Abstract: The present invention includes compositions and methods for the treatment of Th1 and/or Th2 medicated inflammatory diseases, relating to inhibiting CCR5. This is because the present invention demonstrates, for the first time, that expression of IFN-?, IL-13, and CCR5 mediates and/or is associated with Th1 and/or Th2 inflammatory diseases and that inhibiting CCR5 treats, and even prevents, the diseases. Thus, the Invention relates to the novel discovery that inhibiting CCR5 treats and prevents Th1 and/or Th2 mediated inflammatory disease.

Abstract: The invention relates to the novel discovery that antagonizing a C/CLP can be useful for the treatment of diseases associated with the upregulation of one or more C/CLP such as Th2-driven and/or IL-13 mediated inflammatory diseases. Accordingly the present invention provides C/CLP antagonists and also provides compositions and methods for the prevention, management, treatment or amelioration of an inflammatory condition associated with the upregulation of a C/CLP or one or more symptoms thereof and/or the inhibition of IL-13 mediated inflammation.

Abstract: The present invention encompasses compositions and compounds as well as methods of their use for the regulation of a VEGF-induced tissue response. A VEGF-induced tissue response may include angiogenesis, inflammation, increased vascular permeability, increased vascular leak, hemorrhage, or mucus metaplasia. As such, the present invention encompasses methods of treating diseases where a VEGF-induced tissue response is part of the disease's clinical presentation. Specifically, the present invention provides compounds and compositions as well as methods for treating acute lung injury (ALI), acute respiratory distress syndrome (ARDS), asthma, chronic obstructive pulmonary disease (COPD), obstructive sleep apnea (OSA), idiopathic pulmonary fibrosis (IPF), tuberculosis, pulmonary hypertension, pleural effusion, and lung cancer.

Abstract: The present invention encompasses compositions and methods directed to preventing, inhibiting, or treating inflammation, alveolar remodeling, or cell death in lung which results from elevation of IL-18, IFN-?, or PKR where the methods of the present invention comprise administering an IL-18 inhibitor, an IL-18R? inhibitor, and IFN? inhibitor, a PKR inhibitor, and any combination thereof to an individual experiencing inflammation, alveolar remodeling, or cell death in lung. The present invention further encompasses a method of alleviating exacerbations of COPD frequently caused by viral infection by administering inflammation, alveolar remodeling, or cell death in lung to a patient with COPD at risk of developing a viral infection or who has acquired a viral infection.

Abstract: The invention provides methods of treating diseases caused by the over-production of a VEGF polypeptide by administering miRNA or miRNA inhibitor compositions to decrease at least one activity of a VEGF polypeptide.

Abstract: The present invention provides methods of treating a subject diagnosed with, or at risk for developing, pathogenic fibrosis, particularly pulmonary fibrosis. The method of the invention comprises administering to the subject a compound or composition which inhibits semaphorin (SEMA) 7A, SEMA 7A receptors, or downstream effectors. A SEMA 7A inhibitor comprises an antibody, a soluble SEMA 7A receptor, an siRNA, a ribozyme, an antisense, an aptamer, a peptidomimetic, a small molecule, a soluble receptor, or any combinations thereof.

Abstract: An apparatus includes first and second input terminals configured to be coupled to one of multiple types of input sources. The apparatus also includes a diode and a resistor coupled in series between the first and second input terminals. The apparatus further includes a plurality of switches each coupled to at least one of the diode and the resistor. The switches are configured to be opened and closed to reconfigure the apparatus depending on the type of input source. The switches could include a first switch coupled to the first input terminal, a current source, and a first side of the diode. The switches could also include a second switch coupled to the current source, a second side of the diode, and a first side of the resistor. In addition, the switches could include a third switch coupled to the second input terminal and a second side of the resistor.

Abstract: The present invention provides a method for the treatment or prophylaxis of T-helper type 2 (Th2)-mediated disorders using antagonists of IL-11.

Abstract: The present invention includes compositions and methods for the treatment of inflammatory disease (e.g., asthma, COPD, inflammatory bowel disease, atopic dermatitis, atopy, allergy, allergic rhinitis, scleroderma, and the like), relating to inhibiting a chitinase-like molecule. The invention further includes methods to identify new compounds for the treatment of inflammatory disease, including, but not limited to, asthma, COPD and the like. This is because the present invention demonstrates, for the first time, that expression of IL-13, and of a chitinase-like molecule, mediates and/or is associated with inflammatory disease and that inhibiting the chitinase-like molecule treats and even prevents, the disease. Thus, the invention relates to the novel discovery that inhibiting a chitinase-like molecule treats and prevents an inflammatory disease.

Abstract: The present invention includes compositions and methods for the treatment of a Th2 mediated inflammatory disease, relating to inhibiting a VEGF. The invention further includes methods to identify new compounds for the treatment of a Th2 mediated inflammatory disease, including, but not limited to, asthma and the like. This is because the present invention demonstrates, for the first time, that expression of VEGF induces asthma-like phenotype and that inhibiting VEGF reverses the phenotype. Thus, the invention relates to the novel discovery that inhibiting VEGF treats and prevents an Th2 mediated inflammatory disease.

