43results about How to "Inhibit transcription" patented technology

New sub-monomer synthetic methods for the preparation of peptide nucleic acid oligomeric structures are disclosed that provide for the synthesis of both predefined sequence peptide nucleic acid oligomers as well as random sequence peptide nucleic acid oligomers. Further these methods also provide for the incorporation of peptide nucleic acid units or strings of such units with amino acids or strings of amino acids in chimeric peptide nucleic acid-amino acid compounds. Further disclosed are methods of making random libraries of peptide nucleic acids using the fully preformed monomers.

The present invention relates to bacterial luciferase transposon cassettes suitable for conferring bioluminescence properties on a Gram-positive bacteria, Gram-negative bacteria, and other organisms of interest. The invention further includes cells transformed with vectors carrying the transposon cassettes, cells whose genomes have been modified by introduction of such cassettes, and methods of making and using such transposon cassettes, transposon cassette vectors, and cells containing the transposons.

This invention is a method of killing the stealthy intra-cellular bacteria which are key to the pathogenesis of both Acquired Immune Deficiency Syndrome(s) (AIDS) and Cancers. It is currently believed that the disease(s) known as AIDS are caused by a virus, the Human Immunodeficiency Virus (HIV). But much of the long-term (chronic) destruction of the immune system in AIDS is actually caused by tiny, stealthy, antibiotic-resistant bacteria. The HIV virus weakens the immune system so that the stealthy bacteria can proliferate out-of-control, and the damage of AIDS is done just as much by these bacteria as by any virus. These very tiny L-form Cell-Wall-Deficient (CWD) antibiotic-resistant bacteria live within the cytoplasm of cells, including the phagocytic cells (e.g. monocytes, macrophages, lymphocytes, neutrophils and polymorphonuclear cells) of the immune system itself. The cellular proliferation in Cancer is catalysed the action of the same tiny L-form bacteria. They cause the cell nucleus to release mRNA signaling the Th1 cytokine cascade without the need for conventional signaling via, for example, CD4+ T-Lymphocytes. Some of these Cytokines and Chemokines, including, without limitation, Cellular Adhesion Molecule (CAM), create the environment which allows the cellular proliferation to start, and then allows the cancerous growth to gain a foothold in the body. Killing these stealthy pathogens removes the environment needed to initiate and feed the cellular proliferation commonly called ‘Cancer,’ and prevents the chronic phase of the disease AIDS. This invention achieves its objective partly by reducing the ability of these tiny L-form, intra-phagocytic bacteria to translate proteins within their 70S Ribosome. The 30S and 50S subunits of the bacterial ribosome are targeted both individually and collectively. Further, this invention activates the innate immune system with agonist(s) for the VDR Nuclear Receptor, and modulates the availability of endogenous ligands to the PPAR, GCR and CB1 receptors, conditioning the immune system to more easily recognize and kill these tiny bacterial pathogens.

The invention pertains to novel cyclin dependent kinase inhibitors (cdks) and specifically, but not exclusively, as inhibitors of cdk / cyclin complexes. As described herein, the inhibitors of this invention are capable of inhibiting the cell-cycle machinery and consequently may be useful in modulating cell-cycle progression, ultimately controlling cell growth and differentiation. Such compounds would be useful for treating subjects having disorders associated with excessive cell proliferation.