2080 results about "Inflammatory response" patented technology

A method, and apparatus (10) for the controlled acceleration, and/or retardation of the body's inflammatory response generally comprises a foam pad (11) for insertion substantially into a wound site, a heating, a cooling pad (13) for application over the wound site (12), a wound drape (14) or sealing enclosure of the foam pad (11), the heating, and cooling pad (13) at wound site (12). The foam pad (11) is placed in fluid communication with a vacuum source for promotion of the controlled acceleration or retardation of the body's inflammatory response. The heating, and cooling provision controls the local metabolic function as part of the inflammatory response.

A heart valve sewing prosthesis including an intrinsically conductive polymer. The invention includes annuloplasty rings and bands, and sewing rings or cuffs for prosthetic heart valves. Some annuloplasty rings and sewing rings include fabric that is coated with an intrinsically conductive polymer. The coating can be formed over individual filaments or fibers, or on the fabric surface as a surface layer. One intrinsically conductive polymer is polypyrrole. The intrinsically conductive polymer can be doped to facilitate the intrinsic conductivity. Some devices have a polypyrrole surface layer doped with dialkyl-napthalene sulfonate. The intrinsically conductive polymer can be deposited on a fabric using in-situ polymerization of monomeric or oligomeric species, together with a dopant. Animal studies using implanted annuloplasty rings having an intrinsically conductive polymer coating have demonstrated a substantial reduction in pannus formation and inflammatory response.

Silver-containing, sol-gel derived bioactive glass compositions and methods of preparation and use thereof are disclosed. The compositions can be in the form of particles, fibers and/or coatings, among other possible forms, and can be used, for example, for treating wounds, improving the success of skin grafts, reducing the inflammatory response and providing anti-bacterial treatments to a patient in need thereof. Anti-bacterial properties can be imparted to implanted materials, such as prosthetic implants, sutures, stents, screws, plates, tubes, and the like, by incorporating the compositions into or onto the implanted materials. The compositions can also be used to prepare devices used for in vitro and ex vivo cell culture.

Methods for treating xenogenic tissue for implantation into a human body including in-situ polymerization of a hydrogel polymer in tissue, and tissue treated according to those methods, where the polymerization takes place in tissue that has not been fixed with glutaraldehyde. The polymerization may only fill the tissue, bind the polymer to the tissue, or cross-link the tissue through the polymer, depending on the embodiment. One method includes free radical polymerization of a first vinylic compound, and can include cross-linking through use of a second compound having at least two vinyl groups. Another method utilizes nucleophilic addition polymerization of two compounds, one of which can include PEG and can further include hydrolytically degradable regions. In one embodiment, applicants believe the in-situ polymerization inhibits calcification, and that the polymerization of tissue un-fixed by glutaraldehyde allows for improved penetration of the polymer. The methods find one use in the treatment of porcine heart valve tissue, intended to extend the useful life of the valves by inhibiting calcification. The incorporation of degradable hydrogel regions may initially fill the tissue and reduce any initial inflammatory response, but allow for later infiltration by cells to remodel the tissue.

The present invention relates to methods and compositions for symptom-based differential diagnosis, prognosis, and determination of treatment regimens in subjects. In particular, the invention relates to methods and compositions selected to rule in or out SIRS, or for differentiating sepsis, severe sepsis, septic shock and/or MODS from each other and/or from non-infectious SIRS.

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.

Provided are electrokinetically-altered fluids (gas-enriched electrokinetic fluids) comprising an ionic aqueous solution of charge-stabilized oxygen-containing nanostructures in an amount sufficient to provide modulation of at least one of cellular membrane potential and cellular membrane conductivity, and therapeutic compositions and methods for use in treating diabetes and diabetes-associated conditions or disorders (e.g., insulin resistance), or symptoms thereof. Provided are electrokinetically-altered ioinic aqueous fluids optionally in combination with other therapeutic agents. Particular aspects provide for regulating or modulating intracellular signal transduction associated with said inflammatory responses by modulation of at least one of cellular membranes, membrane potential, membrane proteins such as membrane receptors, including but not limited to G-Protein Coupled Receptors (GPCR), and intercellular junctions (e.g., tight junctions, gap junctions, zona adherins and desmasomes). Other embodiments include particular routes of administration or formulations for the electrokinetically-altered fluids (e.g., electrokinetically-altered gas-enriched fluids and solutions) and therapeutic compositions.

