Abstract: A method of inhibiting hyperphosphorylation of the tau protein and/or a TLR4-mediated immune response is disclosed. The method contemplates administering to cells in recognized need thereof such as cells of the central nervous system a FLNA-binding effective amount of a FLNA-binding benzazocine-ring compound or a pharmaceutically acceptable salt thereof such as a) an opioid receptor antagonist compound or b) a mixed opioid receptor agonist and antagonist (agonist/antagonist) compound, c) an opioid receptor agonist compound or d) an enantiomer of an opioid receptor interacting compound, that binds to a pentapeptide of filamin A (FLNA) of SEQ ID NO: 1. The administered compound preferably contains at least four of the six pharmacophores of FIGS. 5-10.

Abstract: The present invention contemplates therapeutic compositions containing a fibrinogen homolog capable of binding to endothelial cells in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Also described are therapeutic compositions containing an ICAM-1 homolog capable of binding to fibrinogen in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Methods of inhibiting endothelial cell and fibrinogen mediated inflammation within a patient by administering a homolog of this invention are also contemplated.

Abstract: The present invention contemplates therapeutic compositions containing a fibrinogen homolog capable of binding to endothelial cells in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Also described are therapeutic compositions containing an ICAM-1 homolog capable of binding to fibrinogen in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Methods of inhibiting endothelial cell and fibrinogen mediated inflammation within a patient by administering a homolog of this invention are also contemplated.

Abstract: The present invention contemplates therapeutic compositions containing a fibrinogen homolog capable of binding to endothelial cells in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Also described are therapeutic compositions containing an ICAM-1 homolog capable of binding to fibrinogen in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Methods of inhibiting endothelial cell and fibrinogen mediated inflammation within a patient by administering a homolog of this invention are also contemplated.

Abstract: The present invention contemplates therapeutic compositions containing a fibrinogen homolog capable of binding to endothelial cells in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Also described are therapeutic compositions containing an ICAM-1 homolog capable of binding to fibrinogen in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Methods of inhibiting endothelial cell and fibrinogen mediated inflammation within a patient by administering a homolog of this invention are also contemplated.

Abstract: The present invention contemplates therapeutic compositions containing a fibrinogen homolog capable of binding to endothelial cells in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Also described are therapeutic compositions containing an ICAM-1 homolog capable of binding to fibrinogen in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Methods of inhibiting endothelial cell and fibrinogen mediated inflammation within a patient by administering a homolog of this invention are also contemplated.

Abstract: The present invention contemplates therapeutic compositions containing a fibrinogen homolog capable of binding to endothelial cells in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Also described are therapeutic compositions containing an ICAM-1 homolog capable of binding to fibrinogen in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Methods of inhibiting endothelial cell and fibrinogen mediated inflammation within a patient by administering a homolog of this invention are also contemplated.

Abstract: The present invention contemplates therapeutic compositions containing a fibrinogen homolog capable of binding to endothelial cells in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Also described are therapeutic compositions containing an ICAM-1 homolog capable of binding to fibrinogen in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Methods of inhibiting endothelial cell and fibrinogen mediated inflammation within a patient by administering a homolog of this invention are also contemplated.

Abstract: Polypeptides corresponding in amino acid residue sequence to T cell stimulating regions of the HBV nucleocapsid protein are disclosed. A method of enhancing the immunogenicity of a polypeptide immunogen comprising operatively linking the polypeptide through an amino acid residue side chain to core protein particles is also disclosed.

Abstract: The present invention contemplates a method for inducing a HIV neutralizing immune response using an OKT4A antibody molecule homolog as an immunogen. Vaccines for practicing an immunization method of this invention are also described.

Abstract: Polypeptides corresponding in amino acid residue sequence to T cell stimulating regions of the HBV nucleocapsid protein are disclosed. A method of enhancing the immunogenicity of a polypeptide immunogen comprising operatively linking the polypeptide through an amino acid residue side chain to core protein particles is also disclosed.

Abstract: Polypeptides corresponding in amino acid residue sequence to T cell stimulating regions of the HBV nucleocapsid protein are disclosed. A method of enhancing the immunogenicity of a polypeptide immunogen comprising operatively linking the polypeptide through an amino acid residue side chain to core protein particles is also disclosed.