44 results about "Inhibitory cell" patented technology

A method of inhibiting the release of a proinflammatory cytokine in a cell is disclosed. The method comprises treating the cell with a cholinergic agonist. The method is useful in patients at risk for, or suffering from, a condition mediated by an inflammatory cytokine cascade, for example endotoxic shock. The cholinergic agonist treatment can be effected by stimulation of an efferent vagus nerve fiber, or the entire vagus nerve.

Signal Transducer and Activator of Transcription (STAT) proteins have a fundamental role cell signaling, and are activated by a large number of cytokines and growth factors. One member of the STAT family, STAT3, has a critical role in oncogenesis. The present invention relates generally to disruption of the pathway of STAT3 signaling in the treatment of human cancer. STAT3 activation is shown to be present in diverse tumor cell lines and tumors, to promote oncogenesis, to inhibit apoptosis, and to reduce sensitivity to chemotherapeutic agents. Inhibition of STAT3 signaling induces apoptosis specifically in tumor cell lines, and increases sensitivity to chemotherapeutic agents. The invention relates more particularly to methods, compositions, means of administering such compositions, and means for identifying such compositions for the inhibition of STAT3 intracellular signaling in the treatment of human cancers.

Textured nanostructured surfaces are described which are highly resistant to cell adhesion. Such surfaces on medical implants inhibit fibroblast adhesion particularly on titanium treated silicone. The surfaces can also be engineered so that other cell types, such as endothelial and osteoblast cells, show little if any tendency to attach to the surface in vivo.

Investigation on the frequency of FLT3/ITD found in various blood cancers has revealed that the frequency is high in acute myeloblastic leukemia in particular. Studies on the effects of FLT3/ITD in the blood cell lines revealed that the tyrosine residues in FLT3/ITD is constitutively phosphorylated in these cell lines and that blood cells into which FLT3/ITD is introduced show IL-3 independent proliferation. Moreover, the blood cells into which FLT3/ITD is introduced are found to be capable of forming tumors and inhibit cell differentiation. The inventors have found that it is possible to screen for pharmaceutical compounds against tumors by using inhibition of these FLT3/ITD functions as an index.

The present invention discloses a peptide of SEQ ID NO:1 and its variants that blocks stretch-activated ion channels. All amino acids in this peptide are D-amino acids. The peptide, designated as D-GsMTx4, is an enantiomer of a peptide GsMTX-4 present in the venom of the spider Grammostola spatulata. The present invention also discloses a method for inhibition of stretch activated ion channels in a cell. This peptide can be used for the treatment of cardiac arrhythmias and other pathologies that involve alteartions in mechanical stress.

The invention discloses application of circRNA in the field of angiogenesis inhibition, and belongs to the fields of biochemistry, molecular biology and medicine. The invention discovers that hsa_circ_0007411 can continuously act on eye vascular endothelial cells, change the structure of angiogenesis and inhibit angiogenesis. By applying the hsa_circ_0007411 to the eye microvascular endothelial cells, 90 percent of angiogenesis can be effectively inhibited, and angiogenesis of neovascularization-related diseases can be effectively inhibited. The effect of hsa_circ_0007411 on cell proliferationand migration is verified, thereby proving that hsa_circ_0007411 can remarkably inhibit cell proliferation and migration, has a remarkable inhibition effect on the proliferation of endothelial cells,and has important guiding significance for diseases related to the proliferation of vascular endothelial cells.

Cell death is induced and/or cell growth is suppressed for a cell having a mutation in the BRAF gene. A drug suppressing GST-π is comprised as an active ingredient.

The polypeptide Fortilin (also known as Translationally Controlled Tumor Protein, TCTP) specifically interacts with p53, a tumor suppressor involved in the induction of apoptosis and the normal growth regulation of a cell. Fortilin also specifically binds MCL1 (Myeloid Cell Leukemia 1). Fortilin has the ability to prevent apoptosis, which may be unregulated in hyperproliferative cells. The present invention is directed at compositions and methods involving a Fortilin modulator, which can induce apoptosis, for the prevention, treatment, or diagnosis of hyperproliferative diseases and conditions, including cancer and atherosclerosis. It is directed also at compositions and methods involving Fortilin, which can inhibit apoptosis, for the treatment of diseases and condition characterized by apoptosis, including certain vascular conditions.