The invention provides a method for alleviating pain associated with neuromuscular or skeletal injury or inflammation by controlled and directed delivery of one or more biological response modifiers to inhibit the inflammatory response which ultimately causes acute or chronic pain. Controlled and directed delivery can be provided by implantable or infusion pumps, implantable controlled release devices, or by sustained release compositions comprising biological response modifiers.

Provided are electrokinetically-altered fluids (e.g., gas-enriched electrokinetic fluids) comprising an ionic aqueous solution of charge-stabilized oxygen-containing nanostructures in an amount sufficient to provide modulation of at least one of cellular membrane potential and cellular membrane conductivity, and therapeutic compositions and methods for use in treating a wound to a surface tissue or a symptom thereof. The electrokinetically-altered fluids or therapeutic compositions and methods include electrokinetically-altered ionic aqueous fluids optionally in combination with other therapeutic agents. Particular aspects provide for regulating or modulating intracellular signal transduction associated with said inflammatory responses by modulation of at least one of cellular membranes, membrane potential, membrane proteins such as membrane receptors, including but not limited to G-Protein Coupled Receptors (GPCR), and intercellular junctions (e.g., tight junctions, gap junctions, zona adherins and desmasomes). Other embodiments include particular routes of administration or formulations for the electrokinetically-altered fluids (e.g., electrokinetically-altered gas-enriched fluids and solutions) and therapeutic compositions.

A modified starch material for biocompatible hemostasis, biocompatible adhesion prevention, tissue healing promotion, absorbable surgical wound sealing and tissue bonding, when applied as a biocompatible modified starch to the tissue of animals. The modified starch material produces hemostasis, reduces bleeding of the wound, extravasation of blood and tissue exudation, preserves the wound surface or the wound in relative wetness or dryness, inhibits the growth of bacteria and inflammatory response, minimizes tissue inflammation, and relieves patient pain. Any excess modified starch not involved in hemostatic activity is readily dissolved and rinsed away through saline irrigation during operation. After treatment of surgical wounds, combat wounds, trauma and emergency wounds, the modified starch hemostatic material is rapidly absorbed by the body without the complications associated with gauze and bandage removal.

The invention relates to a modified starch material for biocompatible hemostasis, biocompatible anti-adhesion, tissue healing promotion, absorbable surgery sealing and tissue adhesion. The invention applies biocompatible modified starch to animal tissues, wherein the modified starch material has the molecular weight of more than 15,000 daltons, and the particle diameter of between 1 and 1,000 mu m. The modified starch hemostatic material has stypticity, reduces hemorrhage, blood oozing and tissue fluid oozing of wounds, maintains relative moistening or drying of wound surfaces or the wounds, inhibits bacterium growth and inflammation reaction, and contributes to locally diminish inflammation of the wounds and relieve pain of patients. Moreover, the modified starch material can wash local parts after operation is over and remove redundant modified starch which does not participate in hemostasis, and can easily remove haemostatic under the condition of debridement treatment after self-help and first-aid treatment of war wounds; and hemostatic materials with a small amount of modified starch can be absorbed by the body, so that the pain of tearing of gauzes and bandages on people is avoided.

Methods are described for preventing or reducing ischemia and/or systemic inflammatory response in a patient such as perioperative blood loss and/or systemic inflammatory response in a patient subjected to cardiothoracic surgery, e.g., coronary artery bypass grafting and other surgical procedures, especially when such procedures involve extra-corporeal circulation, such as cardiopulmonary bypass.

