to methods of modulating ischemic injury in tissues and organs. The invention is further directed to methods of increasing time to ischemic injury in tissues and organs. Such methods utilize compositions comprising cells capable of modulating inflammatory responses, referred to herein as Inflammatory Response Modulating Cells (IRMCs). The IRMCs any be used directly or cell membranes derived from them may be used in practicing the methods of the invention. In addition, the IRMCs and IRMC membranes may be used alone or in combination with each other and/or in combination with various suitable active agents.

Abstract: The invention is directed to novel methods for modulating inflammatory and/or immune responses. Such methods utilize compositions comprising extraembryonic cells (herein referred to as EE cells) including but not limited to extraembryonic HLA-G positive cells (herein referred to as EHP cells) and amnion-derived multipotent progenitor cells (herein referred to as AMP cells); compositions comprising expanded EE cell populations, and/or cell lysates and/or conditioned media derived therefrom, alone or in combination with each other and/or in combination with various extracellular matrices and/or devices and/or other suitable active agents.

Abstract: The invention is directed to novel methods for modulating inflammatory and/or immune responses. Such methods utilize compositions comprising extraembryonic cells (herein referred to as EE cells) including but not limited to extraembryonic HLA-G positive cells (herein referred to as EHP cells) and amnion-derived multipotent progenitor cells (herein referred to as AMP cells); compositions comprising expanded EE cell populations, and/or cell lysates and/or conditioned media derived therefrom, alone or in combination with each other and/or in combination with various extracellular matrices and/or devices and/or other suitable active agents.

Abstract: The invention is directed to novel methods for modulating inflammatory and/or immune responses. Such methods utilize compositions comprising extraembryonic cells (herein referred to as EE cells) including but not limited to extraembryonic HLA-G positive cells (herein referred to as EHP cells) and amnion-derived multipotent progenitor cells (herein referred to as AMP cells); compositions comprising expanded EE cell populations, and/or cell lysates and/or conditioned media derived therefrom, alone or in combination with each other and/or in combination with various extracellular matrices and/or devices and/or other suitable active agents.

Abstract: The invention is directed to substantially purified amnion-derived cell populations, compositions comprising the substantially purified amnion-derived cell populations, and to methods of creating such substantially purified amnion-derived cell populations, as well as methods of use. The invention is further directed to antibodies, in particular, monoclonal antibodies, that bind to amnion-derived cells or, alternatively, to one or more amnion-derived cell surface protein markers. The invention is further directed to methods for producing the antibodies, methods for using the antibodies, and kits comprising the antibodies.

Abstract: The invention is directed to novel compositions and methods for modulating inflammatory and/or immune responses. Such novel compositions are derived from extraembryonic cells (herein referred to as EE cells) including but not limited to extraembryonic HLA-G positive cells (herein referred to as extraembryonic HLA-G positive or “EHP” cells) and Amnion-derived Multipotent Progenitor cells (herein referred to as AMP cells), alone or in combination with each other and/or in combination with various matrices and/or devices and/or other suitable active agents. The novel methods of modulating inflammatory and/or immune responses utilize such novel compositions.

Abstract: The invention is directed to substantially purified amnion-derived cell populations, compositions comprising the substantially purified amnion-derived cell populations, and to methods of creating such substantially purified amnion-derived cell populations, as well as methods of use. The invention is further directed to antibodies, in particular, monoclonal antibodies, that bind to amnion-derived cells or, alternatively, to one or more amnion-derived cell surface protein markers. The invention is further directed to methods for producing the antibodies, methods for using the antibodies, and kits comprising the antibodies.

Abstract: The invention is directed to substantially purified amnion-derived cell populations, compositions comprising the substantially purified amnion-derived cell populations, and to methods of creating such substantially purified amnion-derived cell populations, as well as methods of use. The invention is further directed to antibodies, in particular, monoclonal antibodies, that bind to amnion-derived cells or, alternatively, to one or more amnion-derived cell surface protein markers. The invention is further directed to methods for producing the antibodies, methods for using the antibodies, and kits comprising the antibodies.

Abstract: The invention is directed to novel methods for modulating inflammatory and/or immune responses. Such methods utilize compositions comprising extraembryonic cells (herein referred to as EE cells) including but not limited to extraembryonic HLA-G positive cells (herein referred to as EHP cells) and amnion-derived multipotent progenitor cells (herein referred to as AMP cells); compositions comprising expanded EE cell populations, and/or cell lysates and/or conditioned media derived therefrom, alone or in combination with each other and/or in combination with various extracellular matrices and/or devices and/or other suitable active agents.

