294 results about "Inflammatory mediator" patented technology

This invention comprises administering to a human or animal in need of treatment an effective amount of an antioxidant lipoic acid derivative and/or pharmaceutically acceptable salts and solvates thereof for the treatment or prevention of pathological (inflammatory, proliferative and degenerative diseases, e.g. diabetes mellitus, atherosclerosis, Alzheimer's disease and chronic viral diseases) and non-pathological (e.g. skin aging and wrinkle formation) conditions caused by oxidative damage. Methods of synthesizing novel antioxidant lipoic acid derivatives and their use in preventing or treating diseases or conditions caused by oxidative stress and other free radical mediated conditions are described. Another aspect of this invention is the use of these antioxidant compositions for the protection of skin from damage caused by ultraviolet radiation and dessication, and to provide improved skin feel by desquamating, cleansing and clarifying the skin. The compositions described in this invention increase cellular viability of epidermal cells, promote cytoprotection, and decrease the production of inflammatory mediators such as inflammatory cytokines in these cells. The antioxidant compositions are incorporated into sunscreen products, soap, moisturizing lotions, skin toners, and other skin care products.

This invention relates to a method for the biochemical treatment of persistent pain disorders by inhibiting the biochemical mediators of inflammation in a subject comprising administering to said subject any one of several combinations of components that are inhibitors of biochemical mediators of inflammation. Said process for biochemical treatment of persistent pain disorders is based on Sota Omoigui's Law, which states: ‘The origin of all pain is inflammation and the inflammatory response’. Sota Omoigui's Law of Pain unifies all pain syndromes as sharing a common origin of inflammation and the inflammatory response. The various biochemical mediators of inflammation are present in differing amounts in all pain syndromes and are responsible for the pain experience. Classification and treatment of pain syndromes should depend on the complex inflammatory profile. A variety of mediators are generated by tissue injury and inflammation. These include substances produced by damaged tissue, substances of vascular origin as well as substances released by nerve fibers themselves, sympathetic fibers and various immune cells. Biochemical mediators of inflammation that are targeted for inhibition include but are not limited to: prostaglandin, nitric oxide, tumor necrosis factor alpha, interleukin 1-alpha, interleukin 1-beta, interleukin-4, Interleukin-6 and interleukin-8, histamine and serotonin, substance P, Matrix Metallo-Proteinase, calcitonin gene-related peptide, vasoactive intestinal peptide as well as the potent inflammatory mediator peptide proteins neurokinin A, bradykinin, kallidin and T-kinin.

It has been found that dendritic cells can be prepared which cannot mature. These cells can provide signal 1 to T cells but cannot provide co-stimulatory signal 2. T cells which are stimulated by the permanently immature dendritic cells therefore anergise, so the dendritic cells are tolerogenic rather than immunogenic. The cells are generally CD40^−ve, CD80^−ve and CD86^−ve, and remain so when stimulated by inflammatory mediators such as lipopolysaccharide. The cells can be prepared conveniently by the culturing adherent embryonic stem cells in the presence of GM-CSF.

Administering water-soluble or dispersible synthetic analogs or derivatives of astaxanthin, lutein, zeaxanthin, or lycophyll and/or other carotenoids to a subject may reduce some of the adverse effects of inflammation in a body organ or tissue. The analogs or derivatives may be incorporated into pharmaceutical, over-the-counter, or nutraceutical preparations. Administration of the analogs or derivatives described herein may reduce deposition of inflammatory mediators such as C-reactive protein, complement system proteins or the membrane attack complex (MAC) in tissues. Reduced deposition of these molecules in tissues may reduce cell damage and/or lysis in the tissues.

This invention encompasses methods, pharmaceutical compositions, and kits for modulating (e.g. reducing) the production of pro-inflammatory mediators involved in the pathology of a lung disease, disorder, and/or injury in a patient having the lung disease, disorder, and/or injury. The invention also encompasses methods, pharmaceutical compositions, and kits for inhibiting the production of pro-inflammatory mediators involved in the pathology of a lung disease, disorder, and/or injury in a patient having the lung disease, disorder, and/or injury. In one embodiment, the umbilical cord tissue-derived cells are isolated from human umbilical cord tissue substantially free of blood, are capable of self-renewal and expansion in culture, lack the production of CD117 or CD45, and do not express hTERT or telomerase.

The present invention relates generally to a method of modulating an inflammatory response in a mammal and to agents useful for same. More particularly, the present invention relates to a method of modulating an inflammatory response in a mammal by modulating the functional activity of activin and thereby modulating the pro-inflammatory mediator cascade. The method of the present invention is useful, inter alia, in the treatment and/or prophylaxis of conditions characterised by an aberrant, unwanted or otherwise inappropriate inflammatory response including, inter alia, sepsis and inflammation of the airway. The present invention is further directed to methods for identifying and/or designing agents capable of modulating activin mediated regulation of the inflammatory response.

Permselective asymmetric membranes suitable e.g. for hemodialysis, hemodiafiltration and hemofiltration of blood, and having improved sieving characteristics providing enhanced removal of middle molecular weight substances, e.g. inflammatory mediators having a molecular weight between 20 and 40 kDa. The membranes comprise polyethersulfone and polyvinylpyrrolidone and are coated with hyaluronic acid or copolymers of 2-methacryloyloxyethyl phosphoryl choline and other vinyl polymerizable monomers. Processes for the preparation of these membranes, devices comprising these membranes, and the use of these membranes in hemodialysis, hemodiafiltration and hemofiltration of blood, as well as in bioprocessing, plasma fractionation and the preparation of protein solutions.

