62results about How to "Down-regulated expression" patented technology

The present methods and compositions are of use for treatment of conditions involving fibrosis, such as Peyronie's disease plaque, penile corporal fibrosis, penile veno-occlusive dysfunction, Dupuytren's disease nodules, vaginal fibrosis, clitoral fibrosis, female sexual arousal disorder, abnormal wound healing, keloid formation, general fibrosis of the kidney, bladder, prostate, skin, liver, lung, heart, intestines or any other localized or generalized fibrotic condition, vascular fibrosis, arterial intima hyperplasia, atherosclerosis, arteriosclerosis, restenosis, cardiac hypertrophy, hypertension or any condition characterized by excessive fibroblast or smooth muscle cell proliferation or deposition of collagen and extracellular matrix in the blood vessels and / or heart. In certain embodiments, the compositions may comprise a PDE-4 inhibitor, a PDE-5 inhibitor, a compound that elevates cGMP and / or PKG, a stimulator of guanylyl cyclase and / or PKG, a combination of a compound that elevates cGMP, PKG or NO with an antioxidant that decreases ROS, or a compound that increases MMP activity.

The invention related to intracellular single domain immunoglobulins, and to a method for determining the ability of an immunoglobulin single domain to bind to a target in an intracellular environment, comprising the steps of: a) providing a first molecule and a second molecule, wherein stable interaction of the first and second molecules leads to the generation of a signal; b) providing a single intracellular immunoglobulin domain which is associated with the first molecule, said single immunoglobulin domain being free of complementary immunoglobulin domains; c) providing an intracellular target which is associated with the second molecule, such that association of the immunoglobulin domain and the target leads to stable interaction of the first and second molecules and generation of the signal; and d) assessing the intracellular interaction between the immunoglobulin domain and the target by monitoring the signal.

The present invention provides methods for inducing cell death using hnRNP A1, A1B, A2, and B1 nucleic acid molecules. The invention further provides therapeutic and diagnostic methods for neoplasia treatment relating to hnRNP A1, A1B, A2, and B1 nucleic acid molecules.

The present invention pertains to the use of BMP-2, which is overexpressed in most common cancers, as 1) a target for cancer treatment therapies and 2) a means to diagnose cancer. The therapeutic component of this invention involves administering to a patient a composition that inhibits bone morphogenetic-2 activity. Such inhibition may be accomplished by ligands or antibodies that bind to BMP-2 or BMP-2 receptors. It may also be achieved by preventing the processing of pro-BMP-2, or blocking transcription or replication of BMP-2 DNA or translation of BMP-2 mRNA. The diagnostic component of the invention involves measuring the BMP-2 level in biological samples from both a patient and a subject and comparing those levels. Elevated levels of BMP-2 in the patient compared to the non-cancerous subject indicate cancer.

There is provided a method of preventing a respiratory infection by administering an effective amount of an agent for regulating ICAM-1 expression. Also provided is a composition for the prevention of respiratory infection including an agent which regulates ICAM expression. method of preventing RSV infection by administering an effective amount of an agent that interferes with the binding of RSV to ICAM-1. A method of preventing RSV infection by administering an effective amount of an agent that down regulates the expression of ICAM-1, thereby decreasing RSV binding to ICAM-1 is also provided. There is provided a method of treating RSV infection by administering an effective amount of an agent for down regulating ICAM-1 expression. A method of blocking RSV-ICAM-1 interaction by administering an effective amount of agents for blocking ICAM sites of binding is provided. Also provided is a compound for blocking RSV-ICAM-1 interaction including an agent for blocking ICAM sites of binding.

The invention related to intracellular single domain immunoglobulins, and to a method for determining the ability of an immunoglobulin single domain to bind to a target in an intracellular environment, comprising the steps of: a) providing a first molecule and a second molecule, wherein stable interaction of the first and second molecules leads to the generation of a signal; b) providing a single intracellular immunoglobulin domain which is associated with the first molecule, said single immunoglobulin domain being free of complementary immunoglobulin domains; c) providing an intracellular target which is associated with the second molecule, such that association of the immunoglobulin domain and the target leads to stable interaction of the first and second molecules and generation of the signal; and d) assessing the intracellular interaction between the immunoglobulin domain and the target by monitoring the signal.

A method of increasing tolerance of a plant to an abiotic stress or increasing biomass, vigor or yield of a plant is disclosed. The method comprising upregulating within the plant an exogenous polynucleotide of a microRNA or a precursor thereof, wherein the microRNA is selected from the group consisting of miR-156, miR-169, miR-164, miR-159, miR-167, miR-529, miR-168, ppt-miR395, sof-miR408a, ath-miR408, miR-1039, miR-1091, miR-1118, miR-1134 and miR-1129, thereby increasing the tolerance of the plant to the abiotic stress or increasing the biomass, vigor or yield of the plant.

