Abstract: A vial holder is provided to protect a user's hand from needle sticks. The holder includes a handle and a shield attached to a distal end of the handle. An opening is formed in the distal end of the handle to receive a vial. The vial is placed through the opening and into a passageway of the handle with the upper end of the vial exposed. A user grasps the handle which holds the vial in a stabilized manner. A needle may then safely approach the vial in which inadvertent slippage or movement of the needle results in contact with the needle against the shield and not contact with the user's hand.

Abstract: The present invention is related to the novel discovery of a number of genes that were identified as systemic markers of pulmonary inflammation. This discovery allows for development of a novel tool for reliable, rapid and efficient assessment of therapeutic responses and enables design of novel therapies targeted against diseases associated with pulmonary inflammation. In one embodiment, the present invention allows quantification of therapeutic response in patients who have a disease associated with pulmonary inflammation. In preferred embodiments, the genes are CD64, ADAM9, CD36, IL32, HPSE, PLXND1, HCA112, CSPG2, TLR2, and CD163.

Abstract: Disclosed are Cystatin C (CysC) homologues, including CystC homologues that act as antagonists or inhibitors of transforming growth factor-? (TGF-?). Also disclosed are methods to identify CystC homologues that are antagonists or inhibitors of TGF-? and compositions and therapeutic methods using CystC and homologues thereof to regulate the activity of TGF-?, and TGF-?-mediated tumor malignancy and invasion and other TGF-?-mediated fibrotic or proliferative conditions and diseases.

Abstract: The present invention is related to the novel discovery that HIF-2?, but not HIF-1?, selectively regulates adenosine A2A receptor in endothelial cells, thereby revealing a unique and hitherto unknown pathway by which HIF-2?can regulate angiogenesis independent of HIF-1?. This discovery allows for design of new diagnostic tools and novel therapies targeted against angiogenesis-associated diseases, such as cancer. In another aspect, the present invention shows that A2A receptor expression is a marker of the developing lung, and can be used as a marker of lung diseases, such as pulmonary hypertension.

Abstract: An airway stent with an integral suture anchor is used to prevent migration of the stent within the airway. The suture anchor is incorporated by percutaneous placement of a suture through the neck and into the stent. The distal end of the suture includes an anchor element to secure the suture to the stent. The opposite end of the suture is tensioned and held in place by a suture clamp and a pledget routed over the stent and placed against the neck. Airway stents such as tracheal stents are effective at maintaining airway patency however; a common complication is stent migration. The integral suture anchor provides a reliable, economical, and non-intrusive solution to stent migration.

Abstract: Disclosed are TALL-1 and TALL-1 receptor protein homologues (agonists and antagonists) designed based on the three-dimensional structure of sTALL-1, eBCMA and eBAFF-R; agonist homologues of APRIL; methods of using wild-type APRIL to inhibit the activity of TALL-1; compositions comprising such homologues, nucleic acid molecules encoding such homologues, and therapeutic methods of using such compounds and compositions. Also disclosed are crystalline complexes of sTALL-1 and sTALL-1 in complex with either BCMA or BAFF-R; models of three-dimensional structures of such crystalline complexes and related structures, methods of drug design using any portion of such structures; methods of design and/or identification of regulatory peptides derived from the such structures; compounds identified by drug design using such structures; and the use of such compounds in therapeutic compositions and methods.

Abstract: Compounds may be administered to prevent or rescue organ injury following exposure to alkylating agents, such as sulfur mustards. The compounds may be substituted metalloporphyrins.

Abstract: Particular members of the multisubunit immune recognition receptor (MIRR) family of receptors, specifically, the B cell antigen receptor (BCR), the pre-B cell receptor (pre-BCR), the pro-B cell receptor (pro-BCR), Ig Fc receptors (FcR), and NK receptors, can be physically uncoupled from their associated transducers. The invention describes regulatory compounds and methods for mimicking such dissociation/destabilization for the purposes of receptor desensitization and for treatment of conditions in which receptor desensitization or alternatively, enhanced or prolonged receptor sensitization, is desirable. Compounds and methods for enhancing or prolonging receptor sensitization are also disclosed, as are methods for identifying regulatory compounds suitable for use in the present methods.

Abstract: Disclosed is a rapid, non-invasive and highly specific and sensitive diagnostic assay for the identification of individuals with autoimmune chronic urticaria, which makes use of CD203c, and in some embodiments, additional proteins, as a marker for the disease. Test kits for diagnosis of an individual suspected of having autoimmune chronic urticaria are also disclosed. Also disclosed are a method of identifying compounds useful for treating autoimmune chronic urticaria and a method of treating autoimmune chronic urticaria.

