34results about How to "Modulating level" patented technology

An article of footwear with a dynamically-controlled cushioning system is disclosed. The cushioning system includes a sealed, fluid-filled bladder formed with a plurality of separate cushioning chambers, and a control system. The control system, which includes a CPU, pressure sensors and valves, controls fluid communication between the chambers to dynamically adjust the pressure in the cushioning chambers for various conditions such as the activity that the footwear is used in, the weight of the individual and the individual's running style. Certain adjustments can be made while the footwear is in use.

The invention provides novel heterocyclic compounds, pharmaceutical compositions and methods of treatment that modulate levels of MIF expression and treat disorders associated with high or low levels of MIF expression.

Methods for using tetracycline compounds for the treatment of spinal muscular atrophy are described.

This invention is directed to Indazole Compounds or pharmaceutically acceptable salts, solvates and hydrates thereof. The Indazole Compounds have utility in the treatment or prevention of a wide range of diseases and disorders that are responsive to the inhibition, modulation or regulation of kinases, such as inflammatory diseases, abnormal angiogenesis and diseases related thereto, cancer, atherosclerosis, a cardiovascular disease, a renal disease, an autoimmune condition, macular degeneration, disease-related wasting, an asbestos-related condition, pulmonary hypertension, diabetes, obesity, pain and others. Thus, methods of treating or preventing such diseases and disorders are also disclosed, as are pharmaceutical compositions comprising one or more of the Indazole Compounds. This invention is based, in part, upon the discovery of a novel class of 5-triazolyl substituted indazole molecules that have potent activity with respect to the modulation of protein kinases. Thus, the invention encompasses orally active molecules as well as parenterally active molecules which can be used at lower doses or serum concentrations for treating diseses or disorders associated with protein kinase signal transduction.

The present invention provides methods of producing an isoprenoid or an isoprenoid precursor in a genetically modified host cell. The methods generally involve modulating the level of hydroxymethylglutaryl-CoA (HMG-CoA) in the cell, such that the level of HMG-CoA is not toxic to the cell and/or does not substantially inhibit cell growth, but is maintained at a level that provides for high-level production of mevalonate, IPP, and other downstream products of an isoprenoid or isoprenoid pathway, e.g., polyprenyl diphosphates and isoprenoid compounds. The present invention further provides genetically modified host cells that are suitable for use in a subject method. The present invention further provides recombinant nucleic acid constructs for use in generating a subject genetically modified host cell, including recombinant nucleic acid constructs comprising nucleotide sequences encoding one or more mevalonate pathway enzymes, and recombinant vectors (e.g., recombinant expression vectors) comprising same. The present invention further provides methods for identifying nucleic acids that encode HMG-CoA reductase (HMGR) variants that provide for relief of HMG-CoA accumulation-induced toxicity. The present invention further provides methods for identifying agents that reduce intracellular accumulation of HMG-CoA.

The invention pertains to the development of antibodies that specifically bind amyloid beta protein (Abeta) in its protofibril conformation. The invention also comprises methods of using anti-Abeta protofibril antibodies to diagnose or treat Alzheimer's disease, Down's syndrome Lewybody dementia, vascular dementia, and other neurodegenerative disorders. Furthermore, the invention pertains to the use of anti-Abeta protofibril antibodies to screen and identify substances that will modulate protofibril activity or formation in vitro or in vivo. The invention also pertains to methods for synthesising pure Abeta protofibril antigens as well as to a method for stabilising Abeta protofibrils antigens as well as to a method for stabilising Abeta protofibrils.

The present invention provides a pharmaceutical composition for treating an autoimmune disease comprising a pharmaceutically acceptable carrier and an agent capable of activating CD4+CD25+ regulatory T cells, wherein the composition is to be administered to a subject in a dose of the agent from 0.2 mg to 30 mg.

The invention provides novel heterocyclic compounds, pharmaceutical compositions and methods of treatment that modulate levels of MIF expression and treat disorders associated with high or low levels of MIF expression.

The invention provides NO-releasing polymers and low molecular weight NO-releasing compounds which may be used to for the treatment of medical conditions associated with NO-deficiency. The NO-releasing polymers or the low molecular weight NO-releasing compounds may also be incorporated into medical devices. The invention further provides methods of controlled release of NO for the treatment of diseases and disorders associated with NO-deficiency, wherein the treatment includes systemic or local administration of the NO-releasing polymers or the low molecular weight NO-releasing compounds.

The invention provides novel heterocyclic compounds, pharmaceutical compositions and methods of treatment that modulate levels of MIF expression and treat disorders associated with high or low levels of MIF expression.

A pre-5^th-Generation (5G) or 5G communication system is provided for supporting higher data rates than in 4^th-Generation system. An apparatus of a base station includes: at least one transceiver and at least one processor operatively connected to the transceiver. The transceiver receives channel quality information from a terminal. The processor obtains a first modulation and coding scheme (MCS) level and a number of first resource blocks based on the channel quality information, determines a power boosting value for applying a second MCS level indicating a higher modulation order or a higher code rate than the first MCS level, obtains, based on the power boosting value, a number of second resource blocks corresponding to a transport block size (TBS) value greater than a TBS value corresponding to the number of the first resource blocks in the first MCS level and transmits downlink data based on these determinations.

