149 results about "E2 prostaglandin" patented technology

Disclosed are improvements in human nutrition involving a unique combination of natural products constituting anti-inflammatory compositions which can reduce cardiovascular disease risks as well as play a positive role in other conditions and diseases for which key indicators, especially selected from the group consisting of C-reactive protein (CRP) levels, cyclooxygenase-2 (COX-2), 5-lypoxygenase (5-LOX) expression and prostaglandin E2 (PGE-2) biosynthesis or any combination of these, are indicators. Therapeutic compositions preferably comprise curcumin, bilberry extract, grape seed extract, green tea extract and apple extract, in effective amounts individually and combined to provide a therapeutically significant reduction in one or more key indicators. Another exemplified therapeutic composition comprises: omega-3 rich refined fish oil, resveratrol, blueberry extract, grape seed extract, green tea extract and gamma and / or delta tocopherol, in effective amounts individually for the above benefits.

It has been discovered that the stimulation of beta-adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising beta-adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by beta-adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of beta-adrenergic receptors. It has further been found that the increase in APP synthesis caused by 8Br-cAMP, PG E2, forskolin, or nicotine ditartrate is inhibited by immunosuppressants or anti-inflammatory agents, such as cyclosporin A, and FK-506 (tacrolimus), as well as ion-channel modulators, including ion chelating agents such as EGTA, or calcium / calmodulin kinase inhibitors, such as KN93. The present invention has broad implications in the alleviation, treatment, or prevention of neurological disorders and neurodegenerative diseases, including Alzheimer's Disease.

It has been discovered that the stimulation of beta -adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising beta -adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by beta -adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of beta -adrenergic receptors. It has further been found that the increase in APP synthesis caused by 8Br-cAMP, PG E2, forskolin, or nicotine ditartrate is inhibited by immunosuppressants or anti-inflammatory agents, such as cyclosporin A, and FK-506 (tacrolimus), as well as ion-channel modulators, including ion chelating agents such as EGTA, or calcium / calmodulin kinase inhibitors, such as KN93. The present invention has broad implications in the alleviation, treatment, or prevention of neurological disorders and neurodegenerative diseases, including Alzheimer's Disease.

The present invention relates to engineered multivalent and multispecific binding proteins, methods of making, and specifically to their uses in the prevention, diagnosis, and / or treatment of disease.

The present invention encompasses prostaglandin E2 (PGE2) binding proteins. The invention relates to antibodies that are wild-type, chimeric, CDR grafted and humanized. Preferred antibodies have high affinity for prostaglandin E2 and neutralize prostaglandin E2 activity in vitro and in vivo. An antibody of the invention can be a full-length antibody, or an antigen-binding portion thereof. Methods of making and methods of using the antibodies of the invention are also provided. The antibodies, or antigen-binding portions, of the invention are useful for detecting prostaglandin E2 and for inhibiting prostaglandin E2 activity, e.g., in a human subject suffering from a disorder in which prostaglandin E2 activity is detrimental.

It has been discovered that the stimulation of beta-adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising beta-adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by beta-adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of beta-adrenergic receptors. It has further been found that the increase in APP synthesis caused by 8Br-cAMP, PG E2, or forskolin is inhibited by immunosuppressants, immunophilin ligands, or anti-inflammatory agents, such as cyclosporin A, and FK-506 (tacrolimus), as well as ion-channel modulators, including ion chelating agents such as EGTA, or calcium / calmodulin kinase inhibitors, such as KN93. The present invention has broad implications in the alleviation, treatment, or prevention of neurological disorders and neurodegenerative diseases, including Alzheimer's Disease.