The invention relates to IL-1O Receptor alpha (IL-1ORα) antibodies and subsequences thereof, human and humanized IL-10 Receptor alpha (IL-IORα) antibodies and subsequences thereof, isolated and purified IL-10 Receptor alpha (IL-1ORα) antibodies and subsequences thereof, compositions including IL-10 Receptor alpha (IL-1ORα) antibodies and subsequences thereof, and methods that employ IL-10 Receptor alpha (IL-1ORα) antibodies and subsequences thereof. The invention includes among other things, methods of treating a pathogen infection, pathogen reactivation, and methods of vaccinating or immunizing against a pathogen infection, which include, for example, administering an IL-10 Receptor alpha (IL-1ORα) antibody or subsequence, to treat a pathogen infection, pathogen reactivation or for vaccination or immunization.

Connexin modulation for the treatment of surgical adhesions, and associated methods, compositions, and articles.

The invention discloses a multifunctional contrast agent of oxygen carrying liquid fluorocarbon. The multifunctional contrast agent is of a spherical shell-core structure; the core is prepared from liquid fluorocarbon and indocyanine green. The invention aims at solving the technical problems to provide the multifunctional contrast agent of oxygen carrying liquid fluorocarbon and the preparation method. The multifunctional contrast agent has high biological safety and stability, and is used for the multi-mode nanometer contrast agent guided breast cancer light treatment.

Symptoms, including biochemical correlates, of multiple sclerosis (MS) in a mammal are beneficially affected by administering to the mammal small doses of bodies, such as liposomes, of a size resembling that of mammalian cells, the bodies having phosphate glycerol head groups presented exteriorly on their surfaces. Preferred are liposomes comprised of 50-100% phosphatidylglycerol, with the phospho glycerol headgroups thereof exteriorly presented.

Compositions and methods for treating cardiomyopathy using RNA interference are disclosed. In particular, embodiments of the invention relate to the use of oligonucleotides for treatment of cardiomyopathy, including small interfering RNAs (siRNAs) and short hairpin RNAs (shRNAs) that silence expression of disease-causing mutant alleles, such as the myosin MYL2 allele encoding human regulatory light chain (hRLC)-N47K and the MYH7 allele encoding human myosin heavy chain (hMHC)-R403Q while retaining expression of the corresponding wild-type allele.

The invention discloses a siRNA inhibiting expression of a gene S100A9 and an application of the siRNA and relates to the field of molecular biology. The siRNA inhibiting the expression of the gene S100A9 is characterized in that a sequence of a positive-sense strand is 5'-GCUUCGAGGAGUUCAUCAU-3' and a sequence of an antisense strand is 5'-AUGAUGAACUCCUCGAAGC-3'. The siRNA disclosed by the invention can be used for reducing expression of the gene S100A9, inhibiting expression of a gene MMP7 in a nasopharyngeal carcinoma cell CNE1 and degrading a migration function of the nasopharyngeal carcinoma cell, so that the siRNA can be applied to research of a medicine used for treating nasopharyngeal carcinoma.

All multiple myeloma cell lines examined showed constitutively active IκB kinase (IKK), IκBα phosphorylation and constitutively active NF-κB. Curcumin, a chemopreventive agent, suppressed constitutive IκBα phosphorylation through inhibition of IKK activity and downregulated NF-κB. Curcumin also downregulated expression of NF-κB-regulated gene products such as IκBα, Bcl-2, Bcl-xL, cyclin D1 and interleukin-6. Consequently, curcumin suppressed multiple myeloma cell proliferation and arrested cells at the G1 / S phase of the cell cycle. Curcumin also induced apoptosis and chemosensitivity to vincristine. Overall, results presented herein provide a molecular basis for the treatment of multiple myeloma patients with this pharmacologically safe agent.

The invention discloses a siRNA (small interfering ribonucleic acid) inhibiting PDCD4 (programmed cell death4) gene expression and application of the siRNA. The sense strand sequence is: 5'-GGAGCGGUUUGUAGAAGAA-3', and the anti-sense strand sequence is: 5'-UUCUUCUACAAACCGCUCC-3'. The siRNA inhibiting PDCD4 gene expression provides a novel technical scheme for studying functions of PDCD4 genes, andsensitivity of leukemia cells to chemotherapeutic drugs can be remarkably reduced by using siRNA to silence PDCD4.

Provided are compositions and methods for the treatment of Krabbe and other neurodegenerative diseases, including storage diseases such as GM1 gangliosidosis, Niemann-Pick disease, Tay-Sachs disease, Sandhoff disease, metachromatic leukodystrophy, Canavan disease, Pelizaeus-Merzbacher disease, and storage conditions facilitated by aging of lysosomal functions, which are associated with psychosine (and / or other storage material)-mediated axonal degeneration. Compositions and methods employ (1) one or more inhibitor of a phos-photransferase activity of one or more kinase(s) such as, for example, CDK5, P38, jnk, src, CK2, PKC, GSK3α and β; (2) one or more inhibitor of a phosphotransferase activity of one or more phosphatase(s) such as, for example, the Ser / Thr protein phosphatase PP1 and Tyr protein phosphatase PP2; one or more inhibitor of a caspase / calpain activity of one or more caspases such as caspase 3 and calpains such as calpain 1 and 2; and (4) one or more inhibitor of a sodium / calcium exchange protein such as, for example, NCX1. Inhibitors include small molecules, including the GSK3β inhibitor L803 and the NCX1 inhibitor flecainide, and siRNA molecules that downmodulate cellular levels of one or more mRNA, including siRNA that are capable of downmodulating the cellular expression of PP1. Inhibitors disclosed can cross the blood-brain barrier and, thus, are available to the central nervous system (CNS) and effective in reducing psychosine-mediated axonal degeneration.

