Abstract: Administration of expressible polynucleotides encoding eukaryotic heat shock proteins to mammalian cells leads to the stimulation of an immune response to antigens present in those cells. This makes it possible to stimulate an immune response to target antigens, including target tumor antigens or antigens associated with an infectious disease, without having to isolate a unique antigen or antigen-associated with an infectious disease, without having to isolate a unique antigen or antigen-associated heat shock protein for each target antigen by administering to a mammalian subject or to a group of mammalian cells containing the antigen, an expressible polynucleotide encoding a heat shock protein. The expressed heat shock protein may have the same structure as native heat shock proteins, or may have a modified form adapted to control the trafficking of the expressed heat shock protein within the cells.

Abstract: An intact, assembled T cell receptor (TcR) in soluble form is provided. The soluble TcR is prepared by splicing the extracellular domains of a T cell receptor to the glycosyl phosphatidylinositol (GPI) membrane anchor sequences of Thy-1. The molecule is expressed in the absence of CD3 on the cell surface, and can be cleaved from the membrane by treatment with phosphatidylinositol specific phospholipase C (PI-PLC). The .alpha. and .beta. chains of the soluble molecule are paired in the native conformation as judged by reactivity with the anti-V.sub..beta. 8 monoclonal antibody F23.1, and with the anti-clonotypic monoclonal antibody 1B2. The soluble TcR is a disulfide linked dimer with a molecular mass of 95 kDa on SDS-PAGE under nonreducing conditions, and 47 kDa after reduction.

Abstract: The present invention relates to chimeric antibodies which comprise a B cell epitope, a T cell epitope, and/or an antigen binding site. The chimeric antibodies may be produced by replacing at least a portion of an immunoglobulin molecule with the desired epitope or antigen binding site such that the functional capabilities of the epitope and the parent immunoglobulin are retained. The chimeric antibodies of the invention may be used to enhance an immune response against pathogens and tumor cells in subjects in need of such treatment.

Abstract: The present invention relates to methods and compositions for delivery of a compound, most preferably a polynucleotide, into the cytoplasm of a cell by means of a microparticle, fabricated from a pH-sensitive hydrogel in collapsed phase, and having a size and physical characteristics compatible with uptake via a clathrin-coated pit on the cell surface. The trigger pH at which the hydrogel expands is lower than the physiological pH of the extracellular environment, allowing the microparticle, which comprises the compound to be delivered, to maintain its compact size prior to cellular uptake, thereby providing the additional benefit of protecting the comprised compound from degradation. This protective feature is particularly beneficial in embodiments in which a polynucleotide or a peptide is being delivered. Following uptake via a clathrin-coated pit, the microparticle then enters the intracellular endocytic pathway, where it is subjected to a progressive decrease in pH.

Abstract: The present invention relates to a method of treating and/or preventing gallstones comprising administering a therapeutically effective amount of dehydrocholic acid. It is based, at least in part, on the discovery that consistent usage of dehydrocholic acid resulted in the dissolution of gallstones and prevention, elimination and/or amelioration of biliary colic in four subjects.

Abstract: The present invention relates to the use of diquat bromide as a root control agent. It is based, at least in part, on the results of green house testing in which application of diquat bromide as a dense foam to tree roots resulted in the destruction of the test roots without causing damage to the upper portion of the trees. Without being bound to any particular theory, it is believed that by applying diquat bromide to produce a high local concentration on the target root, the inactivating effects of local organic substances are overcome, and the diquat bromide kills root tissue by its dessicating activity. The inactivation of diquat bromide by organic materials, under these circumstances, becomes an advantage, as it prevents toxic levels of diquat bromide from traveling downstream from the point of application.