Abstract: Provided is a means for inhibiting a function of CD69, whereby allowing suppression of an inflammatory response. That is, provided are: a composition for treating an inflammatory disease which includes an antibody that specifically recognizes a myosin regulatory light chain polypeptide (hereinafter abbreviated as Myl), preferably Myl9, Myl12a, and Myl12b, and inhibits a result of an effect of coexistence of Myl with CD69; a method of treating an inflammatory disease, including administering, to a subject diagnosed as having an inflammatory disease, a therapeutically effective amount of the antibody; and a method of identifying a compound that inhibits a result of an effect of coexistence of Myl with CD69, and a method of identifying a candidate compound for treating an inflammatory disease, including selecting a compound that inhibits the result.

Abstract: A monoclonal antibody recognizing the extracellular region of LAMP5 was produced. The produced antibody demonstrated antibody-dependent cell-mediated cytotoxic activity, and/or cell growth inhibitory activity in the presence of a toxin-labeled secondary antibody, against a multiple myeloma cell line.

Abstract: The present invention provides compositions and methods of use of anti-IGF-1R antibodies or antibody fragments. Preferably the antibodies bind to IGF-1R but not IR; are not agonists for IGF-1R; do not block binding of IGF-1 or IGF-2 to isolated IGF-1R, but effectively neutralize activation of IGF-1R by IGF-1 in intact cells; and block binding of an R1 antibody to IGF-1R. The antibodies may be murine, chimeric, humanized or human R1 antibodies comprising the heavy chain CDR sequences DYYMY (SEQ ID NO:1), YITNYGGSTYYPDTVKG (SEQ ID NO:2) and QSNYDYDGWFAY (SEQ ID NO:3) and the light chain CDR sequences KASQEVGTAVA (SEQ ID NO:4), WASTRHT (SEQ ID NO:5) and QQYSNYPLT (SEQ ID NO:6). Preferably the antibodies bind to an epitope of IGF-1R comprising the first half of the cysteine-rich domain of IGF-1R (residues 151-222). The anti-IGF-1R antibodies may be used for diagnosis or therapy of various diseases such as cancer.

Abstract: The present inventors obtained, from a phage library of human antibodies, an anti-mouse NR 10 neutralizing antibody-expressing BM095 clone that shows a strong proliferation-suppressing activity in an IL-31-dependent Ba/F3 cell proliferation assay system. When this anti-mouse NR 10 neutralizing antibody was administered to NC/Nga mice, a model of atopic dermatitis which is a mouse model of chronic dermatitis that arises as a result of repeated applications of picryl chloride, a mouse model of rheumatoid arthritis, and a mouse model of osteoarthritis, a significant effect of symptom suppression was observed. This revealed that the anti-NR 10 neutralizing antibody is indeed effective as a therapeutic agent for inflammatory diseases. In addition, the present inventors successfully obtained an anti-human NR 10 neutralizing antibody, providing extremely useful therapeutic agents with practical clinical applications.

Abstract: The present invention relates to antibodies that bind to a polypeptide at an epitope in the amino acid sequence of SEQ ID NO: 1 (e.g., a sericin polypeptide). The invention also provides methods and kits using the antibodies of the invention. In some embodiments, the antibody binds to a polypeptide at an epitope in the amino add sequence of SEQ ID NO: 2. In some embodiments, the antibody binds to a polypeptide at an epitope in the amino add sequence of SEQ ID NO: 3. In some embodiments, the polypeptide is a sericin polypeptide (e.g., a sericin isoform 1B polypeptide). In a related aspect, the invention features a method for selectively detecting sericin in a sample.

Abstract: The method for diagnosing sleep apnea includes measuring concentrations of biomarkers in a patient's bodily sample. To determine whether a patient suffers from sleep apnea, or has a predisposition for developing sleep apnea, a sample from the patient is analyzed. If one or more of the following biomarker concentrations are found in the patient's sample, then the patient may be diagnosed as suffering from sleep apnea or having a predisposition for developing sleep apnea: between approximately 992.8 pg/mL and approximately 1309.6 pg/mL of adipsin; between approximately 1,640 pg/mL and approximately 2,900 pg/mL of betatrophin; between approximately 8,090.82 pg/mL and approximately 11,829.07 pg/mL of brain-derived neurotrophic factor (BDNF); between approximately 11.82 pg/mL and approximately 88.26 pg/mL of interleukin-13 (IL-13); between approximately 49.45 pg/mL and approximately 103.29 pg/mL of tumor necrosis factor-? (TNF-?); and between approximately 16.55 pg/mL and approximately 29.

Abstract: Anti-cytokine therapy has revolutionized immunological disease treatment, but is not always effective and subject to treatment resistance as the cytokine cascade is highly redundant and multiple cytokines are involved in inflammation. Targeting a critical common regulator of inflammatory effectors is desirable. Lipopolysaccharide (LPS)-responsive beige-like anchor (LRBA) is a master regulator of multiple genes important for inflammation. Subcellular localization shows that LRBA translocated to the nucleus upon LPS stimulation and colocalized with multiple proteins associated with the endosome membrane system, indicating a critical role in membrane/vesicle trafficking essential for deposition, secretion and signal transduction of immune effectors.

Abstract: A method of treating a mammalian subject with cancer comprises administering to said subject having a cancer, e.g., a metastatic or refractory cancer or tumor, a small molecule inhibitor of a target signaling molecule of the MEK/MAPK pathway that impairs T cell activation, and administering to said subject a molecule that induces T cell proliferation in the presence of said inhibitor. The combination of a small molecule inhibitor of a target of the MEK/MAPK pathway and the T cell proliferation inducer reduces the proliferation of the cancer and tumor cells in vivo. Compositions and kits including these components are also provided.

