648 results about "Inflammatory cell" patented technology

A new class of poly(beta-amino alcohols) (PBAAs) has been prepared using combinatorial polymerization. The inventive PBAAs may be used in biotechnology and biomedical applications as coatings (such as coatings of films or multilayer films for medical devices or implants), additives, materials, excipients, non-biofouling agents, micropatterning agents, and cellular encapsulation agents. When used as surface coatings, these PBAAs elicited different levels of inflammation, both in vitro and in vivo, depending on their chemical structures. The large chemical diversity of this class of materials allowed us to identify polymer coatings that inhibit macrophage activation in vitro. Furthermore, these coatings reduce the recruitment of inflammatory cells, and reduce fibrosis, following the subcutaneous implantation of carboxylated polystyrene microparticles. These polymers may be used to form polyelectrolyte complex capsules for cell encapsulation. The invention may also have many other biological applications such as antimicrobial coatings, DNA or siRNA delivery, and stem cell tissue engineering.

The present invention relates to methods for treating inflammation in body tissues. More specifically, certain disclosed methods relate to selectively inducing apoptosis in inflammatory immune cells by heating cells for a sufficient time and at a sufficient temperature to induce programmed cell death. The disclosed stents can be placed in contact with the inflammatory cells and heated under controlled conditions. The disclosed apparatus and methods are particularly suitable for treating athersclerotic plaques.

Caspase activity and apoptosis are promoted using active, dimeric Smac peptide mimetics of the general formula M1-M2, wherein moieties M1 and M2 are monomeric Smac mimetics and L is a covalent linker. Target cancerous or inflammatory cells are contacted with an effective amount of an active, dimeric Smac mimetic, and a resultant increase in apoptosis of the target cells is detected. The contacting step may be effected by administering to a pharmaceutical composition comprising a therapeutically effective amount of the dimeric mimetic, wherein the individual may be subject to concurrent or antecedent radiation or chemotherapy for treatment of a neoproliferative pathology.

Caspase activity and apoptosis are promoted using active, dimeric Smac peptide mimetics of the general formula M1-L-M2, wherein moieties M1 and M2 are monomeric Smac mimetics and L is a covalent linker. Target cancerous or inflammatory cells are contacted with an effective amount of an active, dimeric Smac mimetic, and a resultant increase in apoptosis of the target cells is detected. The contacting step may be effected by administering to a pharmaceutical composition comprising a therapeutically effective amount of the dimeric mimetic, wherein the individual may be subject to concurrent or antecedent radiation or chemotherapy for treatment of a neoproliferative pathology.

The present invention is directed to an integrated system and a method for utilizing the system to detect and remove blood-borne factors of interest, such as pathogens and / or toxins and / or cytokines, from blood or serum (blood) by contacting the blood with a solid, essentially nonporous substrate which has been surface treated with molecules or chemical groups (the adsorbent media or media) having a binding affinity for the pathogens and / or toxins to be removed (the adsorbents). The invention can be used to remove virulence factors, e.g. toxins, that are released from various pathogens. In one aspect, the invention is for the treatment of sepsis and infection, such as infections associated with battle field trauma.

The present invention relates to a method for extracorporeal removal of a pathogenic microbe, an inflammatory cell or an inflammatory protein from mammalian blood / use of a device comprising a carbohydrate immobilized on a solid substrate, said carbohydrate having a binding affinity for a pathogenic microbe, an inflammatory cell or an inflammatory protein, for extracorporeal removal of said pathogenic microbe, inflammatory cell or inflammatory protein from mammalian blood / use of a carbohydrate having a binding affinity for a pathogenic microbe, an inflammatory cell or an inflammatory protein, wherein said carbohydrate is immobilized on a solid substrate, in the preparation of a device for treatment of a condition caused or aggravated by said pathogenic microbe, inflammatory cell or inflammatory protein / and a method for treatment of a mammalian subject suffering from a condition caused or aggravated by a pathogenic microbe, an inflammatory cell or an inflammatory protein.