The present invention relates to methods and compositions for symptom-based differential diagnosis, prognosis, and determination of treatment regimens in subjects. In particular, the invention relates to methods and compositions selected to rule in or out SIRS, or for differentiating sepsis, severe sepsis, septic shock and/or MODS from each other and/or from non-infectious SIRS.

Methods for decellularizing mammalian tissue for use in transplantation and tissue engineering. The invention includes methods for simultaneous application of an ionic detergent and a nonionic detergent for a long time period, which may exceed five days. One method utilizes SDS as the ionic detergent and Triton-X 100 as the nonionic detergent. A long rinse step follows, which may also exceed five days in length. This long duration, simultaneous extraction with two detergents produced tissue showing stress-strain curves and DSC data similar to that of fresh, unprocessed tissue. The processed tissue is largely devoid of cells, has the underlying structure essentially intact, and also shows a significantly improved inflammatory response relative to fresh tissue, even without glutaraldehyde fixation. Significantly reduced in situ calcification has also been demonstrated relative to glutaraldehyde fixed tissue. Applicants believe the ionic and non-ionic detergents may act synergistically to bind protein to the ionic detergent and may remove an ionic detergent-protein complex from the tissue using the non-ionic detergent. The present methods find one exemplary use in decellularizing porcine heart valve leaflet and wall tissue for use in transplantation.

The invention provides a method for fabricating an implantable medical device to increase biocompatibility of the device, the method comprising: heat setting a polymer construct, wherein the polymer construct is at a temperature range of from about Tg to about 0.6(Tm−Tg)+Tg such that the set polymer construct comprises a crystalline structure having crystals at a size less than about 2 microns; and fabricating an implantable medical device from the heat set polymer construct.

Provided are electrokinetically-altered fluids (gas-enriched (e.g., oxygen-enriched) electrokinetic fluids) comprising an ionic aqueous solution of charge-stabilized oxygen-containing nanostructures in an amount sufficient to provide, upon contact with a cell, modulation of at least one of cellular membrane potential and cellular membrane conductivity, and therapeutic compositions and methods for using same in treating inflammation or at least one symptom thereof. The electrokinetically-altered fluid compositions and methods include electrokinetically-altered ionic aqueous fluids optionally in combination with other therapeutic agents. Particular aspects provide for regulating or modulating intracellular signal transduction associated with inflammatory responses by modulation of at least one of cellular membranes, membrane potential, membrane proteins such as membrane receptors, including but not limited to G-Protein Coupled Receptors (GPCR), and intercellular junctions (tight junctions, gap junctions, zona adherins and desmasomes). Other embodiments include particular routes of administration or formulations for the electrokinetically-generated fluids (electrokinetically-generated gas-enriched fluids and solutions) and therapeutic compositions.

Provided are electrokinetically-altered fluids (e.g., gas-enriched electrokinetic fluids) comprising an ionic aqueous solution of charge-stabilized oxygen-containing nanostructures in an amount sufficient to provide modulation of at least one of cellular membrane potential and cellular membrane conductivity, and therapeutic compositions and methods for use in treating a wound to a surface tissue or a symptom thereof. The electrokinetically-altered fluids or therapeutic compositions and methods include electrokinetically-altered ionic aqueous fluids optionally in combination with other therapeutic agents. Particular aspects provide for regulating or modulating intracellular signal transduction associated with said inflammatory responses by modulation of at least one of cellular membranes, membrane potential, membrane proteins such as membrane receptors, including but not limited to G-Protein Coupled Receptors (GPCR), and intercellular junctions (e.g., tight junctions, gap junctions, zona adherins and desmasomes). Other embodiments include particular routes of administration or formulations for the electrokinetically-altered fluids (e.g., electrokinetically-altered gas-enriched fluids and solutions) and therapeutic compositions.

The invention relates to methods of inhibiting production and function of 3-deoxyglucosone and other alpha-dicarbonyl sugars in skin thereby treating or prevention various diseases, disorders or conditions. Additionally, the invention relates to treatment of various diseases, disorders or conditions associated with or mediated by oxidative stress since 3DG induces ROS and AGEs, which are associated with the inflammatory response caused by oxidative stress.