Abstract: There is disclosed herein a computer-implemented system and method of providing wellness detect and response (WDR) security services for an enterprise, including computing, for the enterprise, a quantitative user-centric security posture, wherein computing the quantitative user-centric security posture comprises calculating, for a user, a quantitative user risk profile according to a combination of user role, user privileges, user behavior, and digital assets assigned to a user and owned by the enterprise.

Abstract: A computer-implemented method provides security services to an enterprise. The method computes, for a plurality of enterprise users, a plurality of user health scores based on respective protection statuses for a plurality of enterprise assets owned by respective users; computes, for the enterprise, an overall enterprise security status score based on the plurality of user health scores; graphically displays to an enterprise administrator the overall enterprise security status score; and presents to the enterprise administrator a plurality of action recommendations to improve the overall enterprise security status score.

Abstract: The present invention provides cell permeable NF-?B inhibitors consist of a polypeptide derived from the p65 subunit of NF-?B and a protein transduction domain derived from antennapedia third helix sequence. The inhibitor suppressed NF-?B activation induced by TNF, LPS, IL-1, okadaic acid, PMA, H2O2 and cigarette smoke condensate. NF-?B-regulated reporter gene expression induced by TNF, TNFR1, TRADD, TRAF2, NIK, IKK and p65 was suppressed by the inhibitor. The inhibitor enhanced TNF- and chemotherapeutic agent-induced apoptosis. Overall these results demonstrate a NF-?B inhibitor that can selectively inhibit NF-?B activation induced by various inflammatory stimuli, down-regulate NF-?B mediated gene expression and upregulate apoptosis.

Abstract: The present invention provides cell permeable NF-?B inhibitors consist of a polypeptide derived from the p65 subunit of NF-?B and a protein transduction domain derived from antennapedia third helix sequence. The inhibitor suppressed NF-?B activation induced by TNF, LPS, IL-1, okadaic acid, PMA, H2O2 and cigarette smoke condensate. NF-?B-regulated reporter gene expression induced by TNF, TNFR1, TRADD, TRAF2, NIK, IKK and p65 was suppressed by the inhibitor. The inhibitor enhanced TNF- and chemotherapeutic agent-induced apoptosis. Overall these results demonstrate a NF-?B inhibitor that can selectively inhibit NF-?B activation induced by various inflammatory stimuli, downregulate NF-?B mediated gene expression and upregulate apoptosis.

Abstract: The present invention provides a RANK (receptor activator of NF-?B) inhibitor consisted of a TRAF-6 (TNF receptor-associated factor-6) binding domain attached to a leader sequence. The peptide inhibitor inhibits RANKL (RANK ligand)-mediated osteoclast differentiation, thus indicating that targeted disruption of interaction between RANK and TRAF6 may prove useful as a therapeutic for metabolic bone disorders, leukemia, arthritis, and metastatic cancer of the bone.

Abstract: The present invention provides cell permeable NF-?B inhibitors consist of a polypeptide derived from the p65 subunit of NF-?B and a protein transduction domain derived from antennapedia third helix sequence. The inhibitor suppressed NF-?B activation induced by TNF, LPS, IL-1, okadaic acid, PMA, H2O2 and cigarette smoke condensate. NF-?B-regulated reporter gene expression induced by TNF, TNFR1, TRADD, TRAF2, NIK, IKK and p65 was suppressed by the inhibitor. The inhibitor enhanced TNF- and chemotherapeutic agent-induced apoptosis. Overall these results demonstrate a NF-?B inhibitor that can selectively inhibit NF-?B activation induced by various inflammatory stimuli, downregulate NF-?B mediated gene expression and upregulate apoptosis.

Abstract: The present invention provides methods for producing exogenous and chimeric antibodies in avians. One aspect of the present invention is a method of producing avians or avian cells lacking endogenous immunoglobulin light chain and heavy chain loci, or portions thereof, and having at least a portion of at least one exogenous immunoglobulin locus. The present invention provides a method for obtaining an avian cell with a deletion in an endogenous immunoglobulin locus by by introducing a targeting construct comprising two regions of sequences which are homologous to the 5′ and 3′ flanking sequences of the region to be deleted in the wild-type locus. In addition, the invention provides methods for inserting exogenous immunoglobulin gene loci into the genome of an avian cell. A second aspect of the invention is the generation of transgenic avian species or transgenic avian cells for producing chimeric antibodies.

Abstract: The present invention provides a RANK (receptor activator of NF-&kgr;B) inhibitor consisted of a TRAF-6 (TNF receptor-associated factor-6) binding domain attached to a leader sequence. The decoy peptide inhibits RANKL (RANK ligand)-mediated osteoclast differentiation, thus indicating that targeted disruption of interaction between RANK and TRAF6 may prove useful as a therapeutic for metabolic bone disorders, leukemia, arthritis, and metastatic cancer of the bone.

Abstract: The present invention concerns transgenic vertebrates that are useful in expressing proteins and in producing antibodies. The present invention discloses methods for producing vertebrates that are transgenic for a bacteriophage RNA polymerase. The present invention further discloses methods for the use of such transgenic vertebrates in protein expression and in antibody production.

Abstract: A method for diagnosing clinically distinct embryonal and alveolar subtypes of rhabdomyosarcoma, including contacting a reagent including an antibody that specifically binds myogenin with a sample that includes at least one rhabdomyosarcoma cell or at least one extract of at least one rhabdomyosarcoma cell, detecting the binding of the antibody to the sample to determine the presence, absence, or amount of myogenin in the sample, and diagnosing clinically distinct embryonal and alveolar subtypes of rhabdomyosarcoma, alveolar rhabdomyosarcoma having an increased amount of binding as compared to embryonal rhabdomyosarcoma.

Abstract: The present invention provides a RANK (receptor activator of NF-&kgr;B) inhibitor consisted of a TRAF-6 (TNF receptor-associated factor-6) binding domain attached to a leader sequence. The peptide inhibitor inhibits RANKL (RANK ligand)-mediated osteoclast differentiation, thus indicating that targeted disruption of interaction between RANK and TRAF6 may prove useful as a therapeutic for metabolic bone disorders, leukemia, arthritis, and metastatic cancer of the bone.

Abstract: The present invention provides methods for producing exogenous and chimeric antibodies in avians. One aspect of the present invention is a method of producing avians or avian cells lacking endogenous immunoglobulin light chain and heavy chain loci, or portions thereof, and having at least a portion of at least one exogenous immunoglobulin locus. The present invention provides a method for obtaining an avian cell with a deletion in an endogenous immunoglobulin locus by by introducing a targeting construct comprising two regions of sequences which are homologous to the 5′ and 3′ flanking sequences of the region to be deleted in the wild-type locus. In addition, the invention provides methods for inserting exogenous immunoglobulin gene loci into the genome of an avian cell. A second aspect of the invention is the generation of transgenic avian species or transgenic avian cells for producing chimeric antibodies.