Abstract: MicroRNAs are shown to be up- and/or down-regulated in inflammation and immune cells using a mouse model of asthma and regulatory T cells as source of RNA, respectively. Modulating the expression of these microRNAs can be effective in redirecting inflammation and immunity and hence, can be beneficial as biomarkers or as therapeutic agents against diverse human immunologic and inflammatory diseases.

Abstract: The present invention provides materials and methods for detecting, quantifying, and/or profiling microRNAs. Advantageously, the present invention is sensitive, specific, convenient, and cost-effective. In one embodiment, the present invention provides a universal primer for reverse transcription of miRNAs, a universal reverse primer for PCR amplification reaction, and a universal probe. In another embodiment, the present invention provides assays that allow the detection and/or quantification of a plurality of target miRNAs using a single reverse transcription reaction and a single qPCR reaction.

Abstract: The present invention pertains to materials and methods for diagnosing and/or determining the prognosis and likelihood of developing asthma. In one embodiment, methods of the invention comprise the use of single nucleotide polymorphic markers of asthma. Markers of the invention are present in the atria natriuretic peptide (NPPA) gene, and serve as a marker for genetic susceptibility of a person or animal in developing asthma.

Abstract: The present invention pertains to a nano-based sensing device (a sensor) comprising a nano-scale working electrode that can be used for the ultra-sensitive detection of blood analytes, disease biomarkers, and other target molecules. The present invention also pertains to a method for detecting target molecules using the sensor as the sensor element of a microfluidic device.

Abstract: The present invention provides miRNA biomarkers useful for diagnosis, prognosis, and/or treatment of airway diseases such as asthma, asthma exacerbation and nasal polyps.

Abstract: The subject invention concerns a method of inhibiting an RNA virus infection within a patient by increasing the amount of 2-5 oligoadenylate synthetase (2-5 AS) activity within the patient. Preferably, the preventative and therapeutic methods of the present invention involve administering a nucleotide encoding 2-5 AS, or at least one catalytically active fragment thereof, such as the p40, p69, p100 subunits, to a patient in need thereof. The present inventors have determined that overexpression of 2-5AS causes a reduction in epithelial cell damage, reduction in infiltration of mononuclear cells in the peribronchiolar and perivascular regions, and reduction in thickening of the septa in the lungs. Levels of chemokines, such as MIP1-?, are also reduced upon overexpression of 2-5AS. The subject invention also pertains to pharmaceutical compositions containing a nucleotide sequence encoding 2-5 AS and a pharmaceutically acceptable carrier, as well as vectors for delivery of the 2-5 AS nucleotide sequence.

Abstract: The subject invention pertains to the development of a novel human mast cell line, USF-MC1. USF-MC1 is a mast cell precursor present in human umbilical cord blood (HUCB) that may be sustained in culture in the absence of exogenous cytokines to serve as a convenient experimental model of human mast cell activation. The SCF-independent human mast cell line USF-MC1 responds to IgE-mediated and IgE-independent stimuli in a way comparable to that of LAD2. USF-MC1 cells are useful for investigation of IgE-mediated activation mechanisms of human mast cells, contributing to the development of effective treatments for allergic disorders and other disorders. The subject invention provides a ready source of human mast cells for research, including pharmacological studies for the screening of various agents, and toxicologic, e.g., for the cosmetic and pharmaceutical industries. The mast cells can also be used as biofactories, for the large-scale production of biomolecules.

Abstract: Compositions and methods for treatment of inflammatory and cell proliferation disorders using natriuretic hormone peptide (NP), polynucleotides encoding NP, or agents that reduce the activity of atrial natriuretic peptide receptor A (NPR-A).

Abstract: A method of delivering a compound of interest to the lungs of a subject by the intravenous injection of Sertoli cells loaded with a plurality of chitosan nanoparticles coupled with the compound of interest is provided. Testis-derived rat Sertoli cells were pre-loaded with chitosan nanoparticles coupled with or without the drug curcumin, pre-labeled with a fluorescent cell marker and then injected intravenously into the control or asthmatic mouse model host. Intact pre-loaded, pre-labeled Sertoli cells were present in the lungs at 15 minutes post-injection, appeared entrapped in the pulmonary pre-capillary vascular bed around alveolar sacs but were not present one hour post-injection although Sertoli cell label and cellular debris was. Most of the of the injected nanoparticle to load (70%) and curcumin load (80%) was present in the lungs 15 minutes post-injection, and remained at 70% and 80%, respectively, one hour post-injection.

Abstract: This invention pertains to inhibitors of atrial natriuretic peptide receptor A (NPRA) function, such as small interfering RNA (siRNA), useful for reducing the inflammation associated with many human diseases, such as asthma, respiratory syncytial virus (RSV) infection, and cancers (such as melanoma, lung cancer, and/or ovarian cancer) by interfering with NPRA gene expression or otherwise reducing NPRA function within a subject; and methods for treating a subject suffering from, or at risk of developing, an inflammatory disease, respiratory allergy (such as allergic rhinitis and asthma), viral infection, and/or cancer by administering such NPRA inhibitors to the subject.

