1079results about How to "Inhibit apoptosis" patented technology

The invention features methods for inhibiting immunostimulatory DNA-associated immune responses, through the administration of specific compounds of the general class of 9-aminoacridines and 4-aminoquiniolines. The invention also features methods of screening compounds useful in inhibiting immunostimulatory DNA-induced immune responses.

The present invention relates to novel Death Domain Containing Receptor-4 (DR4) proteins which are members of the tumor necrosis factor (TNF) receptor family. In particular, isolated nucleic acid molecules are provided encoding the human DR4 proteins. DR4 polypeptides are also provided as are vectors, host cells and recombinant methods for producing the same. The invention further relates to screening methods for identifying agonists and antagonists of DR4 activity and methods for using DR4 polynucleotides and polypeptides. The invention also relates to the treatment of diseases associated with reduced or increased levels of apoptosis using antibodies specific for DR4, which may be agonists and/or antagonists of DR4 activity.

The present invention relates to peptides, proteins, nucleic acids and cells for use in immunotherapeutic methods. In particular, the present invention relates to the immunotherapy of cancer. The present invention furthermore relates to tumor-associated T-cell peptide epitopes, alone or in combination with other tumor-associated peptides that can for example serve as active pharmaceutical ingredients of vaccine compositions that stimulate anti-tumor immune responses, or to stimulate T cells ex vivo and transfer into patients. Peptides bound to molecules of the major histocompatibility complex (MHC), or peptides as such, can also be targets of antibodies, soluble T-cell receptors, and other binding molecules.

The invention relates to a method for in-vitro amplification of NK cells, and in particular relates to a method for massive in-vitro amplification of NK cells, wherein the method comprises the following steps of: a, inoculating a peripheral blood mononuclear cell in a CD3McAb and CD226McAb pre-coated culture bottle for coculture; b, adding 1L-2 and 1L-18, coculturing for 72hours to stimulate amplification of NK cells; c, transferring the NK cells, K562 cells after lethal treatment and a serum-free medium containing 1L-2 and 1L-18 in a cell culture bag for coculture; and d, collecting the NK cells. According to the method for in-vitro amplification of the NK cells, two antibodies CD3McAb and CD226McAb are simultaneously coated, so the cell factor synthesis and ADCC effect are promoted, and killing toxicity of the NK cells is remarkably improved; the activation and amplification on the NK cells are achieved just by the 1L-2 and 1L-18 cell factors, so the amplification multiple and cell toxicity of the NK cells are guaranteed, and the cost of cell culture is reduced.

A method of treating a wound in a subject includes administering directly to the wound or an area proximate the wound an amount of SDF-I effective to promote healing of the wound of the subject.

The invention discloses a mutant human plasminogen kringle5 gene mK5 and an amplification primer of the mK5 gene, the mutant human plasminogen kringle5 gene modified by adding glutathione-S-transferase before the gene mK5, and a method for preparing protein mK5 recombinant protein of two gene codes, glutathioneS transferase (GST)-mK5 fusion protein and two proteins, wherein the mK5 gene and the GST-mK 5 gene can be applied to preparing medicaments for treating angiogenesis diseases. By the invention, the number of exogenous amino acid in the recombinant K5 protein molecules obtained by a gene engineering method is remarkably reduced, the K5 bioactivity of the obtained mK5 is improved, while the mK5 activity of the GST-mK5 fusion protein is maintained, the stability and water solubility of the protein are improved, the purification steps of an expressed product are simplified, and the purity of the product is improved.

The present invention discloses novel compounds of Formula (I), or pharmaceutically acceptable salts thereof, which have glucagon receptor antagonist or inverse agonist activity, as well as methods for preparing such compounds. In another embodiment, the invention discloses pharmaceutical compositions comprising compounds of Formula (I) as well as methods of using them to treat diabetic and other glucagon related metabolic disorders, and the like.

The present invention relates to compounds according to formula (I) as disclosed herein as well as pharmaceutical compositions which include those compounds. Also disclosed are methods of using such compounds, which have activity as agonists or as antagonists of LPA receptors; such methods including inhibiting LPA activity on an LPA receptor, modulating LPA receptor activity, treating cancer, enhancing cell proliferation, treating a wound, treating apoptosis or preserving or restoring function in a cell, tissue, or organ, culturing cells, preserving organ or tissue function, and treating a dermatological condition.

