Abstract: Disclosed herein are methods for determining whether a PAR4 inhibitor should be administered to a human subject, the methods comprising administering a PAR4 inhibitor to a subject determined to have a “G” allele for a single-nucleotide polymorphism (SNP) at rs773902, and not administering a PAR4 inhibitor to a subject determined to have an “A” allele for the SNP at rs773902. A genotyping assay can be used to determine the SNP.

Abstract: Disclosed are anti-miR compositions and methods of use of the same for treatment of or reducing the occurrence of thrombosis and thrombosis related diseases and disorders by reducing platelet activation.

Abstract: The present invention provides fusion proteins that act on the glucocorticoid-induced TNFR family-related gene (GITR) and OX40 signaling pathway. In certain aspects, the proteins of the invention are useful in modulating both regulatory T (Treg) cells and effector T (Teff) cells.

Abstract: Methods and systems include a long-term implantable ultra-filtrate monitoring system that uses micro-porous membranes to produce an ultra-filtrate of tissue interstitial fluid or blood plasma. The ultra-filtrate is transported through a sensor to detect a level of analyte in the ultra-filtrate. The long-term implantable fluid monitoring system thus includes a first porous catheter, a second porous catheter, a sensor configured to measure an amount of analyte in fluid, and a pump configured to move fluid through the first porous catheter to the sensor and from the sensor through the second porous catheter.

Abstract: The present invention relates to systems, devices and methods for diagnosing cancer. In various embodiments, the present invention provides a method for quantifying a 5?-htRNA; a method for quantifying a 3?-htRNA; a method for obtaining a DNA library of 5?-htRNAs and a DNA library of 5?-htRNAs obtained therefrom; and a method for obtaining a DNA library of 3?-htRNAs and a DNA library of 3?-htRNAs obtained therefrom. The invention also teaches a method for determining the presence or absence of a cancer cell in a biological sample; a method of diagnosing cancer in a subject; and a method of prognosing cancer in a subject.

Abstract: The invention provides methods for muscle repair or regeneration comprising administering therapeutically effective amounts of RAR agonists or stem cells that are pretreated with contact with a RAR agonist to a subject at a site of muscle damage. Additionally, the invention provides compositions comprising RAR agonist treated stem cells and methods of use of said cells for muscle repair or regeneration. In one embodiment, the stem cells are mesenchymal stem cells. In one embodiment, the RAR agonist is an RAR? agonist. In one embodiment, administration of the RAR agonist is begun during a period of increased endogenous retinoid signaling in the subject resulting from incurrence of the damaged muscle tissue.

Abstract: Disclosed herein are methods for determining whether a PAR4 inhibitor should be administered to a human subject, the methods comprising administering a PAR4 inhibitor to a subject determined to have a “G” allele for a single-nucleotide polymorphism (SNP) at rs773902, and not administering a PAR4 inhibitor to a subject determined to have an “A” allele for the SNP at rs773902. A genotyping assay can be used to determine the SNP.

Abstract: A chimeric, humanized or single-chain antibody contains a light chain variable region containing the complementarity determining regions of SEQ ID NO: 1, SEQ ID NO:2 and SEQ ID NO:3, and a heavy chain variable region containing the complementarity determining regions SEQ ID NO:4, SEQ ID NO:5 and SEQ ID NO:6. The antibody or antibody fragment thereof is capable of binding the C-terminal telopeptide of the ?2(I) chain of human collagen I, and is useful in the treatment of diseases or disorders associated with excessive collagen fibril.

Abstract: The technology described herein relates to pinacolyl boronate substituted stilbenes for the treatment of cancers, e.g. cancers expressing abnormally high levels of SREBP1.

Abstract: The present disclosure relates to methods of affecting platelet activation by the use of a PC-TP inhibitor. The PC-TP inhibitor can be administered to a subject in need thereof in order to prevent or treat pathologic thrombosis, or to treat a disorder treatable by a PAR4 inhibitor.