The invention discloses a method for promoting cells to differentiate into female genital cells based on overexpression of Figla gene. The Figla gene has the nucleotide sequence shown in SEQ ID. NO.1. The Figla gene is labeled and is used for transfecting pluripotent stem cells so as to promote the pluripotent stem cells to differentiate or transdifferentiate into the female genital cells. After pDsRed1-N1-Figla transfercts mESCs (Mouse Embryonic Stem Cells), RFP (Red Fluorescent Protein) is expressed in noble cells at the cell cloning margin and not expressed in the smooth position at the cloning margin; and the transfected mESCs grow in a flake shape after passage, and most of the transfected mESCs do not form cloning, indicating the Figla gene promotes the differentiation of mESCs.

The invention relates to a biphenyl derivative and a preparation method and medical application thereof. Specifically, the invention relates to the biphenyl derivative represented in a general formula(I), the preparation method of the biphenyl derivative, a medicinal composition containing the biphenyl derivative and the application of the biphenyl derivative as a therapeutic agent, especially inpreparing medicine for treating ischemic cerebral stroke, wherein definitions of substituents in the general formula (I) are the same as definitions in claims.

The invention provides a glioma-targeting composite nanometer preparation, a preparation method and applications thereof, wherein the glioma-targeting composite nanometer preparation is a nasal nanometer complex assembled by coating a coated material hepatoma-derived growth factor delivery shRNA with a coating material losartan-chitosan-polyethyleneimine vector copolymer, and the particle size is50-250 nm. The preparation method comprises: carrying out an oxidation reaction on chitosan and potassium periodate to obtain oxidized chitosan; carrying out a reaction on the oxidized chitosan and polyethyleneimine to obtain a chitosan-polyethyleneimine copolymer; carrying out a Schiff base reaction on the chitosan-polyethyleneimine copolymer and carboxylated losartan to obtain a losartan-chitosan-polyethyleneimine vector copolymer; and assembling the losartan-chitosan-polyethyleneimine vector copolymer and shHDGF to obtain the nasal nanometer complex. According to the present invention, after the nasal cavity product is prepared from the glioma-targeting composite nanometer preparation, the good brain glioma targeting property can be provided.

Provided is a double-chain siRNA molecule targeting a microphthalmia-associated transcription factor MITF coding gene. A sense strand of the siRNA molecule has a sequence of SEQ ID NO: 3 and an anti-sense strand has a sequence of SEQ ID NO: 4, and the anti-sense strand specifically binds to mRNA of the MITF coding gene, to degrade the mRNA, thereby reducing the systhesis of melanin. Further provided is an application of the siRNA molecule in freckle whitening cosmetics or the preparation of medicines for treatment of diseases related to melanin gene.

The invention discloses an application of an expression inhibitor of a pig SIRT1 gene in preparation of a product with an effect of improving development performance of a pig clone reconstructed embryo. The expression inhibitor of the pig SIRT1 gene can effectively improve the development rate of the pig cloned and reconstructed embryo and the embryo quality in a blastula period, so that the development performance of the pig cloned and reconstructed embryo can be effectively improved, so that the cloning efficiency of porcine somatic cell cloning can be improved. The expression inhibitor of the pig SIRT1 gene can be selected from at least one of siRNA capable of inhibiting the expression of the pig SIRT1 gene and a compound capable of specifically inhibiting the expression of the pig SIRT1 gene. The invention also provides three siRNAs capable of inhibiting the expression of the SIRT1 gene of the pig.

Compounds for use in the treatment of sepsis and / or the prevention or treatment of post-sepsis syndrome.

The invention belongs to the technical field of biology and particularly relates to a method for knocking down a fish gene expression based on heat induced miR30-ShRNA. For solving the problem that certain results of a zebrafish siRNA or shRNA knockdown research technique for zebra fish cannot be repeated or poor in effect in the prior art, the method adopts a miR30 mediated shRNA gene knockdown system to establish a corresponding RNAi carrier and achieves the expression level control of a target gene under the heat shock induction condition by introducing a thermal induction regulation and control technique. Results show that a target sequence is an miR30 Apex1shRNA carrier shown as SEQ ID NO.1, heat shock induced knockdown of an Apex1 gene expression can be achieved, and Apex1 gene expression is remarkably reduced.