It has been discovered that the stimulation of beta-adrenergic receptors, which activate cAMP formation, give rise to increased APP and GFAP synthesis in astrocytes. Hence, the in vitro or in vivo exposure of neuronal cells to certain compositions comprising beta-adrenergic receptor ligands or agonists, including, e.g., norepinephrine, isoproterenol and the like, increases APP mRNA transcription and consequent APP overproduction. These increases are blocked by beta-adrenergic receptor antagonists, such as propranolol. The in vitro or in vivo treatment of these cells with 8Br-cAMP, prostaglandin E2 (PG E2), forskolin, and nicotine ditartrate also increased APP synthesis, including an increase in mRNA and holoprotein levels, as well as an increase in the expression of glial fibrillary acidic protein (GFAP). Compositions and methods are disclosed of regulating APP overexpression and mediating reactive astrogliosis through cAMP signaling or the activation of beta-adrenergic receptors. It has further been found that the increase in APP synthesis caused by 8Br-cAMP, PG E2, or forskolin is inhibited by immunosuppressants, immunophilin ligands, or anti-inflammatory agents, such as cyclosporin A, and FK-506 (tacrolimus), as well as ion-channel modulators, including ion chelating agents such as EGTA, or calcium / calmodulin kinase inhibitors, such as KN93. The present invention has broad implications in the alleviation, treatment, or prevention of neurological disorders and neurodegenerative diseases, including Alzheimer's Disease.

The present invention relates to oncolytic vaccinia viruses which have been modified to promote anti-tumor immunity and / or reduce host immunity and / or antibody response against the virus. It is based, at least in part, on the discovery that oncolytic vaccinia virus (i) bearing a genome deletion of a gene that reduces T cell immunity (interleukin-18 binding protein); (ii) treated with a sialidase enzyme which is believed to reduce TLR2 activation and therefore the antibody response; (iii) carrying a gene that enhances cytotoxic T lymphocyte induction (e.g., TRIF) and / or (iv) reduces tumor myeloid-derived suppressor cells by reducing prostaglandin E2 reduces tumor growth. Accordingly, the present invention provides for immunooncolytic vaccinia viruses and methods of using them in the treatment of cancers.

The present invention relates to a method and combination therapy useful in the treatment of cancer. More specifically, the invention relates to the use of COX-2 inhibitors in combination with a therapeutic dendritic cell vaccine for treating cancer. The COX-2 inhibitors of the present invention are believed to inhibit the enzymatic activity of prostaglandineE2 (PGE2); thereby preventing COX-2 overexpressing tumors from evading immune surveillance by antigen-specific cytotoxic T lymphocytes (CTLs). COX-2 inhibitors are believed to suppress PGE2 that COX-2 overexpressing glioma produce, allowing tumor-infiltrating DCs to polarize Th cells toward Th-subset-1 (Th1).

Cationic ophthalmic oil-in-water type emulsions, include colloid particles having an oily core surrounded by an interfacial film, the emulsion including at least one cationic agent and at least one non ionic surfactant, the oily core including a prostaglandin selected from the group comprising in particular latanoprost, unoprostone isopropyl, travoprost, bimatoprost, tafluprost, 8-isoprostaglandinE2, or a mixture thereof, for treating ocular hypertension and / or glaucoma. These emulsions have the property to increase the chemical stability of prostaglandins.

Compositions and methods that employ various combinations of such factors as retinoic acid signaling inhibitors, antioxidants, BMP4, VEGF, prostaglandin E2 pathway stimulants, TPO, SCF, FLT-3, EPO, TGFβ1, p38 MAPK inhibitors, beta adrenergic receptor agonists, cell cycle inhibitors, RXR agonists, Cripto, and chromatin remodelers to drive differentiation of pluripotent stem cells towards primitive blood cells. Uses of such primitive blood cells are provided.

This invention relates to potent selective agonists of the EP, subtype of prostaglandin E2 receptors, their use or a formulation thereof in the treatment of glaucoma and other conditions which are related to elevated intraocular pressure in the eye of a patient. This invention further relates to the use of the compounds of this invention for mediating the bone modeling and remodeling processes of the osteoblasts and osteoclasts.

A method for inhibiting nitric oxide and / or prostaglandin E2 synthesis. The method comprises administering a composition to a subject, wherein the composition comprises an effective amount of butylidene phthalide, citronellol, geraniol or combinations thereof, which can be used to reduce or relieve the syndromes of the inflammation.

This invention relates to potent selective agonists of the EP4 subtype of prostaglandin E2 receptors of formula (I), their use or a formulation thereof in the treatment of glaucoma and other conditions which are related to elevated intraocular pressure in the eye of the patient. This invention further relates to the use of the compounds of this invention for mediating the bone modeling and remodeling processes of the osteoblasts and osteoclasts.

