Abstract: A device for presenting content to a user is utilized in combination with a general purpose computer. The computer has a processor, a computer communications interface, a computer memory and an operating system. The operating system has one or more file management tools. The device has a housing, a device communications interface and a device memory. The device memory comprises a boot partition which includes boot software. The boot software is copied from the device into the computer memory and is executed from the computer memory by the processor. The device memory also comprises a secure partition inaccessible by the file management tools and having content stored thereon. The device memory also comprises content delivery software, which is copied to the computer memory, and when executed by the processor from the computer memory can access the content from the secure partition and present it to the user as sensory data.

Abstract: The present invention provides cell populations that are enriched for mesendoderm and mesoderm, and cell populations that are enriched for endoderm. The cell populations of the invention are useful for generating cells for cell replacement therapy.

Abstract: The present invention provides a method for treating individuals affected with the acid sphingomyelinase-deficient forms of Niemann-Pick disease (i.e., Type A or Type B Niemann-Pick) by administering small molecules as specific molecular “chaperones” for the deficient acid sphingomyelinase (ASM) enzyme associated with the disease. The molecules are ceramide, sphingomyelin, or phosphonucleotide analogues.

Abstract: The present invention pertains to methods to promote outgrowth of, or extension across a substrate of, neuronal cells by inhibiting the interaction between the cytoplasmic tail of the L1-CAM cell surface adhesion molecule and the cytoskeletal protein ankyrin. The invention also pertains to a method to treat diseases characterized by axonal damage such as spinal cord injury, traumatic brain injury, stroke, and neurodegenerative disease by administration of novel peptides that inhibit the binding of the L1-CAM cytoplasmic tail to ankyrin, and to pharmaceutical compositions comprising such peptides. The invention further pertains to a method of blocking calcium flux to protect against neural cell death following stroke or traumatic head injury.

Abstract: Treatment methods and compositions for the treatment of fibrosis are provided. In some embodiments, these methods include augmentation of dendritic cells for treatment of fibrosis. In some embodiments, fms-like tyrosine kinase 3 ligand (Flt3L) is used for the treatment of fibrosis and/or the augmentation of dendritic cells. In certain embodiments, the invention relates to methods for the treatment of fibrosis using Flt3L-expanded dendritic cells. In certain embodiments, the fibrosis is hepatic or pulmonary fibrosis.

Abstract: Disclosed are methods of identifying and diagnosing certain types of cancers and pre-stages thereof in a patient by identifying alternatively spliced isoforms of wild type KLF6 (KLFwt), in particular anyone of the isoforms selected from the group consisting of: KLF6 splice variant-1 (KLF6SV1), KLF6 splice variant-2 (KLF6SV2), and KLF6 splice variant-3 (KLF6SV3). Also disclosed are methods diagnosing cancer using the polypeptides and polynucleotides identified herein, as well as methods of treating certain types of cancers by inhibiting polynucleotides and polypeptides identified herein.

Abstract: New hybrid or chimeric fusion polypeptide transcription regulators which induce interferon target gene expression are provided for use in anti-viral and anti-proliferative applications. The hybrid fusion proteins comprise the p48 interferon regulatory factor protein, or a functional portion thereof, fused to a transcriptional activation domain (TAD), or a functional portion thereof. More specifically, the p48 interferon regulatory factor protein is fused to a STAT transcriptional activation do main (TAD) (p48-STAT TAD). A particular p48-STAT TAD is p48-S2C, in which S2C is the TAD of STAT2. Another p48-TAD is p48-VP16 TAD, in which p48 is fused to the transcriptional activation domain of the VP16 protein of Herpes Simplex Virus (HSV). The p48-TAD nucleic acid sequences and encoded polypeptides can be employed for anti-viral treatment and for the treatment of cancers, tumors and neoplastic diseases.

Abstract: Mutations and polymorphisms in a particular gene, the capillary morphogenesis gene-2 (CMG-2) have been identified. The mutations have been associated with infantile systemic hyalinosis (ISH) and juvenile hyaline fibromatosis (JHF), as well as conditions associated with these disorders. Described herein are variant CMG-2 nucleic acids and variant CMG-2 polypeptides; cells comprising such variant CMG-2 nucleic acids and/or expressing variant CMG-2 polypeptides; and methods of diagnosing and treating such disorders and conditions. Variant CMG-2 proteins include those comprising one or more of E220X, G105D, L329, P257insC, I189T, A357P, and A322S. Variant CMG-2 nucleic acids include those encoding these mutant CMG-2 proteins, as well as silent mutations or polymorphisms.