The present invention relates to novel methods and compositions for gene therapy. The invention also provides methods for treating diseases or disorders of the central nervous system associated with dopaminergic hypoactivity, disease, injury or chemical lesioning, including Parkinson's disease, manic depression, and schizophrenia.

The invention relates to a method to induce apoptosis and to inhibit matrix metalloproteinases in a disease condition in a human or animal by contacting hyperplastic tissue, tumor tissue, or a cancerous lesion with one or more antimicrobial metals, preferably formed with atomic disorder, and preferably in a nanocrystalline form. In another aspect of the invention, there is provided a method of preventing excessive release of matrix metalloproteinases from an inflammatory cell in a disease condition in a human or an animal by contacting the cell with a therapeutically effective amount of a noble metal in a crystalline form characterized by atomic disorder, or with a solution derived therefrom to provide a modulatory effect on one or more matrix metalloproteinases, wherein the one or more noble metals is formed with atomic disorder, and preferably in a nanocrystalline form. The nanocrystalline antimicrobial or noble metal of choice may be used in the form of a nanocrystalline coating of one or more antimicrobial or noble metals, a nanocrystalline powder of one or more antimicrobial or noble metals, or a solution containing dissolved species from a nanocrystalline powder or coating of one or more antimicrobial or noble metals.

The present disclosure relates to preterm infant formulas comprising lutein, lycopene, and beta-carotene, and the use of the preterm infant formulas to modulate inflammation, such as skin inflammation, in preterm infants. Also disclosed are methods of modulating the level of C-reactive protein in a preterm infant using preterm infant formulas comprising mixtures of carotenoids.

Protein complexes are provided comprising FHOS and one or more proteins selected from the group consisting of GROUP1. Methods of using the protein complexes in diagnosing diseases and disorders are also provided. In addition, the protein complexes are also useful in screening assays for identifying compounds effective in treating and/or preventing diseases and disorders associated with FHOS and its interactors.

The present invention relates to methods for modulating the production of ELR+ proinflammatory chemokines in a subject or a cell using either UMLILO IncRNA inhibitors to decrease production of ELR+ proinflammatory cytokines or using UMLILO IncRNA's to increase the production of ELR+ proinflammatory cytokines. The invention also provides for the use of UMLILO IncRNA inhibitors or UMLILO IncRNA's to modulate the expression of ERL+ proinflammatory cytokines.

The disclosure relates to a metabolic transistor in bacteria where a competitive pathway is introduced to compete with a product pathway for available carbon so as to control the carbon flux in the bacteria.

Stimulation of neural activity in a nerve supplying the spleen, wherein the nerve is adjacent to the splenic artery at a position where the splenic artery is not in direct contact with the pancreas, can modulate pro- and anti-inflammatory molecules levels, thereby reducing inflammation and providing ways of treating disorders, such as disorders associated with inflammation. The invention provides improved ways of reducing inflammation with minimized off-target effects, in particular surgical trauma.

The present invention provides an immunomodulating agent and a therapeutic agent for a immune disease, which comprise a lipid vesicle encapsulating a drug capable of suppressing or damaging an immunocyte that expresses or binds to an antibody, the lipid vesicle having an antigen for the antibody bound to the outer surface thereof. Hence, there is provided means for effectively treating an immune disease such as an allergic diseases or an autoimmune disease.

The present invention provides NB-ARC and CARD-containing proteins (NACs), nucleic acid molecules encoding NACs and antibodies specific for at least one NAC. The invention further provides chimeric NAC proteins. The invention also provides screening assays for identifying an agent that can effectively alter the association of a NAC with a NAC-associated protein. The invention further provides methods of modulating apoptosis in a cell by introducing into the cell a nucleic acid molecule encoding a NAC or an antisense nucleotide sequence. The invention also provides a method of using a reagent that can specifically bind to a NAC to diagnose a pathology that is characterized by an increased or decreased level of apoptosis in a cell.

The disclosure relates to a metabolic transistor in microbes such as bacteria and yeast where a competitive pathway is introduced to compete with a product pathway for available carbon so as to control the carbon flux in the microbe.

Provided is a simple and safe immunization procedure to reduce cancer incidence and increase longevity by modulating IGF-1 levels in the body. Described are cancer preventive vaccines and methods that elicit circulating antibodies specific to insulin-like growth factor 1 (IGF-1) in the body. Many cancers will be less likely to occur and spread in the absence or reduced levels of the stimulatory signals provided by IGF-1. Longevity also can be extended by immunologically lowering the level of bioavailable IGF-1 in adult animals. This prolongation of lifespan resulting from lower IGF-1 levels is produced independently of the inhibitory effects on carcinogenesis. However, the two IGF-1-mediated processes are linked mechanistically. Methods of active and passive immunization to suppress IGF-1 activity are included. Also described are methods for increasing longevity or reducing one or more symptoms of aging in a warm-blooded animal comprising administering anti-IGF-1 antibodies such that IGF-1 is inactivated or suppressed or administering IGF-1 antigen such that the animal produces endogenous antibodies to IGF-1.