873results about How to "Reduce secretion" patented technology

A method for the treatment of obesity or other disorders by electrical activation or inhibition of nerves is disclosed. This activation or inhibition can be accomplished by stimulating a nerve using an electrode. Dynamic stimulation through ramped cycling of electrical stimulation, stimulation frequency alteration, and / or duty cycle variance can produce therapeutic benefits.

A method for the treatment of obesity or other disorders, by wireless electrical activation or inhibition of the sympathetic nervous system. This activation or inhibition can be accomplished by wirelessly stimulating the greater splanchnic nerve or other portion of the sympathetic nervous system using a wireless electrode inductively coupled with a radiofrequency field. The source of radiofrequency energy may be internal or external to the patient. This nerve activation can result in reduced food intake and increased energy expenditure.

A responsive gastrointestinal stimulation device is provided where one or more sensors sense data corresponding to a subject or the gastrointestinal tract of a subject and responds to sensing the data by stimulating, adjusting stimulation, or stopping stimulation of the gastrointestinal tract. A stimulation device is also provided to stimulate the gastrointestinal tract to produce a sensation of satiety or to control hunger or food consumption.

A method for the treatment of obesity or other disorders, by electrical activation or inhibition of the sympathetic nervous system. This activation or inhibition can be accomplished by electrically stimulating the greater splanchnic nerve or other portion of the sympathetic nervous system using an implantable pulse generator. This nerve activation can result in reduced food intake and increased energy expenditure. Reduced food intake may occur through a variety of mechanisms that reduce appetite and cause satiety. Increased adrenal gland hormone levels will result in increased energy expenditure. Fat and carbohydrate metabolism, which are also increased by sympathetic nerve activation, will accompany the increased energy expenditure.

A method for the treatment of obesity or other disorders by electrical activation or inhibition of nerves is disclosed. This activation or inhibition can be accomplished by stimulating a nerve using an electrode. Dynamic stimulation through ramped cycling of electrical stimulation, stimulation frequency alteration, and / or duty cycle variance can produce therapeutic benefits.

A method for the treatment of obesity or other disorders by electrical activation or inhibition of nerves is disclosed. This activation or inhibition can be accomplished by stimulating a nerve using an electrode. The method further comprises performing a surgical procedure and / or administering a weight loss drug.

The present invention relates to pharmaceutical compositions of linagliptin, pharmaceutical dosage forms, their preparation, their use and methods for treating metabolic disorders.

Methods and systems are disclosed for phototreatment in which replaceable containers comprising one or more adjuvant (consumable or re-useable) substances are employed. The adjuvant substance can be, for example, a topical substance or a coolant. Systems are disclosed for using a topical substance to detect contact of a phototreatment device with a tissue, detect speed of a phototreatment device over the tissue, detect regions of tissue that have been treated by a phototreatment device and / or to provide other benefits to the tissue such as improved skin tone and texture, tanning, etc. Safety systems are also disclosed that ensure that a proper consumable substance and / or container is connected to a phototreatment device and / or directed to a proper target. Additionally, cooling systems and methods that utilize phase change materials for extracting heat from a light generating device are disclosed.

The present invention discloses a treatment for syndrome-X, and resulting complications, that include hyperlipidemia, hypertension, central obesity, hyperinsulinemia and impaired glucose intolerance. Diabetic complications include excess proinsulin levels.

The invention features a method for treating a patient diagnosed with, or at risk of developing, an immunoinflammatory disorder by administering a non-steroidal immunophilin-dependent immunosuppressant (NsIDI) and a Group A enhancer (e.g., antifungal agent, antigout agent, anti-infective agent, antiprotozoal agent, antiviral agent, humectant, sunscreen, vitamin D compound, microtubuline inhibitor, or zinc salt) or analog or metabolite thereof to the patient. The invention also features a pharmaceutical composition containing an NsIDI and Group A enhancer or analog or metabolite thereof for the treatment or prevention of an immunoinflammatory disorder.