Abstract: The subject invention concerns a method of inhibiting an RNA virus infection within a patient by increasing the amount of 2-5 oligoadenylate synthetase (2-5 AS) activity within the patient. Preferably, the preventative and therapeutic methods of the present invention involve administering a nucleotide encoding 2-5 AS, or at least one catalytically active fragment thereof, such as the p40, p69, p100 subunits, to a patient in need thereof. The present inventors have determined that overexpression of 2-5AS causes a reduction in epithelial cell damage, reduction in infiltration of mononuclear cells in the peribronchiolar and perivascular regions, and reduction in thickening of the septa in the lungs. Levels of chemokines, such as MIP1-?, are also reduced upon overexpression of 2-5AS. The subject invention also pertains to pharmaceutical compositions containing a nucleotide sequence encoding 2-5 AS and a pharmaceutically acceptable carrier, as well as vectors for delivery of the 2-5 AS nucleotide sequence.

Abstract: There is provided a method of preventing a respiratory infection by administering an effective amount of an agent for regulating ICAM-1 expression. Also provided is a composition for the prevention of respiratory infection including an agent which regulates ICAM expression. method of preventing RSV infection by administering an effective amount of an agent that interferes with the binding of RSV to ICAM-1. A method of preventing RSV infection by administering an effective amount of an agent that down regulates the expression of ICAM-1, thereby decreasing RSV binding to ICAM-1 is also provided. There is provided a method of treating RSV infection by administering an effective amount of an agent for down regulating ICAM-1 expression. A method of blocking RSV-ICAM-1 interaction by administering an effective amount of agents for blocking ICAM sites of binding is provided. Also provided is a compound for blocking RSV-ICAM-1 interaction including an agent for blocking ICAM sites of binding.

Abstract: The present invention pertains to nanoparticles, comprising a metal and/or polymer core, with 7-alpha hydroxylase, or an enzymatically active fragment thereof, nicotinamide adenine dinucleotide (NADH) and antibodies, or antibody fragments, specific for low density lipoprotein (LDL), attached to the core. The invention also concerns methods for reducing LDL cholesterol in a human or animal subject by administering nanoparticles of the invention. In a preferred embodiment, both circulating LDL and plasma cholesterol levels are reduced in the subject.

Abstract: MicroRNAs are shown to be up- and/or down-regulated in inflammation and immune cells using a mouse model of asthma and regulatory T cells as source of RNA, respectively. Modulating the expression of these microRNAs can be effective in redirecting inflammation and immunity and hence, can be beneficial as biomarkers or as therapeutic agents against diverse human immunologic and inflammatory diseases.

Abstract: The subject invention provides for the utilization of bone-marrow derived stem cells in the treatment of allergic and inflammatory diseases. In one embodiment, the invention provides for treatment of asthma. Bone-marrow derived stem cells can be used for decreasing inflammation and alter the course of immune response in the lung.

Abstract: The present invention pertains to materials and methods for diagnosing and/or determining the prognosis and likelihood of developing asthma. In one embodiment, methods of the invention comprise the use of single nucleotide polymorphic markers of asthma. Markers of the invention are present in the atria natriuretic peptide (NPPA) gene, and serve as a marker for genetic susceptibility of a person or animal in developing asthma.

Abstract: The present invention pertains to a method for treatment of allergic diseases by administering a natriuretic hormone peptide (NHP), or a nucleic acid sequence encoding NHP, to a patient in need thereof. In another aspect, the present invention concerns an expression vector comprising a nucleic acid sequence encoding NHP. In another aspect, the present invention concerns a host cell genetically modified with a nucleic acid sequence encoding NHP. In another aspect, the present invention concerns a pharmaceutical composition comprising NHP or a nucleic acid sequence encoding NHP and a pharmaceutically acceptable carrier. In another aspect, the present invention pertains to novel fragments of atrial natriuretic peptide (ANP) exhibiting bronchodilatory and anti-inflammatory activity, and isolated nucleic acid sequences encoding the fragments.

Abstract: The present invention pertains to methods and pharmaceutical compositions for modulating an immune response. The method of the present invention involves administration of an effective amount of nucleic acid molecules encoding interleukin-12 (IL-12), interferon-gamma (IFN-?), or a combination thereof, to a patient in need of such treatment. The pharmaceutical compositions of the invention contain nucleic acid molecules encoding IL-12 and/or IFN-? and an operably-linked promoter sequence. In another aspect, the present invention concerns expression vectors containing a nucleotide sequence encoding IL-12 and IFN-?, and an operably-linked promoter sequence. In another aspect, the present invention concerns cells genetically modified with a nucleotide sequence encoding IL-12 and IFN-?.

Abstract: The present invention pertains to methods and pharmaceutical compositions for modulating an immune response. The method of the present invention involves administration of an effective amount of nucleic acid molecules encoding interleukin-12 (IL-12), interferon-gamma (IFN-?), or a combination thereof, to a patient in need of such treatment. The pharmaceutical compositions of the invention contain nucleic acid molecules encoding IL-12 and/or IFN-? and an operably-linked promoter sequence. In another aspect, the present invention concerns expression vectors containing a nucleotide sequence encoding IL-12 and IFN-?, and an operably-linked promoter sequence. In another aspect, the present invention concerns cells generally modified with a nucleotide sequence encoding IL-12 and IFN-?.

Abstract: The subject invention concerns a method of inhibiting respiratory syncytial virus (RSV) infection in a patient by decreasing the endogenous protein kinase C (PKC) activity within the patient. Preferably, the preventative and therapeutic methods of the present invention involve administration of a PKC inhibitor. The present inventor has determined that decreasing normal endogenous PKC activity is inhibitory to RSV infection of human cells. The subject invention also pertains to pharmaceutical compositions containing a PKC inhibitor and a pharmaceutically acceptable carrier.