The invention belongs to the field of pharmacy, and relates to application of a hydrogen sulfide donor to the preparation of a medicine for treating central nervous system disease, in particular to application of the hydrogen sulfide donor, namely sodium hydrosulfide, or allyl cysteine and analogues thereof to the preparation of the medicine for treating the central nervous system disease. Integral animal model experiments prove that the sodium hydrosulfide and propargyl cysteine can reduce the learning and memory impairment of rats, increase the content of hydrogen sulfide in hippocampus tissues of the rats, inhibit the messenger ribonucleic acid (mRNA) expression of a tumor necrosis factor alpha and a receptor I thereof, inhibit an inflammatory mediator in the hippocampus tissues of rats with dementia and inhibit inflammation-related enzymes in the hippocampus tissues of the rats, and can be used as a medicine for treating Alzheimer disease and other inflammation-related central nervous system degenerative diseases such as Parkinson disease.

The present invention provides modulators of TNF, particularly peptides and their derivatives, particularly GEP peptides, which antagonize TNF and TNF-mediated responses, activity or signaling. The invention provides methods of antagonizing TNF and the modulation of TNF-mediated diseases or responses, including inflammatory diseases and conditions. Compositions of GEP peptides, including in combination with other inflammatory mediators, are provided. Methods of treatment, alleviation, or prevention of TNF-mediated diseases and inflammatory conditions, including rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, psoriasis, inflammatory bowel diseases, Chrohn's disease, ulcerative colitis, uveitis, inflammatory lung diseases, chronic obstructive pulmonary disease, are provided.

The invention discloses an adsorption material for blood purification and a preparation method thereof. The adsorption material is prepared by coupling a functionalization area with at least one ligand, wherein the functionalization area is formed by a carrier with 0.05-2mm particle size alone or by performing surface modifying on the carrier with 0.05-2mm particle size; and the ligand is capable of binding to at least one pathogenic component in blood or plasma, so that at least one pathogenic composition in whole blood or plasma can be selectively adsorbed. For the adsorption material disclosed by the invention, functional polymers and different ligands are introduced onto the surface of the carrier by using different methods according to different blood purification requirements, so as to achieve an effect of reducing circulating pathogenic substances and harmful pro-inflammatory mediators in a human body, and achieve personalized and functional aims of the adsorption material for blood purification. The adsorption material has the good market value and application prospect.

The invention provides a method of ameliorating systemic inflammation in a patient involving administering to the patient a therapeutically effective dose of composition including polystyrene divinyl benzene copolymer and a polyvinyl pyrrolidone polymer. More particularly, the method relates to using these polymers as an enteral sorbent preparation to remove inflammatory mediators, such as cytokines, from the intestinal lumen. The polymers can be in the form of a preparation of polystyrene divinyl benzene copolymer beads with a biocompatible polyvinyl pyrrolidone polymer coating.

A method and apparatus for preventing and treating septicemia in patient blood is provided. The extracorporeal system includes an antimicrobial device to inactivate at least 99% of bloodborne microorganisms, a hemoconcentrator/filtration unit to remove approximately 50-75% of target molecules from the patient blood and a filter unit to remove target molecules from patient blood from the sieved plasma filtrate. Target molecules are produced by microorganisms, as well as by the patient's cells. These molecules include endotoxins from Gram negative bacteria, exotoxins from Gram negative and Gram positive bacteria, as well as RAP protein mediator from Staphylococcus aureus, and cell mediators such as tumor necrosis factor-alpha, and interleukin 1-beta, interleukin 6, complement proteins C3a and C5a, and bradykinin.

Animal models for severe acute respiratory syndrome-coronavirus infection of humans are needed to elucidate SARS pathogenesis and develop vaccines and antivirals. Transgenic mice were developed expressing human angiotensin-converting enzyme 2, a functional receptor for the virus, under the regulation of a global promoter. A transgenic lineage, designated AC70, was among the best characterized against SARS coronavirus infection, showing weight loss and other clinical manifestations before reaching 100% mortality within 8 days after intranasal infection. Inflammatory mediators were also detected in these tissues, coinciding with high levels of virus replication. In contrast, infected transgene-negative mice survived without showing any clinical illness. The severity of the disease developed in these transgenic mice, AC70 in particular, makes these mouse models valuable not only for evaluating the efficacy of antivirals and vaccines, but also for studying SARS coronavirus pathogenesis and infection by other coronaviruses utilizing human ACE2 for viral entry into cells.

The invention relates to the technical field of drugs, and discloses a sponge-derived triterpene compound dysiarenone. The chemical structural formula of the compound is as follows in the description.The invention further discloses a preparation method of dysiarenone. The compound dysiarenone shows strong inhibitory activity on expression of COX-2 enzymes and release of inflammatory mediator PGE2 and can be used for preparing anti-inflammatory and anti-tumor drugs.

The invention concerns a product consisting of distilled water or of an aqueous solution hypotonic or substantially isotonic with respect to blood plasma or, less preferably, hypertonic with respect to blood plasma, to be administered on the nasal mucosa according to a specific operation mode in order to cause an inflammation of an irritative kind, for use in a treatment of stimulation of the endogenous production of inflammatory mediators, in the therapy and prevention of neurological disorders, in particular of degenerative disorders of the central and peripheral nervous system. The inflammatory mediators the endogenous production of which is stimulated comprise NGF, neurotrophin-3, neurotrophin-4, serotonin, substance P, heparin, ECF-A.