A polypeptide consisting essentially of the amino acid sequence NCEHFVTYCRYG (SEQ ID NO: 1), ENCEHFVNELRYG (SEQ ID NO: 2), NCEHFVNELRYG (SEQ ID NO: 3), RNCEHFVAQLRYG (SEQ ID NO: 4), NCEHFVAQLRYG (SEQ ID NO: 5), or NCEHFVTYLRYG (SEQ ID: 6), or a variant of any of the foregoing, a composition comprising same, a nucleic acid consisting essentially of a nucleotide sequence encoding the amino acid sequence of any of SEQ ID NOS: 1-6 or a variant thereof, a composition comprising same, a host cell comprising an above-described nucleic acid molecule, a method of inhibiting cancerous cell growth comprising contacting a collection of cancerous cells with a cell growth-inhibiting effective amount of one or more of the foregoing, a method of modulating gene expression comprising contacting a collection of cells with a gene expression-modulating effective amount of at least one above-described nucleic acid or a composition comprising same, and a method of enhancing the immune response-inducing effect of a vaccine, which method comprises adding to the vaccine at least one above-described polypeptide, or a variant thereof.

It is intended to provide a substance having an effect of shrinking pores by analyzing the mechanism of making pores perceptible and compositions such as a skin preparation for external use which exerts the above effect to thereby make pores imperceptible. As means for solving these problems, there are provided a parakeratosis inhibitor and a pore-shrinking agent comprising an antagonist to an excitatory cell receptor, for example, a glutamate receptor such as N-methyl-D-aspartic acid receptor or an ATP receptor such as P2X receptor, or an agonist to an inhibitory cell receptor such as a γ-aminobutyrate receptor such as bicuculline-sensitive receptor having the Cl— channel therein or glycine receptor, as well as a skin preparation for external use aiming at inhibiting parakeratosis and a skin preparation for external use aiming at shrinking pores each containing such an antagonist to an excitatory cell receptor or an agonist to an inhibitory cell receptor as described above. Owing to the effects of inhibiting parakeratosis and shrinking pores, the skin can be maintained in a healthy state without perceptible pores.

The present invention includes methods of inhibiting or suppressing cellular secretory processes. More specifically the present invention relates to inhibiting or reducing the release of inflammatory mediators from inflammatory cells by inhibiting the mechanism associated with the release of inflammatory mediators from granules in 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. Peptide fragments and variants thereof of MANS peptide as disclosed in the present invention are useful in such methods.

The invention discloses application of inhibitory cells derived from a medullary system in preparation of diagnostic reagents for autoimmune diseases. It is found that MDSCs and its subgroup G-MDSCs,M-MDSCs are obviously different in normal people and patients with autoimmune diseases, and only peripheral blood and/or joint fluid sampling is needed, the ratio can be judged by flow cytometry, a specific value is calculated, and the detection is very simple and convenient; in addition, by setting a cut-off value (mean value of normal human + 3SD), higher accuracy can be further ensured, the autoimmune disease can be determined without comprehensive judgment combined with other markers, good indication can be provided for diagnosis and drug treatment effects of the autoimmune disease, and clinical application is facilitated.

Nectin-4 and Nectin-1 in cancer progression/development and as a therapeutic target for cancer.

The invention relates to novel application of berberine, in particular to application of the berberine to preparing a drug for preventing and treating familial adenomatous polyp (FAP). The FAP is an autosomal dominant hereditary disease which is characterized by multiple adenomatous polyps in the digestive tract, mainly comprises CFAP (Classical Familial Adenomatous Polyp) and AFAP (Attenuated Familial Adenomatous Polyp) and is not rare in clinic; and early intervention is significant. In the invention, the applied berberine can bring inhibitory action to the cell growth of colon cancer cells and FAP cell line (IMCE), wherein the mechanism includes inhibiting cell proliferation, promoting apoptosis, down regulating expression of COX-2 and AP-1, inhibiting synthesis of PGE2 (Prostaglandin E2) and activation of EGFR (Epidermal Growth Factor Receptor) and Akt and brings out well effect when applied to FAP patients in a long term. The invention provides a novel safe, effective, and economic method for preventing and treating the FAP.