This invention relates to potent selective agonists of the EP4 subtype of prostaglandin E2 receptors of formula (1), their use or a formulation thereof in the treatment of glaucoma and other conditions which are related to elevated intraocular pressure in the eye of the patient.

This invention relates to potent selective agonists of the EP4 subtype of prostaglandin E2 receptors, their use or a formulation thereof in the treatment of glaucoma and other conditions, which are related to elevated intraocular pressure in the eye of a patient. This invention further relates to the use of the compounds of this invention for mediating the bone modeling and remodeling processes of the osteoblasts and osteoclasts.

This invention is related to the use of at least one oligonucleotide with a length of from about 8 to about 30 nucleotide building blocks for manufacturing a pharmaceutical preparation for the prophylaxis and / or the treatment of diseases, that are modulated by TGF-beta2, TGF-beta1, TGF-beta3, VEGF, interleukin-10, c-jun, c-fos, and / or prostaglandin E2 in a mammal, wherein said oligonucleotide hybridizes with a messenger RNA of a TGF-beta2, TGF-beta1, TGF-beta3, VEGF, interleukin-10, c-jun, c-fos and / or prostaglandin E2 gene and wherein said preparation comprises said oligonucleotide in a concentration of about 1 microM to about 25 microM.

This invention relates to the use of EP2 receptor subtype selective prostaglandin E2 agonists to augment bone mass including the prevention and treatment of skeletal disorders in mammals, including humans.

The invention discloses a tumor tissue 3D culture method suitable for culturing various tumor tissues. The tumor tissue 3D culture method comprises the following steps: 1) dropwise adding hydrogel into a pore plate, transferring cut tumor tissue blocks into the hydrogel, dropwise adding a culture solution, and standing in a CO2 incubator in order to freeze the hydrogel; 2) adding the culture solution into the pore plate for culturing, taking the cultured tumor tissue blocks out and fixing, wherein the culture solution is prepared from an Advanced DMEM / F12 culture solution, 1*GlutaMAX, an epidermis growth factor (EGF), a fibroblast growth factor FGF10, N-acetyl-L-cysteine (NAC), prostaglandin E2 PGE2, Nicotinamide and 50*B27. Moreover, the invention further discloses a tumor tissue 3D culture solution. The method is suitable for a plurality of tumor tissues, can be used for rating the medicinal effects of antitumor drugs more rapidly and accurately, and overcomes the defects in cell 2D culturing and animal experiment rating methods; a more convenient and economical modeling method is provided for clinical medicament researches and new medicament development.

The invention discloses hydrogel for repairing injured tissue and a preparation method thereof. The preparation method comprises the following steps: dissolving a hydrogel material through sterile distilled water, and swelling to obtain hydrogel; dissolving PGE2 powder into a phosphate buffering solution to prepare a PGE2 solution; dropwise adding the PGE2 solution into the hydrogel; stirring for 3-5 hours under the temperature of 2-8 DEG C; storing or storing by freezing, wherein the PGE2 is the abbreviation of prostaglandin E2. With the adoption of the hydrogel, the release time of PGE2 can be certainly prolonged; the hydrogel is directly applicable to the treatment of tissue injury, and is capable of promoting the recovery of injured skin tissue and function; the hydrogel is capable of inducing macrophage at the injured site to polarize to reach M2 type so as to inhibit inflammatory, thereby accelerating the healing of the injured tissue; in addition, the blood vessel at the injured part is promoted to regrow in early stage. Additionally, the hydrogel is free from cytotoxicity, can directly coat the surface of the injured tissue, is convenient to use, and low in price, and has an effective treatment effect.

The present invention discloses recombinant escherichia coli. The recombinant escherichia coli over-expresses an encoding gene of prostaglandin H synthase and an encoding gene of prostaglandin E synthase. The present invention also discloses an application of the recombinant escherichia coli in production of prostaglandin E2. The present invention also discloses a method for producing the prostaglandin E2. Arachidonic acid is used as a substrate and the recombinant escherichia coli is used to produce the prostaglandin E2. The escherichia coli strain capable of expressing the prostaglandin H synthase and the prostaglandin E2 synthetase is constructed and the expressed enzymes can directly catalyze conversion of the arachidonic acid into the prostaglandin E2.