The subject invention relates to monoclonal antibodies that have the ability to bolster the function of the GLP-1 receptor and may therefore have utility in the treatment of mammalian metabolic disorders such as, for example, diabetes. In particular, the invention describes the generation of fully human monoclonal antibodies made against extracellular domains of the human GLP-1 receptor which are capable of binding the intact receptor and activating it in a manner similar to the native ligand. Additionally, the invention describes methods used to generate and develop allosteric modulator antibodies of the human GLP-1 receptor with potential therapeutic uses.

A method for the treatment of obesity or other disorders by electrical activation or inhibition of the sympathetic nervous system is disclosed. This activation or inhibition can be accomplished by stimulating the greater splanchnic nerve or other portion of the sympathetic nervous system using an electrode. This nerve activation can result in reduced food intake and increased energy expenditure.

This invention relates to antibodies and antigen binding fragments and conjugates containing same, and / or alternative scaffolds, specific for LSR molecules, which are suitable drugs for immunotherapy and treatment of specific cancer.

Antibody to human IL-20 protein, a method for generation thereof and cells producing this antibody are disclosed. The antibody of the present invention has specificity to neutralizing hIL-20W-induced CPAE proliferation activity, and is useful for treating IL-20-induced inflammation, such as artheriosclerosis and rheumatoid arthritis.

A unique DHA product, 10, 17S-docosatriene (“Neuroprotectin D1” or “NPD1”), was found to provide surprisingly effective neuroprotection when administered right after an experimental stroke. Moreover, both nerve cells and retinal pigment epithelial (RPE) cells were found to synthesize 10,17S-docosatriene (NPD1) from DHA. NPD1 also potently counteracted H2O2 / TNFα oxidative stress-mediated cell apoptotic damage. Under the same oxidative-stress conditions, NPD1 up-regulated the anti-apoptotic Bcl-2 proteins, Bcl-2 and Bcl-xL, and decreased expression of the pro-apoptotic proteins, Bad and Bax. Moreover, in RPE cells NPD1 inhibited oxidative stress-induced caspase-3 activation, IL-1β-stimulated human COX-2 promoter expression, and apoptosis due to N-retinylidene-N-retinylethanolamine (A2E). Overall, NPD1 protected both nerve and retinal pigment epithelial cells from cellular apoptosis and damage due to oxidative stress. NPD1 concentration in the brain of Alzheimer's patients was found to be significantly decreased from that of controls. In cultured human brain cells, NPD1 synthesis was up-regulated by neuroprotective soluble β amyloid, and NPD1 was found to inhibit secretion of toxic β amyloid peptides.

The invention concerns a cosmetic composition for treating or preventing disorders associated with a greasy skin, in particular by an activity reducing sebum secretion, comprising as active principle at least one dicarboxylic fatty acid or one derivative of such a fatty acid. The invention concerns in particular cosmetic compositions for topical administration. The invention also concerns a cosmetic method for treating or preventing disorders associated with hyperseborrhea.

Pharmaceutical compositions containing a proanthocyanidin polymer composition which are useful for the treatment and prevention of secretory diarrhea are provided. The invention specifically relates to pharmaceutical formulations of a proanthocyanidin polymer composition which has been isolated from a Croton spp. or a Calophyllum spp. In particular, the invention relates to a formulation of a proanthocyanidin polymer composition which protects the composition from the effects of stomach acid after oral administration, particularly to those formulations which are enteric coated. The invention also relates to methods of producing a directly compressible proanthocyanidin polymer composition, as well as compositions containing the directly compressible proanthocyanidin polymer composition.

Mesenchymal stem cells that selectively promote or suppress inflammation are provided, as well as methods of producing and using the same.