The present invention includes methods of modulating cellular secretory processes. More specifically the present invention relates to modulating or reducing the release of inflammatory mediators from inflammatory cells by inhibiting the mechanism associated with the release of inflammatory mediators from the vesicles or granules in the inflammatory cells. In this regard, the present invention discloses an intracellular signaling mechanism that illustrates several novel intracellular targets for pharmacological intervention in disorders involving secretion of inflammatory mediators from vesicles in inflammatory cells. MANS peptide and active fragments thereof are useful in such methods.

A polymeric biomaterial that facilitates cell-specific ingrowth. The polymeric biomaterial encourages the ingrowth of cell types while reducing the ingrowth of undesirable cell types. This activity encourages proper integration of prosthetic implants or scaffolds utilizing this biomaterial by discouraging encapsulation or the accumulation of inflammatory cells such as macrophages, while encouraging infiltration by desirable cells such as endothelial or smooth muscle cells. Short peptide sequences are included in a polymeric biomaterial that result in complementary activities. Peptide sequences that are specifically cleaved by proteases found within preferred cells are used to cross-link the biomaterial and lead to degradation by those cells. Peptide sequences taken from proteins involved in cell adhesion can also be attached to the biomaterial to encourage adhesion by preferred cells. Combined use of both peptides in the polymeric biomaterial provides both specific adhesion and selective ingrowth.

The present invention relates (a) to new compounds represented by Formula I:wherein M represents a macrolide subunit (macrolide moiety) derived from macrolide possessing the property of accumulation in inflammatory cells, V represents an anti-inflammatory steroid or nonsteroid subunit, or an antineoplastic or antiviral subunit and L represents a linking group covalently linking M and V; (b) to their pharmacologically acceptable salts, prodrugs and solvates, (c) to processes and intermediates for their preparation, and (d) to their use in the treatment of inflammatory / neoplastic / viral diseases and conditions in humans and animals.

An encapsulation system for use in the treatment of diabetes (Types 1 or 2, and LADA) are provided. The system has (1) a delivery vehicle comprising a selectively permeable membrane that allows passage of glucose, insulin and other nutrients through the membrane, but prevents large molecules such as antibodies or inflammatory cells from passing through the membrane; (2) a population of islet cells or insulin producing cells encapsulated by said membrane; and (3) a biological response modifier that may be in contact with the membrane or encapsulated by the membrane. Generally, the biological response modifier is a compound, including resolved enantiomers, diastereomers, tautomers, salts and solvates thereof, having the following formula:wherein:X, Y and Z are independently selected from a member of the group consisting of C(R3), N, N(R3) and S;R1 is selected from a member of the group consisting of hydrogen, methyl, C(5-9)alkyl, C(5-9)alkenyl, C(5-9)alkynyl, C(5-9)hydroxyalkyl, C(3-8)alkoxyl, C(5-9)alkoxyalkyl, the R1 being optionally substituted;R2 and R3 are independently selected from a member of the group consisting of hydrogen, halo, oxo, C(1-20)alkyl, C(1-20)hydroxyalkyl, C(1-20)thioalkyl, C(1-20)alkylamino, C(1-20)alkylaminoalkyl, C(1-20)aminoalkyl, C(1-20)aminoalkoxyalkenyl, C(1-20)aminoalkoxyalkynyl, C(1-20)diaminoalkyl, C(1-20)triaminoalkyl, C(1-20)tetraaminoalkyl, C(5-15)aminotrialkoxyamino, C(1-20)alkylamido, C(1-20)alkylamidoalkyl, C(1-20)amidoalkyl, C(1-20)acetamidoalkyl, C(1-20)alkenyl, C(1-20)alkynyl, C(3-8)alkoxyl, C(1-11)alkoxyalkyl, and C(1-20)dialkoxyalkyl.

The present invention relates to methods for the detection and therapy of inflamed tissue, whereby immune modulators are used to increase the uptake of diagnostic or therapeutic compositions by inflammatory cells.

