Abstract: A portable temperature transfer device for transferring thermal energy to and/or from a laboratory plate is provided as well as its methods of use. The temperature transfer device comprises a base and a raised stage that comprises a thermal conductive material and an encasement that interfaces with the base to create a cavity that encloses a laboratory plate. The raised stage allows direct contact between individual wells of the laboratory plate and the temperature transfer device. The encasement completes the thermally conductive environment for the laboratory plate.

Abstract: The present invention provides a method of treating autoimmune diseases. In particular, it provides a method for the treatment of Crohn's disease or psoriasis comprising administering to a subject in need thereof a therapeutically effective amount of an antibody against interferon ?.

Abstract: The present invention concerns double-stranded NF-?B decoy oligodeoxynucleotide (NF-?B dsODN) molecules that contain a core sequence capable of specific binding to an NF-?B transcription factor. In a particular aspect, the invention concerns NF-?B decoy molecules that preferentially bind p50/p65 and/or cRel/p50 heterodimers over p50/p50 homodimers. In another aspect, the invention concerns NF-?B decoy molecules with improved binding affinity to p65.

Abstract: The present invention concerns double-stranded NF-?B decoy oligodeoxynucleotide (NF-?B dsODN) molecules that contain a core sequence capable of specific binding to an NF-?B transcription factor. In a particular aspect, the invention concerns NF-?B decoy molecules that preferentially bind p50/p65 and/or cRel/p50 heterodimers over p50/p50 homodimers. In another aspect, the invention concerns NF-?B decoy molecules with improved binding affinity to p65.

Abstract: The present invention concerns double-stranded NF-?B decoy oligodeoxynucleotide (NF-?B dsODN) molecules that contain a core sequence capable of specific binding to an NF-?B transcription factor. In a particular aspect, the invention concerns NF-?B decoy molecules that preferentially bind p50/p65 and/or cRel/p50 heterodimers over p50/p50 homodimers. In another aspect, the invention concerns NF-?B decoy molecules with improved binding affinity to p65.

Abstract: The present invention concerns methods and formulations for non-parental delivery of nucleic acid molecules to cells. In particular, the present invention relates to methods and formulations that enhance the transport of poly- and oligonucleotides across biological membranes.

Abstract: The present invention concerns double-stranded NF-?B decoy oligodeoxynucleotide (NF-?B dsODN) molecules that contain a core sequence capable of specific binding to an NF-?B transcription factor. In a particular aspect, the invention concerns NF-?B decoy molecules that preferentially bind p50/p65 and/or cRel/p50 heterodimers over p50/p50 homodimers. In another aspect, the invention concerns NF-?B decoy molecules with improved binding affinity to p65.

Abstract: The present invention provides a method of treating autoimmune diseases. In particular, it provides a method for the treatment of Crohn's disease or psoriasis comprising administering to a subject in need thereof a therapeutically effective amount of an antibody against interferon ?.

Abstract: The present invention provides a method of treating autoimmune diseases. In particular, it provides a method for the treatment of Crohn's disease or psoriasis comprising administering to a subject in need thereof a therapeutically effective amount of an antibody against interferon &ggr;.

Abstract: Methods and compositions are provided for the creation and screening of non-human animal models having chronic inflammation. Immunocompromised host animals are injected with a population of immunocompetent effector cells, depleted of CD25+ T cells. The effector cells are tolerant of the host major histocompatibility antigens, but reactive to at least one antigen present in the host animal. The transferred cells are preferably stimulated and localized by administration of an immunostimulant at a local site. The animals are useful for a variety of screening assays and for investigation into disease causes and pathways. A variety of chronic inflammatory diseases may be studied with this model, including psoriasis, rheumatoid arthritis, diabetes, inflammatory bowel disease and multiple sclerosis.

Abstract: Methods and compositions are provided for the creation and screening of non-human animal models having chronic inflammation. Immunocompromised host animals are injected with a population of immunocompetent effector cells, depleted of CD25+ T cells. The effector cells are tolerant of the host major histocompatibility antigens, but reactive to at least one antigen present in the host animal. The transferred cells are preferably stimulated and localized by administration of an immunostimulant at a local site. The animals are useful for a variety of screening assays and for investigation into disease causes and pathways. A variety of chronic inflammatory diseases may be studied with this model, including psoriasis, rheumatoid arthritis, diabetes, inflammatory bowel disease and multiple sclerosis.

Abstract: Methods and compositions are provided for the creation and screening of non-human animal models having many of the histologic characteristics of human psoriasis. Immunocompromised host animals are injected with a purified population of CD45Rb positive cells, which are tolerant of the host major histocompatibility antigens, but are mismatched at one or more minor antigens. The injected cells are stimulated with a pro-inflammatory cytokine, e.g. IL-12, and a polyclonal activating agent. The injected animals develop a chronic skin disorder that includes histological features observed in human psoriasis, e.g. rete pegs, severe acanthosis and infiltration of Th1 cells into the dermis.

Abstract: Methods and compositions are provided for the creation and screening of non-human animal models having many of the histologic characteristics of human psoriasis. Immunocompromised host animals are injected with a purified population of CD45Rb positive cells, which are tolerant of the host major histocompatibility antigens, but are mismatched at one or more minor antigens. The injected cells are stimulated with a pro-inflammatory cytokine, e.g. IL-12, and a polyclonal activating agent. The injected animals develop a chronic skin disorder that includes histological features observed in human psoriasis, e.g. rete pegs, severe acanthosis and infiltration of Th1 cells into the dermis.

Abstract: Methods and compositions are provided for the creation and screening of non-human animal models having many of the histologic characteristics of human psoriasis. Immunocompromised host animals are injected with a purified population of CD45Rb positive cells, which are tolerant of the host major histocompatibility antigens, but are mismatched at one or more minor antigens. The injected cells are stimulated with a pro-inflammatory cytokine, e.g. IL-12, and a polyclonal activating agent. The injected animals develop a chronic skin disorder that includes histological features observed in human psoriasis, e.g. rete pegs, severe acanthosis and infiltration of Th1 cells into the dermis.