36 results about "Clinical reaction" patented technology

The invention discloses pills for treating a rheumatic heart disease and a preparation method thereof and belongs to the field of traditional Chinese medicines. Active ingredients of the pills comprise: by weight, 50 to 70 parts of cassia twig, 50 to 65 parts of mix-fried licorice root, 45 to 60 parts of dwarf lilyturf tuber, 45 to 60 parts of Chinese magnoliavine fruit, 40 to 55 parts of poria cocos, 40 to 50 parts of mix-fried milkvetch root, 40 to 50 parts of curcumae, 35 to 45 parts of pubescent holly root, 35 to 45 parts of red sage root, 30 to 40 parts of Chinese arborvitae kernel, 25 to 40 parts of snakegourd fruit, 20 to 30 parts of longan pulp, 20 to 30 parts of sichuan lovage rhizome, 15 to 30 parts of stir-fried milkwort root, 15 to 25 parts of grassleaf sweetflag rhizome and 10 to 25 parts of syzygium jambos seed. The pills utilizes the unique traditional Chinese medicines, has a good formula, has effects of tonifying qi, nourishing yin, dispelling wind, dissipating heat, relaxing muscles and tendons, invigorating the circulation of blood, strengthening vital qi and eliminating pathogens, and has good absorption effects, obvious curative effects, no toxic and side effect and no adverse clinical reactions. A clinical experiment proves that the pills have good effects of treatment on a rheumatic heart disease, and postoperative recovery.

A method for treating a subject afflicted with an autoimmune disease with a pharmaceutical composition comprising glatiramer acetate and a pharmaceutically acceptable carrier, comprising the steps of administering a therapeutic amount of the pharmaceutical composition to the subject, determining whether the subject is a glatiramer acetate responder or a glatiramer acetate hypo- / non-responder by measuring the value of a biomarker selected from the group consisting of IL-10 concentration, IL-17 concentration, IL-18 concentration, TNF-α concentration, BDNF concentration, caspase-1 concentration, IL-10 / IL-18 ratio and IL-10 / IL-17 ratio in the blood of the subject, and comparing the measured value to a reference value for the biomarker to identify the subject as a glatiramer acetate responder or a glatiramer acetate hypo- / non-responder, and continuing the administration if the subject is identified as a glatiramer acetate responder, or modifying treatment of the subject if the subject is identified as a glatiramer acetate hypo- / non-responder.

It has been determined that allergens, which are characterized by both humoral (IgE) and cellular (T cell) binding sites, can be modified to be less allergenic by modifying the IgE binding sites. The IgE binding sites can be converted to non-IgE binding sites by masking the site with a compound that prevents IgE binding or by altering as little as a single amino acid within the protein, most typically a hydrophobic residue towards the center of the IgE-binding epitope, to eliminate IgE binding. The method allows the protein to be altered as minimally as possible, other than-within the IgE-binding sites, while retaining the ability of the protein to activate T cells, and, in some embodiments by not significantly altering or decreasing IgG binding capacity The examples use peanut allergens to demonstrate alteration of IgE binding sites. The critical amino acids within each of the IgE binding epitopes of the peanut protein that are important to immunoglobulin binding have been determined. Substitution of even a single amino acid within each of the epitopes led to loss of IgE binding. Although the epitopes shared no common amino acid sequence motif, the hydrophobic residues located in the center of the epitope appeared to be most critical to IgE binding.

We identify markers capable of guiding the decision to incorporate epidermal growth factor receptor (EGFR) inhibitors, in particular EGFR tyrosine kinase inhibitors (TKIs), into chemotherapeutic regimens. Mitogen-inducible gene 6 (Mig6), a negative regulator of EGFR, is selectively upregulated during the development of resistance to the EGFR tyrosine kinase inhibitor (TKI) erlotinib, resulting in decreased EGFR phosphorylation. The ratio of Mig6 / EGFR expression highly correlates with erlotinib sensitivity. A low Mig6 / EGFR ratio correlates with a high response rate to gefitinib and a marked increase in progression-free survival for patients. The ratio of Mig6 to EGFR is a major predictor of biologic and clinical responses to EGFR inhibitors.