Abstract: In one embodiment, a masked monoclonal antibody (mAb) is provided, the mAb, encoded by a nucleic acid sequence or an amino acid sequence molecule comprising a signal sequence, a masking epitope sequence, a linker sequence that is cleavable by a protease specific to a target tissue; and an antibody or a functional fragment thereof. In another embodiment, a cross-masked mAb heterodimer complex is provided, comprising a first masked mAb, comprising a first signal sequence, a first masking epitope sequence, a first linker that is cleavable by a protease specific to a target tissue, and a first antibody or fragment thereof; and a second masked mAb, comprising a second signal sequence, a second masking epitope sequence, a second linker that is cleavable by a protease specific to a target tissue, and a second antibody or fragment thereof.

Abstract: The technology described herein relates to pinacolyl boronate substituted stilbenes for the treatment of cancers, e.g. cancers expressing abnormally high levels of SREBP1.

Abstract: Antibodies and antigen-binding fragments of antibodies that bind GCC are disclosed. In some embodiments, the antibodies are humanized, chimeric or human. Nucleic acids and vectors encoding the antibodies or portions thereof, recombinant cells that contain the nucleic acids, and compositions comprising the antibodies or antigen-binding fragments are also disclosed. The invention also provides therapeutic and diagnostic methods utilizing the antibodies and antigen-binding.

Abstract: Provided are fusion proteins comprising a first domain and a second domain, wherein the first domain comprises a polypeptide that binds to and triggers PD-1 and the second domain comprises a polypeptide that binds to and triggers a TRAIL receptor or Fas. In some embodiments, the polypeptide that binds to and triggers PD-1 comprises at least a portion of the extracellular domain of PD-L1 or PD-L2 and the second domain comprises at least a portion of the extracellular domain of TRAIL or Fas ligand. Also provided are methods for treating autoimmune, alloimmune or inflammatory diseases, and methods for treating cancer, using the fusion proteins.

Abstract: An implantable vital sign sensor including a housing including a first portion, the first portion defining a first open end, a second open end opposite the first end, and a lumen there through, the first portion being sized to be implanted substantially entirely within the blood vessel wall of the patient. A sensor module configured to measure a blood vessel blood pressure waveform is included, the sensor module having a proximal portion and a distal portion, the distal portion being insertable within the lumen and the proximal portion extending outward from the first open end.

Abstract: An implantable medical device having a sheath formed of a polymer material, wherein the sheath forms a reservoir attached to or around the implantable medical device, and wherein the reservoir is sealed with a biocompatible pressure responsive coating; wherein the biocompatible coating is stable for at least 7-day post implantation into a body, and can be mechanically ruptured by application of an exterior pressure generating force.

Abstract: The present invention relates to a genetically modified plant having an increased amount of oil in its green biomass as compared to the oil in the green biomass of its non-genetically modified counterpart. The plants may be used for producing bio-fuels such as biodiesel fuel.

Abstract: Disclosed herein are methods for determining whether a PAR4 inhibitor should be administered to a human subject, the methods comprising administering a PAR4 inhibitor to a subject determined to have a “G” allele for a single-nucleotide polymorphism (SNP) at rs773902, and not administering a PAR4 inhibitor to a subject determined to have an “A” allele for the SNP at rs773902. A genotyping assay can be used to determine the SNP.

Abstract: MicroRNA genes are highly associated with chromosomal features involved in the etiology of different cancers. The perturbations in the genomic structure or chromosomal architecture of a cell caused by these cancer-associated chromosomal features can affect the expression of the miR gene(s) located in close proximity to that chromosomal feature. Evaluation of miR gene expression can therefore be used to indicate the presence of a cancer-causing chromosomal lesion in a subject. As the change in miR gene expression level caused by a cancer-associated chromosomal feature may also contribute to cancerigenesis, a given cancer can be treated by restoring the level of miR gene expression to normal. microRNA expression profiling can be used to diagnose cancer and predict whether a particular cancer is associated with an adverse prognosis. The identification of specific mutations associated with genomic regions that harbor miR genes in CLL patients provides a means for diagnosing CLL and possibly other cancers.