This disclosure concerns methods for evaluating inflammatory cells and modulators of the inflammatory response in tumor tissue and other relevant tissue types. The methods entail: obtaining a tissue sample and processing said tissue sample to produce histologic slides of tissue sections; staining of the tissue sections to identify inflammatory cells and modulators of the inflammatory response; digitizing slides to produce an image of the stained tissue sections; digitally stratifying the tissue sample into tumor and other relevant tissue compartments; and using digital image analysis to quantify cell-based and cell population-based features. The quantification of cell-based and cell population-based features within a tissue compartment of interest is used to develop a summary score of the immune system-tissue compartment of interest interaction. Patient stratification and selection as candidates for a therapeutic approach is ultimately based on the summary score value.

The current invention relates to a process for increasing the efficacy of cancerous disease inhibiting therapeutic agents delivered to a treatment region of a tissue structure, such as a tumor. The multi-step procedure takes advantage of the resulting thermal stress response occurring as a result of exposure to the cold. Coordinating the thermal related stress response with the timing of cancerous disease inhibiting agent action provides a unique therapeutic regiment to treat tumors which provides a maximized effect on the tumor, protects normal cells, and activates local pro-inflammatory cells.

The invention belongs to the field of traditional Chinese medicine pharmacy, and relates to the novel medical usage of icaritin, in particular to the usage of icaritin in preparation of medicine for preventing and treating endotoxemia. Lipopolysaccharide (LPS) is used for stimulating the macrophage system RAW264.7 of a mouse and establishing an extraneous endotoxic inflammation model, LPS is used for stimulating the C57BL / 6J mouse and establishing the endotoxemia animal model, icaritin is adopted for intervention, and dexamethasone is used as reference. The experiment result shows that the icaritin can reduce the death rate, the level of the inflammatory factor, the inflammatory mediator and the adhesion molecules and infiltration of inflammatory cells of the tissue after the mouse is attacked by endotoxin, and proves that the icaritin can effectively prevent and treat endotoxemia and can be used for further preparing effective drug for preventing and treating endotoxemia, including dosage forms such as oral and enteric capsules or intravenous injections.

The present invention relates to methods for the detection and therapy of active atheromatous plaques, and in particular vulnerable plaques, whereby immune modulators are used to increase the uptake of diagnostic or therapeutic compositions by the inflammatory cells associated with such plaques.

A method for modifying access of cells to extravascular spaces and regions comprising administering to a patient an enzyme that cleaves chondroitin sulfate proteoglycans is provided. It has been found that administration of an enzyme that cleaves chondroitin sulfate proteoglycans to a patient disrupts extravasation of cells from the blood stream into tissue. The present invention provides methods of reducing penetration of cells associated with inflammation into tissue of a patient. Several methods are also provided for the regulation and suppression of inflammation comprising administering enzymes that digest chondroitin sulfates. Also provided are methods of treating and preventing inflammation associated with infection, injury and disease.

The present invention relates to a method for extracorporeal removal of a pathogenic microbe, an inflammatory cell or an inflammatory protein from mammalian blood / use of a device comprising a carbohydrate immobilized on a solid substrate, said carbohydrate having a binding affinity for a pathogenic microbe, an inflammatory cell or an inflammatory protein, for extracorporeal removal of said pathogenic microbe, inflammatory cell or inflammatory protein from mammalian blood / use of a carbohydrate having a binding affinity for a pathogenic microbe, an inflammatory cell or an inflammatory protein, wherein said carbohydrate is immobilized on a solid substrate, in the preparation of a device for treatment of a condition caused or aggravated by said pathogenic microbe, inflammatory cell or inflammatory protein / and a method for treatment of a mammalian subject suffering from a condition caused or aggravated by a pathogenic microbe, an inflammatory cell or an inflammatory protein.