The present invention provides diagnostic methods for predicting therapeutic efficacy in an individual being treated for an autoimmune or an inflammatory disease. In addition, the present invention also provides novel methods for monitoring azathioprine therapy or optimizing clinical responsiveness to azathioprine therapy in an individual by measuring 6-thioguanosine nucleotide levels in a sample from the individual.

It has been determined that allergens, which are characterized by both humoral (IgE) and cellular (T cell) binding sites, can be modified to be less allergenic by modifying the IgE binding sites. The IgE binding sites can be converted to non-IgE binding sites by masking the site with a compound that prevents IgE binding or by altering as little as a single amino acid within the protein, most typically a hydrophobic residue towards the center of the IgE-binding epitope, to eliminate IgE binding. The method allows the protein to be altered as minimally as possible, other than-within the IgE-binding sites, while retaining the ability of the protein to activate T cells, and, in some embodiments by not significantly altering or decreasing IgG binding capacity The examples use peanut allergens to demonstrate alteration of IgE binding sites. The critical amino acids within each of the IgE binding epitopes of the peanut protein that are important to immunoglobulin binding have been determined. Substitution of even a single amino acid within each of the epitopes led to loss of IgE binding. Although the epitopes shared no common amino acid sequence motif, the hydrophobic residues located in the center of the epitope appeared to be most critical to IgE binding.

The present invention provides a method to quantitatively measure the response of a patient to an immune-modulator drug that will aid clinicians in the determination of the optimal combination / posology of immunosuppressant / immune-modulator drugs. In addition, this method will open the possibility for clinicians to make the necessary adjustments in immunosuppressive therapy, as a way to avoid organ rejection to actually take place. Furthermore, this method will significantly reduce side effects of immunosuppressant drugs, optimizing therapeutic scheme and dosages, enabling the determination of the most effective immunosuppression regimen at the lower dosages for each patient individually and monitoring of treatment efficiency along time, thus opening the door to treatment personalization.

The invention relates to methods for determining the likelihood of the formation of a clinical response in an individual to therapy with an immunomodulatory agent for treatment of a disease or condition of the individual.

The present invention generally relates to diagnostic assays using cell cultures, in particular to chimeric antigen receptor (CAR) expressing reporter cell assays to analyze samples, in particular patient samples, to diagnose cancer by quantifying the expression of tumor antigens and / or predicting clinical response to cancer immunotherapies. A further aspect of the present invention is to improvesafety of e.g., cancer immunotherapies.

The invention relates to methods for predicting a clinical response to B-lymphocyte inhibiting or depleting therapies (BCIDT) using expression levels of genes of the Type I INF pathway. In another aspect, the invention relates to a method for evaluating a pharmacological effect of a treatment with B-lymphocyte inhibiting or depleting therapy. More in particular, the invention relates to a method for prognosticating the clinical response of a patient to treatment with a soluble BCID or TCID agent, said method comprising the steps of obtaining at least two samples from said patient wherein a first sample has not been exposed to a soluble BCID or TCID agent and wherein at least a second sample has been exposed to a soluble BCID or TCID agent, determining the level of an IFN-I type response in said at least two samples, comparing the level of the IFN-I type response in said first sample with the level of the IFN-I type response in said at least second sample and prognosticating said clinical response from said comparison.

The invention provides a method for predicting the clinical response to a cancer vaccine in a patient having cancer, a method for determining the immune response to a cancer vaccine in a patient having cancer who has been administered a cancer vaccine, a method for determining the long-term survival in a patient having cancer, corresponding kits therefor, as well as methods of for improving the efficacy of a virus-based vaccine.