The invention discloses a proliferation accelerator for human adipose-derived stem cells and an application method thereof. The proliferation accelerator for the human adipose-derived stem cells comprises insulin, hydrocortisone, parathyroid hormone, estradiol, testosterone, a platelet-derived growth factor-AB, an epidermal growth factor, a basic fibroblast growth factor, L-glutamine, 2-mercaptoethanol, a leukemia inhibitory factor, L-ascorbic acid, biotin, dexamethasone, an IGF-I (Insulin-like Growth Factor-I) and a SCF (Stem Cell Factor). The proliferation accelerator for the human adipose-derived stem cells, disclosed by the invention, is applied to proliferation and subculture of the adipose-derived stem cells, can be used to not only specifically promote the growth sped and the proliferation quantity of the adipose-derived stem cells to increase in the form of geometric progression, but also suppress early differentiation and maturity of the adipose-derived stem cells so as to prevent apoptosis or premature senility of the stem cells during culturing and keep the vigorous and active differentiation potentials of the adipose-derived stem cells. The proliferation accelerator for the human adipose-derived stem cells, disclosed by the invention, has good application prospect in the field of culture of the adipose-derived stem cells.

The invention discloses nutrient gel for sterilizing and healing a wound surface and belongs to the technical field of anti-bacteria gel. The nutrient gel for sterilizing and healing the wound surface is prepared from hydroxyethyl cellulose, chitosan and derivatives thereof, guanidine polymers, glycerinum and compound amino acid. The hydroxyethyl cellulose serves as a gel substrate, the gel which is used for sterilizing and healing the wound surface and contains the guanidine polymers, the chitosan and derivatives thereof and the compound amino acid is prepared through a simple process, and the nutrient gel has good skin compliance, is non-irritant, has sterilization and anti-inflammation functions, provides a certain nutrition support for the wound surface, effectively promotes healing and recovery of the wound surface, has no side effects and is safe and environment-friendly.

The invention relates to a method for culturing gamma-delta-T cells, and in particular relates to a method for in-vitro amplification of gamma-delta-T cells, wherein the method comprises the following operating steps of: pre-coating a T75 culture bottle by a TCR-gamma-delta resisting antibody and CD28McAb for later use use; isolating the peripheral blood mononuclear cell (PBMC) of a patient; regulating the PBMC concentration to 1*10<6> 6/ml by a serum-free culture medium which contains 5% of autologous plasma, and transferring PBMC cell suspension into the T75 culture bottle; adding an initial culture medium which contains proper concentrations of Zoledronat, HSP70, 1L-2, 1L-7 and 1L-15; culturing in a saturated humid environment containing 5% of CO2 at 37 DEG C; depending on growth situation of the cell, changing the culture medium every 2-3days, to control the cell concentration at about 2.5*10<6>/ml; meanwhile, compensating full doses of Zoledronat, HSP70, 1L-2, 1L-7 and 1L-15; and continuously culturing for 12-16days, to obtain a great amount of gamma-delta-T cells which are comparatively high in purity.

We have discovered that administering anti-ceramide antibody treats and prevents an array of diseases mediated by cytolytic T lymphocyte (CTLs)-induced killing and by damage to endothelial microvasculture, including radiation-induced GI syndrome, Graft vs. Host diseases, inflammatory diseases and autoimmune diseases. We have also discovered new anti-ceramide monoclonal antibodies, that have therapeutic use preferably in humanized form to treat or prevent these diseases.

The invention belongs to the genetic engineering field, and especially relates to an application of long-chain non-coding RNA in the preparation of non-small cell lung cancer treatment drugs. The change of the lnc-uc002llc.1 expression has influences on the apoptosis, proliferation, the drug susceptibility and the like of non-small cell lung cancer cells, so the reduction of the lnc-uc002llc.1 expression can realize the apoptosis promotion, proliferation inhibition and chemotherapy drug susceptibility enhancement of the non-small cell lung cancer cells.