The invention relates to application of CART (Cocaine Amphetamine Regulated Transcript) in preparing medicaments for treating alzheimers diseases. In the invention, CART is prepared into injection preparations for treating alzheimers diseases, and the defects of the traditional medicaments for enhancing cholinergic action and N-methyl-D-aspartic acid (NMDA) receptor antagonists are overcome. The novel medicament has multiple target point actions on the generation and the degradation of A beta as well as the influence of the neurotoxicity and the molecular mechanism of the A beta. The invention has effects on effectively treating dementia with estrogen and up-regulating intracephalic CART; more CARTs are distributed in intracephalic hippocampus; CART exists in intracephalic acetylcholine neurons and can promote the release of acetylcholine; and mitochondrial dysfunction induced by A beta neurotoxicity is the main pathway for the A beta to cause neuronal apoptosis. The CART has a directaction on mitochondrial succinodehydrogenase subunit B and can maintain the respiration of mitochondria and the generation of energy, alleviate oxidative stress, stabilize mitochondrial membrane potential and prevent the mitochondria from being damaged, thereby inhibiting apoptosis.

In one aspect the present invention provides methods for inhibiting cell death or inflammation in a mammal, wherein the methods each include the step of administering to a mammal a Bcl protein in an amount sufficient to inhibit cell death or inflammation in the mammal. The invention also provides methods for identifying a Bcl protein that inhibits cell death or inflammation when administered to a mammal.

The invention relates to an application of a KDM1A micro-molecular inhibitor in the inhibition of the growth and the transfer of tumor cells. The KDM1A micro-molecular inhibitor can inhibit the activity of histone demethylase KDM1A in cells and inhibit demethylation of histone H3K4me2 in order to cause up-regulation of the TIMP3 expression and promote down-regulation of extracellular MMP2 expression, inhibits the activity of JNK kinase in the cells, and effectively inhibits the invasion and the transfer of tumor cells; and the KDM1A micro-molecular inhibitor is 2-PCPA. The lung cancer cell proliferation, migration and invasion inhibition molecular mechanism of the KDM1A micro-molecular inhibitor 2-PCPA is explicated in the invention, the lung cancer treatment effect of the KDM1A micro-molecular inhibitor is researched on the basis of the molecular mechanism, the gap in the field of lung cancer treatment using an epigenetic medicine is filled, and the 2-PCPA can be used for preparing micro-molecular medicines for inhibiting the proliferation and the transfer of lung cancer cells, so the lung cancer treatment effect is improved, and the life of lung cancer patients is prolonged.

The invention discloses a use of a hypoxia-inducible factor prolyl hydroxylase activity inhibitor in the preparation of a drug for preventing and treating acute kidney injury. The HIF prolyl hydroxylase activity inhibitor is Roxadustat (FG-4592). The HIF prolyl hydroxylase activity inhibitor is an HIF family selective inhibitor, and can alleviate pathological damages of cisplatin-induced acute kidney injury to kidneys and improve the functions of the kidneys. The FG-4592 can reduce apoptosis of renal tubular cells and renal tubular functions, improve the pathological injury and renal functionsof the kidneys and protect the structures and the functions of the kidneys in the acute kidney injury by activating HIF1alpha, promoting the expression of EPO and HO-1, inhibit apoptosis and down-regulate the release of inflammatory factors. The FG-4592 is currently in a Phase III clinical research stage in the field of prevention and treatment of chronic renal anemia, and it is found that the FG-4592 is highly possible to provide the effective clinical drug for preventing and treating the AKI.

Neonatal seizure is different from adult seizure, and many anti epileptic drugs that are effective in adults often fail to treat neonatal seizure. Gluconic acid, a natural organic acid enriched in fruits and honey, and the glucose oxidase enzyme, is shown herein to potently inhibit neonatal epilepsy both in vitro and in vivo. Sodium gluconate is shown to inhibit epileptiform burst activity in cell cultures and protect neurons from kainic acid-induced cell death. Sodium gluconate also inhibited epileptiform burst activity in brain slices in a manner that was much more potent in neonatal animals than in older animals. Consistently, in vivo EEC recordings also revealed that sodium gluconate inhibited the epileptic seizure activity in a manner that was much more potent in neonates than in adult animals. Mechanistically, sodium gluconate inhibits voltage-dependent CLC-3 C1⁻ channels both in neuronal cultures and in hippocampal slices. Together, these data suggest a novel antiepileptic drug gluconate that potently inhibits neonatal seizures through blocking CLC-3 C1⁻ channels.