The present invention provides a method for treating a human subject afflicted with multiple sclerosis or a single clinical attack consistent with multiple sclerosis with a pharmaceutical composition comprising glatiramer acetate and a pharmaceutically acceptable carrier, comprising the steps of:a) determining whether the human subject is a glatiramer acetate responder by evaluating expression of a biomarker selected from the group consisting of ERAP2, SIGLEC1, AAK1, KIAA1671, PLEKHA2, LOC730974, IFIT3, RWDD3, MYO6 SCARA3 and IFI44L, or a combination thereof, in human subject; andb) administering the pharmaceutical composition comprising glatiramer acetate and a pharmaceutically acceptable carrier to the human subject only if the human subject is identified as a glatiramer acetate responder.

The invention discloses a double gene-deleted strain of a pseudorabies virus variant, a construction method and an application thereof. The invention provides the pseudorabies virus strain with gI and gE genes being deleted. The pseudorabies virus variant is assigned the access number CGMCC. NO.8786. The invention further provides the construction method for the double gene-deleted strain. The construction method includes: (1) constructing a pseudorabies virus TJ strain transfer vector containing complete expression cassettes of EGFP and Neo; (2) transfecting the transfer vector to a cell which is inoculated with a pseudorabies virus TJ strain to obtain a transitional virus; and (3) performing an enzyme digestion process to a transitional viral genome, co-transfecting the enzyme digested transitional viral genome with the transfer vector and performing a plague screening process to obtain the double gene-deleted strain. The double gene-deleted strain is completely attenuated, is free of any clinical reaction after immunization of pigs, can rapidly induce generation of a specific antibody of pseudorabies virus, is high in neutralizing antibody titer and can provides a complete immune protection which aims at an attack of a presently-epidemic pseudorabies virus variant.

The invention provides a preparation method for a rhesus ovary and ovarian follicle generation model. According to the method, female rhesus monkeys are used as test objects, and each rhesus monkey is injected with 60 IU of luteinizing hormone LH each time and is injected twice everyday for seven days successively to prepare the rhesus ovary and ovarian follicle generation model. The invention also provides application of luteinizing hormone LH in preparing medicines for activating ovary and stimulating ovarian follicle thereof to grow. According to the invention, monkeys are used in the method for preparing the model, background data in physiology, hematology, blood biochemistry and the like of monkeys are abundant and easily available, monkeys have a biological background resembling to human beings, and therefore, test results of monkeys can well indicate clinical reactions of medicines; multi-aspect and multi-angle assessment are carried out, and obtained results can well and objectively indicate drug action on a reproductive system; animals (monkeys) and instruments (a B-mode ultrasonoscope, a microscope, a cell culture device, etc.) used in the model are simple and easily available, and the model has versatility.

The invention discloses a pill for treating chronic lymphocytic thyroiditis and a preparation method, belonging to the field of traditional Chinese medicines. The effective components of the pill disclosed by the invention are composed of the following raw materials: 65-80 g of Chinese yam, 63-76 g of radix pseudostellariae, 60-73 g of immature bitter orange, 57-70 g of wolfberry, 55-67 g of semen litchi, 53-65 g of radix bupleuri, 50-62 g of white atractylodes rhizome, 43-55 g of the root of three-nerved spicebush, 40-52 g of glossy privet fruit, 38-50 g of stellaria aquatica, 35-47 g of tendril-leaved fritillary bulb, 32-45 g of pericarpium citri reticulatae viride, 30-42 g of fructus forsythiae, 28-40 g of rhizoma atractylodis, 25-37 g of liquorice, 23-35 g of allium macrostemon, 20-33 g of rose, 18-30 g of fingered citron, 15-28 g of selfheal, 12-25 g of sea horse, 9-22 g of oyster, 6-15 g of turtle shell, 4-10 g of pumex, and 2-7 g of air potato. The selected medicinal materials in the invention accord with monarch, ministerial and adjuvant principles; aiming at pathogenesis, treatment is carried out according to different symptoms; both symptoms and root causes are treated; the pill disclosed by the invention has the effects of tonifying the spleen and kidney, promoting blood circulation to remove blood stasis and resolving hard lump, and has the advantages of being good in absorption effect, obvious in curative effect and free from toxic and side effects and poor in clinical reaction; and in addition, found from clinical verifications, the pill disclosed by the invention has higher curative rate to chronic lymphocytic thyroiditis.