Abstract: Disclosed are TALL-1 and TALL-1 receptor protein homologues (agonists and antagonists) designed based on the three-dimensional structure of sTALL-1, eBCMA and eBAFF-R; agonist homologues of APRIL; methods of using wild-type APRIL to inhibit the activity of TALL-1; compositions comprising such homologues, nucleic acid molecules encoding such homologues, and therapeutic methods of using such compounds and compositions. Also disclosed are crystalline complexes of sTALL-1 and sTALL-1 in complex with either BCMA or BAFF-R; models of three-dimensional structures of such crystalline complexes and related structures, methods of drug design using any portion of such structures; methods of design and/or identification of regulatory peptides derived from the such structures; compounds identified by drug design using such structures; and the use of such compounds in therapeutic compositions and methods.

Abstract: Particular members of the multisubunit immune recognition receptor (MIRR) family of receptors, specifically, the B cell antigen receptor (BCR), the pre-B cell receptor (pre-BCR), the pro-B cell receptor (pro-BCR), Ig Fc receptors (FcR), and NK receptors, can be physically uncoupled from their associated transducers. The invention describes regulatory compounds and methods for mimicking such dissociation/destabilization for the purposes of receptor desensitization and for treatment of conditions in which receptor desensitization or alternatively, enhanced or prolonged receptor sensitization, is desirable. Compounds and methods for enhancing or prolonging receptor sensitization are also disclosed, as are methods for identifying regulatory compounds suitable for use in the present methods.

Abstract: Disclosed are Cystatin C (CysC) homologues, including CystC homologues that act as antagonists or inhibitors of transforming growth factor-? (TGF-?). Also disclosed are methods to identify CystC homologues that are antagonists or inhibitors of TGF-? and compositions and therapeutic methods using CystC and homologues thereof to regulate the activity of TGF-?, and TGF-?-mediated tumor malignancy and invasion and other TGF-?-mediated fibrotic or proliferative conditions and diseases.

Abstract: Methods for therapy of cystic fibrosis and other conditions such as cancer are provided. The methods comprise one or more agents capable of increasing thiol-containing compound transport via a transporter system (i.e. ABC transporters such as MDR-1 or MRP-2) in cells. Other embodiments include the use of agents to modulate transport of thiol-containing compounds within the cell. Therapeutic methods involve the administration of such agents to a patient afflicted with cystic fibrosis, cancer and/or another condition responsive to stimulation of thiol-containing compound transport.

Abstract: Disclosed is a method to reduce airway hyperresponsiveness, such as allergen-induced airway hyperresponsiveness, in a mammal by administering an agent that increases the biological activity of a CGRP receptor. Also disclosed are methods for identifying compounds useful in the present method.

Abstract: Disclosed are Cystatin C (CysC) homologues, including CystC homologues that act as antagonists or inhibitors of transforming growth factor-? (TGF-?). Also disclosed are methods to identify CystC homologues that are antagonists or inhibitors of TGF-? and compositions and therapeutic methods using CystC and homologues thereof to regulate the activity of TGF-?, and TGF-?-mediated tumor malignancy and invasion and other TGF-?-mediated fibrotic or proliferative conditions and diseases.

Abstract: Disclosed are compositions and methods for decreasing the viscosity and/or cohesiveness of and/or increasing the liquefaction of excessively or abnormally viscous or cohesive mucus or sputum. The composition contains a protein or peptide containing a thioredoxin active-site in reduced state and optionally further contains a reducing system.

Abstract: Disclosed is a method for regulation of airway hyperresponsiveness by modulating the action of ?? T cells in a patient. Also disclosed are methods for identifying compounds that regulate airway hyperresponsiveness by modulating ?? T cell action.

Abstract: Disclosed are compositions and methods for decreasing the viscosity and/or cohesiveness of and/or increasing the liquefaction of excessively or abnormally viscous or cohesive mucus or sputum. The composition contains a protein or peptide containing a thioredoxin active-site in reduced state and optionally further contains a reducing system.

Abstract: A joint aspirate-facilitating device is provided including a flexible main panel that is secured to the joint to be aspirated. An inflatable bladder is secured to the main panel and is placed in contact with the soft tissues overlying and surrounding the joint space. The bladder is used to apply pressure to selected areas of the joint to compress the fluid sacs in the joint. An access opening is formed in the main panel designating the location where joint fluid is to be aspirated. The joint fluid is directed to flow to the area of the joint exposed at the access opening based on the shape of the bladder that compresses surrounding areas of the fluid sacs. A conventional hand pump may pressurize the bladder or the bladder may be filled with a viscous gel material to generate pressure. Multiple access openings may be formed on the main panel designating locations where aspiration is to be conducted.