The invention discloses a firming and repairing fair mask product which is prepared by soaking mask paper with the liquid prepared from the following raw materials in parts by weight: 0.1-3 parts of hyaluronic acid oligomer, 0.1-2.5 parts of hyaluronic acid, 0.7-30 parts of synthetic egg white powder, 1-7 parts of an aloe extract, 0.7-9 parts of propylene glycol, 5-50 parts of 1,2-butylene glycol, 5-30 parts of glycerol, 40-80 parts of a ginseng extract, 10-50 parts of a milkvetch root extract, 20-50 parts of a baical skullcap root extract, 20-80 parts of a small cucumber extract, 0.1-1 part of a licorice extract, 0.3-2 parts of arbutin, 1-10 parts of superoxide dismutase, 1-10 parts of a coenzyme q10, 0.1-5 parts of beta-glucan, and the balance of water which is added until the total amount is 1000 parts. The mask product can reduce skin injuries, repair damaged cells, delay skin wrinkling, relieve the generation of facial dark stains and replenish and lock water, and is antiallergic.

The present invention provides a smart contact lens including a sensor capable of non-invasively sensing an eye disease in real time and a drug reservoir, and smart glasses for controlling the smart contact lens.

The invention provides a novel approach to increase immunoglobulin expression in non-human transgenic animals. For instance, the invention provides a method to increase humanized immunoglobulin production in animals genetically engineered to express one or several human or humanized immunoglobulin transloci. This can be done by overexpressing the apoptosis inhibitor, i.e. a rabbit bcl-2, whose expression is driven by a B-cell specific promoter specifically in the B-cell of the animal, thereby enhancing the survival of B-cells. This invention further relates to a method for selectively enhancing the survival of exogenous B-cells, that is B-cells expressing any immunoglobulin transgene locus, over the survival of endogenous B-cells that do not express the transgene locus. Selectivity is achieved by expressing the apoptosis-inhibitor only within exogenous B-cells, that is, by coupling exogenous immunoglobulin expression with apoptosis inhibitor expression. This latter method allows for increased expression and production of the transgene encoded product(s) over the endogenously produced immunoglobulin of the transgenic animal. The invention also provides a novel apoptosis-inhibitor, rabbit bcl-2.

The invention provides a vector encoding a derivative of EBNA-1 that is not cytotoxic when expressed efficiently in cells, which supports extrachromosomal replication, maintenance and transcription from extrachromosomal oriP containing vectors but does not substantially activate transcription from host cell genes. Also provided is a vector having oriP and encoding a derivative of EBNA-1. The vectors of the invention may be employed in vitro and in gene therapy.

The invention discloses a method for separating and culturing primary chicken hepatocytes. According to the method, EGTA (Ethylene Glycol Tetraacetic Acid) with low hepatotoxicity is added into a perfusate A to loosen the junction between hepatocytes, so that the dispersion degree of the to-be-separated hepatocytes is increased; double resistance is added into the perfusate A, a perfusate B and D-Hanks flushing fluid, so that the pollution is further prevented; and circulating perfusion digestion is adopted during digestion perfusion, so that the perfusion cost is greatly reduced. A serum-free cultural method of the chicken hepatocytes is established; compared with a traditional serum cultural method, the method disclosed by the invention has the same effect on the aspects of cell quantity, activity, function and the like, so that the problems caused by the existence of serum are solved and a foundation is laid for the substance metabolism study and biological product preparation on the basis of the chicken hepatocyte culture.

The present invention discloses compounds of Formula I: (I) having 11beta-HSD type 1 antagonist activity, as well as methods for preparing such compounds. In another embodiment, the invention discloses pharmaceutical compositions comprising compounds of Formula I, as well as the use of the Fomula I and compositions as medicaments to treat diabetes, hyperglycemia, obesity, hypertension, hyperlipidemia, Syndrome X, and other conditions associated with hyperglycemia.

Mitogen induced nuclear orphan receptor (MINOR) is described as inducing apoptosis in dendritic cells (DCs). Downregulation of its expression results in a downregulation of apoptosis. A novel approach of inhibiting DC apoptosis is described employing small interfering RNA (siRNA) that targets MINOR. Improved DC-based vaccines exhibiting longer lifespan of DCs, increased potency of DCs, and enhanced immunogenicity are described.