Abstract: The invention is directed to novel methods for modulating inflammatory and/or immune responses. Such methods utilize compositions comprising extraembryonic cells (herein referred to as EE cells) including but not limited to extraembryonic HLA-G positive cells (herein referred to as EHP cells) and amnion-derived multipotent progenitor cells (herein referred to as AMP cells); compositions comprising expanded EE cell populations, and/or cell lysates and/or conditioned media derived therefrom, alone or in combination with each other and/or in combination with various extracellular matrices and/or devices and/or other suitable active agents.

Abstract: The invention is directed to novel methods for modulating inflammatory and/or immune responses. Such methods utilize compositions comprising extraembryonic cells (herein referred to as EE cells) including but not limited to extraembryonic HLA-G positive cells (herein referred to as EHP cells) and amnion-derived multipotent progenitor cells (herein referred to as AMP cells); compositions comprising expanded EE cell populations, and/or cell lysates and/or conditioned media derived therefrom, alone or in combination with each other and/or in combination with various extracellular matrices and/or devices and/or other suitable active agents.

Abstract: The invention is directed to methods of modulating ischemic injury in tissues and organs. The invention is further directed to methods of increasing time to ischemic injury in tissues and organs. Such methods utilize compositions comprising cells capable of modulating inflammatory responses, referred to herein as Inflammatory Response Modulating Cells (IRMCs). The IRMCs any be used directly or cell membranes derived from them may be used in practicing the methods of the invention. In addition, the IRMCs and IRMC membranes may be used alone or in combination with each other and/or in combination with various suitable active agents.

Abstract: The invention is directed to novel methods for modulating inflammatory and/or immune responses. Such methods utilize compositions comprising extraembryonic cells (herein referred to as EE cells) including but not limited to extraembryonic HLA-G positive cells (herein referred to as EHP cells) and amnion-derived multipotent progenitor cells (herein referred to as AMP cells); compositions comprising expanded EE cell populations, and/or cell lysates and/or conditioned media derived therefrom, alone or in combination with each other and/or in combination with various extracellular matrices and/or devices and/or other suitable active agents.

Abstract: The invention is directed to substantially purified amnion-derived cell populations, compositions comprising the substantially purified amnion-derived cell populations, and to methods of creating such substantially purified amnion-derived cell populations, as well as methods of use. The invention is further directed to antibodies, in particular, monoclonal antibodies, that bind to amnion-derived cells or, alternatively, to one or more amnion-derived cell surface protein markers. The invention is further directed to methods for producing the antibodies, methods for using the antibodies, and kits comprising the antibodies.

Abstract: The invention is directed to substantially purified amnion-derived cell populations, compositions comprising the substantially purified amnion-derived cell populations, and to methods of creating such substantially purified amnion-derived cell populations, as well as methods of use. The invention is further directed to antibodies, in particular, monoclonal antibodies, that bind to amnion-derived cells or, alternatively, to one or more amnion-derived cell surface protein markers. The invention is further directed to methods for producing the antibodies, methods for using the antibodies, and kits comprising the antibodies.

Abstract: The invention is directed to substantially purified amnion-derived cell populations, compositions comprising the substantially purified amnion-derived cell populations, and to methods of creating such substantially purified amnion-derived cell populations, as well as methods of use. The invention is further directed to antibodies, in particular, monoclonal antibodies, that bind to amnion-derived cells or, alternatively, to one or more amnion-derived cell surface protein markers. The invention is further directed to methods for producing the antibodies, methods for using the antibodies, and kits comprising the antibodies.

Abstract: Biotinidase deficiency is detected by determining the activity of the biotinidase enzyme utilizing a newborn dried blood spot and calorimetric end point analysis. The four mutations most commonly associated with complete biotinidase deficiency are G98: d7i3, Q456H, R538C, and the double mutation D444H:A171T. Partial biotinidase deficiency is almost universally attributed to the D444H mutation. To more effectively distinguish between profound and partial biotinidase deficiency, a panel of assays utilizing real time PCR and melting curve analysis is developed to detect those mutations listed above. In newborn screening for biotinidase deficiency, the analysis of common mutations is useful to distinguish between partial and complete enzyme deficiency. Combining biotinidase enzyme analysis with genotypic data also increases the sensitivity of screening for biotinidase deficiency and provides information useful to clinicians earlier than would otherwise be possible.

Abstract: A method is disclosed for detecting galactosemia-causing mutations in the GALT gene, comprising amplifying a portion of the GALT gene from isolated DNA and allowing a pair of labeled probes to hybridize to the portion. One of the labeled probes is adapted to match to a sequence that includes the galactosemia-causing mutation, and another of the labeled probes hybridizes to an adjacent sequence, thereby forming a hybrid. Melting curves of each hybrid are then analyzed, wherein peaks of the curves are produced at an acquired fluorescence and melting temperature, Tm; and a genotype is assigned based on the Tm of the hybrid. Resulting melting peaks are compared to reference sample peaks derived from samples characterized to contain the mutations, wherein the reference sample curves indicate a temperature change, &Dgr;Tm, between mutant and wild type peaks.