Methods and systems are disclosed for phototreatment in which replaceable containers comprising one or more adjuvant (consumable or re-useable) substances are employed. The adjuvant substance can be, for example, a topical substance or a coolant. Systems are disclosed for using a topical substance to detect contact of a phototreatment device with a tissue, detect speed of a phototreatment device over the tissue, detect regions of tissue that have been treated by a phototreatment device and / or to provide other benefits to the tissue such as improved skin tone and texture, tanning, etc. Safety systems are also disclosed that ensure that a proper consumable substance and / or container is connected to a phototreatment device and / or directed to a proper target. Additionally, cooling systems and methods that utilize phase change materials for extracting heat from a light generating device are disclosed.

A method for treatment of obesity or other disorders by electrical activation or inhibition of nerves is disclosed. This activation or inhibition can be accomplished by stimulating a nerve using an electrode. The method further comprises performing a surgical procedure and / or administering a weight loss drug.

The present invention relates generally to a method of reducing unwanted airway tissue mucus secretion in a mammal and to agents useful for same. More particularly, the present invention relates to a method of reducing airway tissue mucus hypersecretion in a mammal by downregulating the functional level of activin or upregulating the functional level of follistatin. The method of the present invention is useful, inter alia, in the treatment and / or prophylaxis of conditions characterised by airway tissue mucus dysfunction, such as overproduction of mucus or decreased mucus clearance, and where a reduction in mucus secretion levels would thereby alleviate the condition.

Disclosed herein are methods of treating benign, pre-cancerous, or non-metastatic tumors using an anti-VEGF-specific antagonist. Also disclosed are methods of treating a subject at risk of developing benign, pre-cancerous, or non-metastatic tumors using an anti-VEGF-specific antagonist. Also disclosed are methods of treating or preventing recurrence of a tumor using an anti-VEGF-specific antagonist as well as use of VEGF-specific antagonists in neoadjuvant and adjuvant cancer therapy.

A dosage unit for treating constipation in a human patient is described. The dosage unit of the invention comprises a halogenated prostaglandin analog and a pharmaceutically suitable excipient. The dosage unit relieves constipation without substantial side effects.

The present invention provides compositions that contain botulinum toxin and a hyaluronidase, and that lack human or recombinant serum albumin. The present invention also provides methods of administering the pharmaceutical composition to a subject in need thereof.

The invention involves the treatment, prevention, and reduction of immunoinflammatory disorders involving the combination of an agent that increases the signal activity of a glucocorticoid receptor (e.g., glucocorticoid receptor agonist) and an agent that modulates the signaling activity of one or more signaling pathways selected from the NF-κB pathway, NFAT pathway, AP-1 pathway, and Elk-1 pathway such that proinflammatory cytokine secretion or production, or any other inflammatory response, is reduced. Further, screening methods are provided for identifying candidate compounds and strategies useful for treating, preventing, or reducing such conditions.

The present invention provides improved formulations of botulinum toxin that increase delivery of the botulinum toxin to neural and associated tissues and exhibit a higher specific neurotoxicity and higher potency (in LD50 Units) than available formulations of botulinum toxins. These improved formulations enable physicians to treat a wide variety of pathological conditions with a lower toxin load that reduces the risk of inducing an immune response against the toxin and its associated proteins that may ultimately lead to the development of toxin resistance. These benefits are particularly important in the treatment of conditions that require high-dose or chronic administration of botulinum toxin. Additionally, the decreased in LD50 Unit doses of inventive formulations allows for controlled administration limits diffusion. The present invention also provides methods of treating neuromuscular diseases and pain, using low-dose botulinum toxin.

The present invention relates to treatment of mucus hypersecretion, to compositions therfor and manufacture of those compositions. The present invention relates particularly, though not exclusively, to the treatment of chronic bronchitis in chronic obstructive pulmonary disease (COPD), asthma and other clinical conditions involving COPD.

The present invention relates to glucagon receptor polypeptide antagonists which inhibit the binding of the hormone glucagon to its receptor. More particularly, the present invention relates to high affinity glucagon receptor antibodies or Fab fragments thereof that inhibit binding of glucagon to its receptor and their use in the treatment or prevention of type 2 diabetes (NIDDM) and related disorders in mammalian species.