The present invention discloses novel compounds of Formula I, or pharmaceutically acceptable salts thereof, which have glucagon receptor antagonist or inverse agonist activity, as well as methods for preparing such compounds. In another embodiment, the invention discloses pharmaceutical compositions comprising compounds of Formula I as well as methods of using them to treat diabetic and other glucagon related metabolic disorders, and the like.

Disclosed is an AGE production inhibitor or the like, which effectively inhibits the production of an advanced glycation end product (AGE), while having improved biological safety. Specifically disclosed is an AGE production inhibitor or the like, which contains an extract of cherry (preferably blossoms or leaves thereof) and/or a processed product of the extract as an active ingredient. The AGE production inhibitor or the like contains, as an active ingredient, at least one compound that is selected from the group consisting of 1-O-(E)-caffeoyl-ss-D-glucopyranoside, 1-O-(E)-coumaroyl-ss-D-glucopyranoside, 1-O-(E)-cinnamoyl-ss-D-glucopyranoside, kaempferol 3-O-ss-D-glucopyranoside, quercetin 3-O-ss-D-glucopyranoside, kaempferol 3-O-(6"-malonyl)-ss-D-glucopyranoside, and quercetin 3-O-(6"-malonyl)-ss-D-glucopyranoside.

The present invention provides compounds of formula I that are useful as potent and selective inhibitors of 11-beta hydroxysteroid dehydrogenase 1. The present invention further provides a pharmaceutical composition which comprises a compound of Formula I, or a pharmaceutical salt thereof, and a pharmaceutically acceptable carrier, diluent, or excipient. In addition, the present invention provides compositions comprising compounds of formula I for the treatment of metabolic syndrome, diabetes, hyperglycemia, obesity, hypertension, hyperlipidemia, other symptoms associated with hyperglycemia, and related disorders. Formula (I) wherein, Ru⁰ is (II), or (III) G¹ is methylene or ethylene; L is a divalent linking group selected from —(C₁-C₄) alkylene-, —S—, —CH(OH)—, or —O—; A is methylene, —S—, —O—, or —NH—; and the other substituents are as defined in the claims.

The invention discloses moisturizing lotion for repairing skin barriers and resisting free radicals. The moisturizing lotion comprises, in weight percent, 2%-6% of polyhydric alcohols, 0.2%-3% of thickening suspending agents, 1%-5% of natural squalane, 2.5%-4.5% of emulsifying agents, 0.1%-3% of ceramide NP, 0.1%-5% of nicotinamide, 0.1%-2% of lycopene, 0.5%-3% of grape seed extracts, 0.1%-1% of ferulic acid, 0.1%-2% of coenzyme Q10, 0.1%-2% of vitamin E and the balance water. By the aid of the proportion and combination of different components, a novel local treatment formula can be developedaccording to skin lesion relevant to a plurality of cuticles and skin damage and resistance of the free radicals. The components in the formula are necessary components forming skin permeability barriers and have synergistic interaction between antioxidant components, the skin barriers can be repaired, protection films are formed on the surfaces of skins, the moisturizing lotion resists oxidationand the free radicals, damage of external factors to the skins is avoided, transepidermal water loss rate is effectively reduced, and the moisturizing lotion has good moisturizing effects on the skins.

The present invention provides compounds of formula I that are useful as potent and selective inhibitors of 11-beta hydroxysteroid dehydrogenase 1. The present invention further provides a pharmaceutical composition which comprises a compound of Formula I, or a pharmaceutical salt thereof, and a pharmaceutically acceptable carrier, diluent, or excipient. In addition, the present invention compositions containing these compounds for the treatment of metabolic syndrome, diabetes, hyperglycemia obesity, hypertension, hyperlipidemia, other symptoms associated with hyperglycemia, and related disorders. Formula I wherein G¹ is methylene or ethylene; L is —(C₁-C₄)alkylene-, —S—, —CH(OH)—, or —O—; R⁰ is Formula II or Formula III and the other substituents are as defined in the claims.