Abstract: A free radical quenching composition is disclosed comprising a liposome containing at least two antioxidants selected from the following group: beta-carotene, vitamin E, vitamin C, glutathione, niacin, and optionally at least one trace metal (Zn, Se, Cr, Cu, Mn). Also disclosed is a method for reducing the undesirable side effects of free radicals in a mammal by administering to a mammal in need of such antioxidants an effective amount of liposomes containing at least two antioxidants.

Abstract: The present invention provides novel conjugates of camptothecin compounds and long-chain unsaturated fatty acid. The novel conjugates can be used to treat mammalian cell proliferative diseases such as cancer.

Abstract: This invention relates to antisense oligonucleotides which modulate the expression of the ribonucleotide reductase or the secA genes in microorganisms. This invention is also related to methods of using such oligonucleotides in inhibiting the growth of microorganisms. These antisense oligonucleotides are particularly useful in treating pathological conditions in mammals which are mediated by the growth of microorganisms.

Abstract: In summary of this disclosure, the present invention provides a method of nucleic acid, including DNA, immunization of a host, including humans, against disease caused by infection by a strain of Chlamydia, specifically C. pneumoniae, employing a vector, containing a nucleotide sequence encoding an POMP91B precursor protein of a strain of Chlamydia pneumoniae and a promoter to effect expression of the POMP91B precursor gene in the host. Modifications are possible within the scope of this invention.

Abstract: The present invention provides novel aminoadamantane derivatives, methods of making the derivatives, compositions including the novel aminoadamantane derivatives, and methods for the treatment and prevention of neurological diseases using the derivatives and compositions.

Abstract: A method for producing analgesia or for neuroprotection in a mammal comprising administering a therapeutically effective amount of a conantokin to the mammal.

Abstract: In summary of this disclosure, the present invention provides a method of nucleic acid, including DNA, immunization of a host, including humans, against disease caused by infection by a strain of Chlamydia, specifically C. pneumoniae, employing a vector, containing a nucleotide sequence encoding a lorf2 protein of a strain of Chlamydia pneumoniae and a promoter to effect expression of the lorf2 gene in the host. Modifications are possible within the scope of this invention.

Abstract: In summary of this disclosure, the present invention provides a method of nucleic acid, including DNA, immunization of a host, including humans, against disease caused by infection by a strain of Chlamydia, specifically C. pneumoniae, employing a vector, containing a nucleotide sequence encoding an PilG-like protein of a strain of Chlamydia pneumoniae and a promoter to effect expression of the PilG-like gene in the host. Modifications are possible within the scope of this invention.

Abstract: The invention disclosed herein provides methods and compositions for the computer-assisted design of morphogen analogs. Practice of the invention is enabled by the use of at least a portion of the atomic co-ordinates defining the three-dimensional structure of human osteogenic protein-1 (hOP-1) as a starting point in the design of the morphogen analogs. In addition, the invention provides methods for producing morphogen analogs of interest, and methods for testing whether the resulting analogs mimic or agonize human OP-1-like biological activity. The invention also provides a family of morphogen analogs produced by such methods.

Abstract: Disclosed are methods of utilizing a morphogenically active fragment of 60A protein to induce tissue morphogenesis, including methods for increasing a progenitor cell population in a mammal, methods for stimulating progenitor cells to differentiate and maintain their differentiated phenotype in vivo or in vitro, methods for inducing tissue-specific growth in vivo and methods for the replacement of diseased or damaged tissue in vivo.

Abstract: Disclosed are a family of synthetic proteins having affinity for a preselected antigen. The proteins are characterized by one or more sequences of amino acids constituting a region which behaves as a biosynthetic antibody binding site (BABS). The sites comprise 1) non-covalently associated or disulfide bonded synthetic VH and VL dimers, 2) VH-VL or VL-VH single chains wherein the VH and VL are attached by a polypeptide linker, or 3) individual VH or VL domains. The binding domains comprise linked CDR and FR regions, which may be derived from separate immunoglobulins. The proteins may also include other polypeptide sequences which function e.g., as an enzyme, toxin, binding site, or site of attachment to an immobilization media or radioactive atom. Methods are disclosed for producing the proteins, for designing BABS having any specificity that can be elicited by in vivo generation of antibody, and for producing analogs thereof.

Abstract: The invention provides methods for alleviating immune cell mediated inflammatory responses to injury to mammalian tissue. The present methods make use of osteogenic protein 1(OP-1), which is appreciated herein as tissue morphogen, i.e., a substance competent to induce tissue-specific morphogenesis of mammalian body tissues in addition to bone and/or cartilage. Alternatively, the present methods make use of other naturally-occurring or biosynthetic proteins sharing a defined structural and functional relationship with OP-1 and thus appreciated herein also to be tissue morphogens. The invention is particularly adapted to alleviating tissue damage associated with ischemia-reperfusion injury or hyperoxia injury in mammals, including humans.

Abstract: Disclosed herein are methods and compositions for identifying morphogen analogs. The preferred methods and compositions relate to the discovery that morphogen upregulation of the mouse type X collagen promoter activity is mediated by a MEF-2 like sequence and requires an adjacent AP-1 sequence. Certain methods rest on the use of test cells comprising DNA defining a morphogen-responsive transcription activating element operatively associated with a reporter gene. Other methods rest on the use of DNAs for measuring morphogen-inducible DNA-binding. In certain preferred embodiments, the methods and DNAs involve an osteogenic protein 1 (OP-1) responsive transcription activating element. Substances that mediate interaction with and/or activate the OP-1 responsive transcription activating element are considered herein likely to be useful for reproducing in vivo effects of morphogens such as OP-1.

Abstract: The present invention relates to complexes of the CDK2 protein with proteins identified as interacting with CDK2 by a modified yeast two hybrid assay system. The proteins identified to interact with CDK2 are cyclin H, cyclin I, ERH, and two gene products, hsReq*-1 and hsReq*-2, which are splice variants of the gene hsReq. Thus, the invention provides complexes of CDK2 and cyclin H, cyclin I, ERH, hsReq*-1, and hsReq*-2, and derivatives, fragments and analogs thereof. The invention also provides nucleic acids encoding the hsReq*-1 and hsReq*-2, and proteins and derivatives, fragments and analogs thereof. Methods of screening the complexes for efficacy in treating and/or preventing certain diseases and disorders, particularly cancer, atherosclerosis and neurodegenerative disease are also provided.

Abstract: This invention relates to methods and compositions of controlling cell distribution within a bioartificial organ by exposing the cells to a treatment that inhibits cell proliferation, promotes cell differentiation, or affects cell attachment to a growth surface within the bioartificial organ. Such treatments include (1) genetically manipulating cells, (2) exposing the cells to a proliferation-inhibiting compound or a differentiation-inducing compound or removing the cells from exposure to a proliferation-stimulating compound or a differentiation-inhibiting compound; exposing the cells to irradiation, and (3) modifying a growth surface of the BAO with ECM molecules, molecules affecting cell proliferation or adhesion, or an inert scaffold, or a combination thereof. These treatments may be used in combination.