The metabolic fingerprint and anti-inflammatory activity and anti-HIV activity of H. gentianoides is disclosed. High performance liquid chromatography (HPLC) analysis shows that H. gentianoides contains a family of compounds, including some not previously observed in other Hypericum species. H. gentianoides extracts and fractions from these extracts reduce prostaglandin E2 synthesis in mammalian macrophages and inhibit HIV in infected HeLa cells. The present invention provides extracts and fractions thereof from H. gentianoides for use in pharmaceutical compositions and methods for the treatment or inhibition of inflammation, prostaglandin E-mediated disease, disorder or condition, a cyclooxygenase-mediated disease, disorder or condition, or an HIV infection.

The invention provides a laetiporus sulphureus extract. The weight percentage of trametenloic acid B in the extract is 1-12 percent. The invention also provides application of the extract and the compound trametenloic acid B therein. The laetiporus sulphureus is a common edible fungus, has good safety, and can be prepared by large-scale fermentation; the prepared laetiporus sulphureus extract is stable in quality and strong in controllability; the laetiporus sulphureus extract and the traametenloic acid B obtained by separation have remarkable anti-inflammatory activity, can be used for treating acute and chronic rheumatic arthritis and rheumatoid arthritis, acute and chronic hepatitis, mastitis and other inflammatory diseases, can inhibit COX2 and reduce release of PGE2 (prostaglandin E2) and other inflammatory mediums, and provides a novel administration choice for clinical application.

The invention encompasses compositions and methods for effectively treating and / or preventing osteoporosis and related disorders such as osteoarthritis and rheumatoid arthritis, and for promoting overall bone and joint health. This is accomplished by totally addressing the multiple mechanisms that lead to such disorders. The invention includes compositions comprising a combination of agents that effectively suppress, regulate or interfere with the various biochemical processes and mechanisms that increase the risk for development of osteoporosis. The present compositions and methods simultaneously promote bone formation and reduce bone resorption by (a) stimulating osteoblast formation and osteogenesis; (b) suppressing adipocyte differentiation; (c) inhibiting osteoclast formation; and (d) increasing apoptosis of osteoclasts. The inventive compositions used for administration to human and other mammalian subjects having or at risk for development of osteoporosis comprise (1) at least one agent capable of modulating expression and / or activity of one or more of peroxisome activated protein receptor gamma (PPAR-γ), CAAT / enhancer binding protein-α (C / EBPα) and Sterol Regulatory Element-Binding Protein (SREBP-1); (2) at least one agent that activates expression and / or activity of one or more of the osteogenic transcription factors (Runx2 / Cbfα1, Dlx5, Osterix, Msx2); (3) at least one agent that activates expression and / or activity of one or more of bone morphogenetic proteins (BMPs: BMP 2 and 4), alkaline phosphatase (ALP), and osteocalcin; (4) at least one agent capable of activating Wnt / β-catenin signaling pathway; (5) at least one agent that inhibits the activity of pro-oxidants including reactive nitrogen species and reactive oxygen species (ROS); (6) at least one agent that suppresses one or more of inflammatory mediators including interleukins IL-1α, IL-1β, IL-6, NF-κB, TNF-α, matrix metalloproteinases (MMPs) and prostaglandin E2 (PGE2); and (7) at least one agent that induces the expression of and / or activates one or more of adenosine monophosphate-activated protein kinase (AMPK), sirtuin (SIRT1) and adiponectin (AP).

This invention relates to potent selective agonists of the EP4 subtype of prostaglandin E2 receptors, their use or a formulation thereof in the treatment of glaucoma and other conditions which are related to elevated intraocular pressure in the eye of a patient. This invention further relates to the use of the compounds of this invention for mediating the bone modeling and remodeling processes of the osteoblasts and osteoclasts.

Use of a benzoyl derivative of 3-aminocarbazole to produce a drug for the preventive or therapeutic treatment of a disorder selected form the group comprising inflammatory processes, pain, fever, tumours, Alzheimer's disease and atherosclerosis. Method for the preventive or therapeutic treatment of a disorder selected from the group comprising inflammatory processes, pain, fever, tumours, Alzheimer's disease and atherosclerosis in which a therapeutically effective quantity of a benzoyl derivative of 3-aminocarbazole according to the invention is administered to an individual.