Use of IL-31 agonists, including IL-31, are used to treat agonists are used to treat asthma, airway hyper-responsiveness or allergic rhinitis. The method comprise inhibiting, reducing, limiting or minimizing production of proimflammatory cytokines and include administration of the IL-31 agonsit during sensitization or challenge resulting in the asthma, airway hyper-responsiveness or allergic rhinitis state.

A medicament having inhibitory activity against NF-κB activation, which comprises a compound represented by the following general formula (I) or a pharmacologically acceptable salt as an active ingredient:wherein X represents a connecting group, A represents hydrogen atom or acetyl group, E represents an aryl group or a heteroaryl group, and ring X represents an arene or a heteroarene.

The present invention provides methods and compositions to modulate inflammation and inflammatory responses using Netrin polypeptides and Netrin receptors. Methods of the present invention comprise the use of Netrin polypeptides and Netrin receptors to decrease migration of inflammatory cells of the immune system to a site of injury or infection.

New recombinant oncolytic viral vectors have been constructed based on a known herpes simplex virus-1 with a single 34.5 gene and a synctial mutation (called OncSyn (OS) virus), which was designed to be more immunogenic than the parental OS virus largely due to deletion of the viral gene viral host shutoff (vhs) gene (the “OSV” virus). In another embodiment, the OSV virus was constructed to constitutively express 15-PGDH (the “OSVP” virus), the principal enzyme responsible for degradation of PGE2. OSVP was shown to decrease both breast tumors and prostate cancer tumors in mice models. In addition, OSVP was shown to trigger substantial inflammatory cytokine production and pro mote anti-tumor immune responsiveness. These altered viruses, OSV and OSVP, can be used to treat various cancers including breast, prostate, liver, colon, and other tissues. Other exogenous genes can be added to either OSV or OSVP to improve the therapeutic response.

A combination drug treatment for inhibiting stenosis or restenosis is disclosed. The combination treatment is an active component containing both an anti-inflammatory substance and an anti-thrombotic substance which, together, contribute to an inhibiting effect on the initial stages of stenosis or restenosis. The active component can be delivered to a site of treatment by being carried on a device, such as a stent.

The present invention relates (a) to new compounds represented by Formula I: wherein M represents a macrolide subunit (macrolide moiety) derived from macrolide possessing the property of accumulation in inflammatory cells, S represents a steroid subunit (steroid moiety) derived from steroid drug with anti-inflammatory activity and L represents a linker molecule linking M and S, (b) to their pharmacologically acceptable salts, prodrugs and solvates, (c) to processes and intermediates for their preparation, and (d) to their use in the treatment of inflammatory diseases and conditions in humans and animals. Such compounds inhibit many cytokines and immune mediators involved in immune responses which cause inflammation, allergy, or alloimmunity, including without limitation IL-1, 2, 4, 5, 6, 10, 12, GMCSF, ICAM, and TNF-α. Importantly, anti-inflammatory steroids exert a direct anti-inflammatory effect through binding to the glucocorticosteroid receptor.

The present invention provides methods or kits with inflammatory cytokines to pretreat 1-ISCs to augment their immune modulatory effect, in prevention and treatment of various diseases such as multiple sclerosis, arthritis, lupus, sepsis, hepatitis, cirrhosis, Parkinson's disease, chronic infections, and GvHD. The present invention relates to novel methods for enhancing the immunosuppressive or the immune stimulatory activities of mesenchymal stem cells (JvfSCs).

The present invention provides for uses of an anti-TNFα antibody or an antigen-binding fragment thereof for the manufacture of a medicament for use in the treatment of asthma or airway inflammation in an individual in need thereof. The present invention also provides for use of an anti-TNFα antibody or an antigen-binding fragment thereof for the manufacture of a medicament for use in reducing accumulation in lungs of inflammatory cells in an individual in need thereof.

An ophthalmological device comprises an implant member carrying an antifibrotic agent that is released slowly over a prolonged period when inserted into a wound in an eye produced by surgery. The member is placed in the vicinity of a wound created during the surgery to inhibit inflammatory cell proliferation, thereby preventing the growth of fibrous tissue after the eye surgery.