Abstract: The present invention includes compositions and methods for the treatment of inflammatory disease (e.g. asthma, COPD, inflammatory bowel disease, atopic dermatitis, atopy, allergy, allergic rhinitis, scleroderma, and the like), relating to inhibiting a chitinase-like molecule. The invention further includes methods to identify new compounds for the treatment of inflammatory disease, including, but not limited to, asthma, COPD and the like. This is because the present invention demonstrates, for the first time, that expression of IL-13, and of a chitinase-like molecule, mediates and/or is associated with inflammatory disease and that inhibiting the chitinase-like molecule treats and even prevents, the disease. Thus, the invention relates to the novel discovery that inhibiting a chitinase-like molecule treats and prevents an inflammatory disease.

Abstract: The present invention includes compositions and methods for the treatment of inflammatory disease (e.g. asthma, COPD, inflammatory bowel disease, atopic dermatitis, atopy, allergy, allergic rhinitis, scleroderma, and the like), relating to inhibiting a chitinase-like molecule. The invention further includes methods to identify new compounds for the treatment of inflammatory disease, including, but not limited to, asthma, COPD and the like. This is because the present invention demonstrates, for the first time, that expression of IL-13, and of a chitinase-like molecule, mediates and/or is associated with inflammatory disease and that inhibiting the chitinase-like molecule treats and even prevents, the disease. Thus, the invention relates to the novel discovery that inhibiting a chitinase-like molecule treats and prevents an inflammatory disease.

Abstract: The present invention includes compositions and methods for the treatment of Th1 and/or Th2 medicated inflammatory diseases, relating to inhibiting CCR5. This is because the present invention demonstrates, for the first time, that expression of IFN-?, IL-13, and CCR5 mediates and/or is associated with Th1 and/or Th2 inflammatory diseases and that inhibiting CCR5 treats, and even prevents, the diseases. Thus, the Invention relates to the novel discovery that inhibiting CCR5 treats and prevents Th1 and/or Th2 mediated inflammatory disease.

Abstract: An analog signal scrambler/de-scrambler includes a receiver for receiving an analog signal and converting the signal into an intermediate frequency signal. A generator generates a pseudo-random gaussian frequency distribution signal, which is multiplied with the intermediate frequency signal by a frequency converter to scramble/de-scramble the analog signal.

Abstract: The present invention includes compositions and methods for the treatment of inflammatory disease (e.g., asthma, COPD, inflammatory bowel disease, atopic dermatitis, atopy, allergy, allergic rhinitis, scleroderma, and the like), relating to inhibiting a chitinase-like molecule. The invention further includes methods to identify new compounds for the treatment of inflammatory disease, including, but not limited to, asthma, COPD and the like. This is because the present invention demonstrates, for the first time, that expression of IL-13, and of a chitinase-like molecule, mediates and/or is associated with inflammatory disease and that inhibiting the chitinase-like molecule treats and even prevents, the disease. Thus, the invention relates to the novel discovery that inhibiting a chitinase-like molecule treats and prevents an inflammatory disease.

Abstract: The invention relates to the novel discovery that antagonizing a C/CLP can be useful for the treatment of diseases associated with the upregulation of one or more C/CLP such as Th2-driven and/or IL-13 mediated inflammatory diseases. Accordingly the present invention provides C/CLP antagonists and also provides compositions and methods for the prevention, management, treatment or amelioration of an inflammatory condition associated with the upregulation of a C/CLP or one or more symptoms thereof and/or the inhibition of IL-13 mediated inflammation.

Abstract: This invention is directed to the use of an inhibitor of cathepsin-S or -B, or composition thereof, to treat or prevent chronic obstruction pulmonary disease, or physiological condition associated therewith. Such a therapy would occur using at least one of such inhibitors alone or in combination with the other, or further in combination with an anti-inflammatory agent.

Abstract: The present invention includes compositions and methods for the treatment of inflammatory disease (e.g., asthma, COPD, inflammatory bowel disease, atopic dermatitis, atopy, allergy, allergic rhinitis, scleroderma, and the like), relating to inhibiting a chitinase-like molecule. The invention further includes methods to identify new compounds for the treatment of inflammatory disease, including, but not limited to, asthma, COPD and the like. This is because the present invention demonstrates, for the first time, that expression of IL-13, and of a chitinase-like molecule, mediates and/or is associated with inflammatory disease and that inhibiting the chitinase-like molecule treats and even prevents, the disease. Thus, the invention relates to the novel discovery that inhibiting a chitinase-like molecule treats and prevents an inflammatory disease.

Abstract: This invention is directed to the use of an inhibitor of cathepsin-S or -B, or composition thereof to treat or prevent chronic obstruction pulmonary disease, or physiological condition associated therewith. Such a therapy would occur using at least one of such inhibitors alone or in combination with the other, or further in combination with an anti-inflammatory agent.