Abstract: The present invention relates to the identification of host cell proteins that interact with viral proteins required for virus replication, and high throughput assays to identify compounds that interfere with the specific interaction between the viral and host cell protein. Interfering compounds that inhibit viral replication can be used therapeutically to treat viral infection. The invention is based, in part, on the Applicants' discovery of novel interactions between viral proteins and a human host cell proteins. One of these host cell proteins, referred to herein as NPI-1, interacts with influenza virus protein NP. Also, host cell proteins, referred to herein as NS1I-1 and NS1-BP interact with influenza virus protein NS1. In addition, host cell proteins containing WW domains that interact with viral proteins such as Rhabdoviral M protein are described.

Abstract: The present invention provides methods for adenoassociated virus-mediated site-specific integration of a transgene into a stem cell. Stem cells having a transgene integrated therein, and differentiated cells generated from the stem cells are also provided.

Abstract: A method of enhancing the activity of lysosomal ?-Galactosidase A (?-Gal A) in mammalian cells and for treatment of Fabry disease by administration of 1-deoxy-galactonojirimycin and related compounds.

Abstract: The present invention relates to novel therapies for cancer and, in particular, to therapies that are particularly suited to tumor cells resistant to other types of therapies, such as radiation therapy, chemotherapy, or a combinations thereof. The invention provides methods for identifying and implementing strategies to inhibit a transcription factor involved in promoting resistance and inhibition of apoptosis. The invention provides a compound that alters ATF2 activity, specifically amino-terminal fragments of ATF2 that retain the JNK binding domain. The invention provides methods for inhibiting tumor cell growth and for sensitizing tumor cells to apoptosis with such peptides.

Abstract: The present invention provides populations of human cardiovascular progenitor cells, methods of making such cells, and methods of using the cells for production of populations of cardiovascular colonies and populations of cardiomyocytes. Methods of cardiomyocytes replacement therapy are also provided.

Abstract: Compounds and methods of selectively inhibiting an immunoproteasome are described. Also described are methods of treating a cancer, an inflammation, and/or an autoimmune disease and methods of suppressing endogenous antigenic peptide generation by administering to a subject in need of treatment thereof a therapeutic amount of an immunoproteasome specific inhibitor.

Abstract: The present invention relates, in general, to attenuated negative-strand RNA viruses having an impaired ability to antagonize the cellular interferon (IFN) response, and the use of such attenuated viruses in vaccine and pharmaceutical formulations. The invention also relates to the development and use of IFN-deficient systems for selection of such attenuated viruses. In particular, the invention relates to attenuated influenza viruses having modifications to the NS1 gene that diminish or eliminate the ability of the NS1 gene product to antagonize the cellular IFN response. The mutant viruses replicate in vivo but demonstrate reduced pathogenicity, and therefore are well suited for live virus vaccines, and pharmaceutical formulations.

Abstract: The present invention relates to the discovery, identification and characterization of a receptor protein, referred to herein as T1R3, which is expressed in taste receptor cells and associated with the perception of bitter and sweet taste. The invention encompasses T1R3 nucleotides, host cell expression systems, T1R3 proteins, fusion protein, transgenic animals that express a T1R3 transgene, and recombinant “knock-out” animals that do not express T1R3. The invention further relates to methods for identifying modulators of the T1R3-mediated taste response and the use of such modulators to either inhibit or promote the perception of bitterness or sweetness. The modulators of T1R3 activity may be used as flavor enhancers in food, beverages and pharmaceuticals.

Abstract: The present invention provides cell populations that are enriched for mesendoderm and mesoderm, and cell populations that are enriched for endoderm. The cell populations of the invention are useful for generating cells for cell replacement therapy.

Abstract: The present invention relates to compounds and methods for treating cancers in which the autocrine Wnt canonical signaling pathway is activated. In particular, there is provided a method for inhibiting growth of a tumor cell or sensitizing a cancer cell to treatment by contacting such a tumor cell with a compound that alters Wnt signaling. The compound that alters Wnt signaling can be a Wnt antagonist, a Wnt receptor antagonist, or a combination thereof.

Abstract: Diagnostic and therapeutic applications for certain types of cancer and precancerous conditions, including those deriving from hematologic cells, are described. Of particular interest are those cancers and precancerous conditions associated with increased signaling in the RAS-MAP kinase pathway. The diagnostic and therapeutic applications described herein are based on certain mutations in the protein tyrosine phosphatase gene PTPN11 and its expression product, PTPN11, promoting a gain-of-function in PTPN11 activity. Also described are nucleotide sequences, amino acid sequences, probes, and primers related to PTPN11 and PTPN11 variants, and cells expressing such variants.

Abstract: The present invention relates to a method for diagnosing Alzheimer's disease and Parkinson's disease in a subject by analyzing the expression of Semaphorin 3 and downstream effectors. It also provides a method for identifying a substance useful in the prevention or treatment of Alzheimer's disease and Parkinson's disease, and a method of using such substance in the treatment of Alzheimer's disease and Parkinson's disease.