Abstract: This invention relates to the production and genotyping of mice lacking both Angiopoietin 1 and Angiopoietin 2. This invention also relates to the use of Tie2 receptor activation for treatment of open angle glaucoma, congenital glaucoma and cystic kidney disease, and more specifically to the use of angiopoietin 1 recombinant proteins, peptides, VE-PTP phosphatase inhibitors, and Tie2— peptomimetics to improve lymphatic drainage in the Schlemm's canal and corneal limbal lymphatic system for open angle glaucoma and congenital glaucoma patients, and to slow and/or reduce the growth of cysts in patients with cystic kidney disease.

Abstract: The invention provides methods for the treatment of coronary heart disease, peripheral vascular disease, stroke, and ischemia featuring agents that interfere with the expression or activity of Cthrc1. The invention also provides the use of Cthrc1 peptide as a therapeutic agent for the treatment of acute or chronic cardiac deficiencies. The invention further provides detection and monitoring of Cthrc1 peptide in blood or serum to assess or monitor cardiac function.

Abstract: The invention features compositions featuring (a) one or more of connective tissue growth factor (CTGF) and human C-terminal CTGF peptide; and (b) one or more of insulin and IGF-1; and methods of using such compositions to reduce cardiac tissue damage associated with an ischemic event or to enhance engraftment of a cell in a cardiac tissue.

Abstract: The present invention provides antibodies and related molecules that bind to chemokine receptor 4 (CXCR4). The invention further provides antibody-drug conjugates comprising such antibodies, antibody encoding nucleic acids, and methods of obtaining such antibodies. The invention further relates to therapeutic methods for use of these antibodies and anti-CXCR4 antibody-drug conjugates for the treatment of a disorder associated with CXCR4 function or expression (e.g., cancer), such as colon, RCC, esophageal, gastric, head and neck, lung, ovarian, pancreatic cancer or hematological cancers.

Abstract: Provided is a monoclonal antibody or a fragment thereof that selectively inhibits the enzymatic activity of vascular endothelial lipase and pharmaceutical compositions containing the same as an active ingredient useful for the treatment of arteriosclerosis or metabolic syndrome.

Abstract: The invention discloses application of irisin in the preparation of drugs for preventing myocardial ischemia reperfusion injuries. Experimental results show that irisin can decrease the myocardial infarction area caused by ischemia reperfusion, reduce the increase of the contents of lactate dehydrogenase (LDH), troponin (cTnI), creatine kinase (CK), and other myocardial enzyme markers caused by ischemia reperfusion, meanwhile reducing the inflammatory response, myocardial apoptosis, and oxidative stress response caused by myocardial ischemia reperfusion, promote peroxysome proliferator-activated receptor ? nuclear translocation, and inhibit nuclear transcription factor NF-?B nuclear translocation and accordingly decrease myocardial structure injuries and load increase caused by ischemia reperfusion. Therefore, irisin can be used for preventing and decreasing myocardial reperfusion injuries and has important clinical significance on the treatment of myocardial ischemia.

Abstract: The present invention relates to Pharmaceutical compositions comprising an antibody specifically binding to human proprotein convertase subtilisin/kexin type 9 (PCSK9), to methods for treating diseases or conditions in which proprotein convertase subtilisin/kexin type 9 (PCSK9) expression or activity causes an impact by administration of PCSK9-specific antibodies or antigen-binding fragments thereof and preferably by additional administration of an inhibitor of 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMG-CoA reductase). The present invention further relates to PCSK9-specific antibodies or antigen-binding fragments thereof for use in the treatment of diseases or conditions in which PCSK9 expression or activity causes an impact.

Abstract: A method of treating or preventing a gum disease or gum disorder or gum injury in a mammal by administering to the mammal at least one inflammation modulatory or anti-inflammatory protein or polypeptide, such as TSG-6 protein, or a biologically active fragment, derivative, or analogue thereof. Gum diseases or gum disorders or gum injuries that may be treated include periodontal gum disease, and gum wounds resulting from gum surgeries.

Abstract: The invention provides stabilized aqueous pharmaceutical etanercept compositions suitable for long-term storage of etanercept, methods of manufacture of these compositions, methods of administration, and kits containing same.

Abstract: The present application relates to antibodies that specifically bind to hepcidin and methods of using the antibodies. Another aspect relates to antibodies which bind hepcidin and regulate iron homeostasis. Another aspect relates to the use of humanized antibodies which bind hepcidin for the treatment of a disease or condition associated with hepcidin.

Abstract: The present invention provides apelin receptor (APLNR) modulators that bind to APLNR and methods of using the same. The invention includes APLNR modulators such as antibodies, or antigen-binding fragments thereof, which inhibit or attenuate APLNR-mediated signaling. The invention includes APLNR modulators such as antibodies, or antibody fusion proteins thereof, that activate APLNR-mediated signaling. According to certain embodiments of the invention, the antibodies or antigen-binding fragments or antibody fusion proteins are fully human antibodies that bind to human APLNR with high affinity. The APLNR modulators of the invention are useful for the treatment of diseases and disorders associated with APLNR signaling and/or APLNR cellular expression, such as cardiovascular diseases, angiogenesis diseases, metabolic diseases and fibrotic diseases.

Abstract: The present invention relates to antibodies anti-sPLA2-IIA and uses thereof.