159results about How to "Restore sensitivity" patented technology

The present invention provides diagnostic and prognostic methods for predicting the effectiveness of treatment of a cancer patient with an EGFR kinase inhibitor. Methods are provided for predicting the sensitivity of tumor cell growth to inhibition by an EGFR kinase inhibitor, comprising assessing whether the tumor cell has undergone an epithelial to mesenchymal transition (EMT), by determining the expression level of epithelial and / or mesenchymal biomarkers, wherein tumor cells that have undergone an EMT are substantially less sensitive to inhibition by EGFR kinase inhibitors. Improved methods for treating cancer patients with EGFR kinase inhibitors that incorporate the above methodology are also provided. Additionally, methods are provided for the identification of new biomarkers that are predictive of responsiveness of tumors to EGFR kinase inhibitors. Furthermore, methods for the identification of agents that restore the sensitivity of tumor cells that have undergone EMT to inhibition by EGFR kinase inhibitors are also provided.

Nucleic acid vectors encoding light-gated cation-selective membrane channels, in particular channelrhodopsin-2 (Chop2), converted inner retinal neurons to photosensitive cells in photoreceptor-degenerated retina in an animal model. Such treatment restored visual perception and various aspects of vision. A method of restoring light sensitivity to a retina of a subject suffering from vision loss due to photoreceptor degeneration, as in retinitis pigmentosa or macular degeneration, is provided. The method comprises delivering to the subject by intravitreal or subretinal injection, the above nucleic acid vector which comprises an open reading frame encoding a rhodopsin, to which is operatively linked a promoter and transcriptional regulatory sequences, so that the nucleic acid is expressed in inner retinal neurons. These cells, normally light-insensitive, are converted to a light-sensitive state and transmit visual information to the brain, compensating for the loss, and leading to restoration of various visual capabilities.

The present invention provides diagnostic and prognostic methods for predicting the effectiveness of treatment of a cancer patient with an EGFR kinase inhibitor. Methods are provided for predicting the sensitivity of tumor cell growth to inhibition by an EGFR kinase inhibitor, comprising assessing whether the tumor cell has undergone an epithelial to mesenchymal transition (EMT), by determining the expression level of epithelial and / or mesenchymal biomarkers, wherein tumor cells that have undergone an EMT are substantially less sensitive to inhibition by EGFR kinase inhibitors. Improved methods for treating cancer patients with EGFR kinase inhibitors that incorporate the above methodology are also provided. Additionally, methods are provided for the identification of new biomarkers that are predictive of responsiveness of tumors to EGFR kinase inhibitors. Furthermore, methods for the identification of agents that restore the sensitivity of tumor cells that have undergone EMT to inhibition by EGFR kinase inhibitors are also provided.

The present invention relates to therapeutic compositions for treating cancer or preventing the growth of cancer cells, e.g., tumor growth, in a subject. The present invention also relates to methods for treating cancer, e.g., inhibiting tumor growth, in a subject who has become resistant to treatment, by administering to a subject an effective amount of a proteasome inhibitor and an effective amount of a therapeutic agent, e.g., a chemotherapeutic agent. The present invention further relates to methods for purging bone marrow, i.e., removing cancer cells from bone marrow, by exposing the bone marrow cells to a proteasome inhibitor and a therapeutic agent, e.g., a chemotherapeutic agent.

Guanosine triphosphate pathway tetrahydrobiopterin synthesis antagonist and / or pterin salvage pathway tetrahydrobiopterin synthesis antagonists are administered to inhibit nitric oxide synthesis from arginine in vascular cells in a subject in need of such inhibition (e.g., for prophylactic or curative effect for endotoxin- or cytokine-induced hypotension or for restoration of vascular contractile sensitivity to pressor agents in the treatment of such hypotension). The tetrahydrobiopterin synthesis antagonist may be administered with alpha 1-adrenergic agonist or with nitric oxide synthase inhibitor. The tetrahydrobiopterin synthesis antagonists are also administered to attenuate inflammation caused by induced nitric oxide production in immune cells. Unwanted counterproductive or side effects can be eliminated or ameliorated by administration additionally of levodopa with or without carbidopa and L-5-hydroxytryptophane.

The present invention is a method of improving the persistence of electrical neural stimulation, and specifically a method of improving the persistence of an image supplied to a retina, or visual cortex, through a visual prosthesis. A continuously stimulated retina, or other neural tissue, will desensitize after a time period in the range of 20 to 150 seconds. However, an interruption of the stimulation on the order of a few milliseconds will restore the retinal sensitivity without the user perceiving the interruption, or with the user barely perceiving the interruption.

Nucleic acid vectors encoding light-gated cation-selective membrane channels, in particular channelrhodopsin-2 (Chop2), converted inner retinal neurons to photosensitive cells in photoreceptor-degenerated retina in an animal model. Such treatment restored visual perception and various aspects of vision. A method of restoring light sensitivity to a retina of a subject suffering from vision loss due to photoreceptor degeneration, as in retinitis pigmentosa or macular degeneration, is provided. The method comprises delivering to the subject by intravitreal or subretinal injection, the above nucleic acid vector which comprises an open reading frame encoding a rhodopsin, to which is operatively linked a promoter and transcriptional regulatory sequences, so that the nucleic acid is expressed in inner retinal neurons. These cells, normally light-insensitive, are converted to a light-sensitive state and transmit visual information to the brain, compensating for the loss, and leading to restoration of various visual capabilities.

The present invention provides a rational basis for combining targeted therapies together with selected chemotherapeutics, which does not currently exist for the treatment of melanoma. The present invention is based on the present inventors' discovery that Akt3 regulates apoptosis and V599E B-Raf regulates growth and vascular development in melanoma. Inventors are the first to recognize an effective combined targeted therapeutic for treating melanoma. In one embodiment, the invention provides a method for inducing apoptosis in a melanoma tumor cell by reducing Akt3 activity. In yet another embodiment, the invention provides a method for inducing apoptosis in a melanoma tumor cell comprising contacting a melanoma tumor cell with an agent that reduces Akt3 activity. Consequently, the method provided restores normal apoptotic sensitivity to a melanoma tumor cell, thereby allowing the administration of a lower concentration of chemotherapeutic agents resulting in decreased toxicity to a patient. The present inventors' contemplate a method for treating a melanoma tumor in a mammal comprising: administering to a melanoma tumor an effective amount of an agent to induce apoptosis; and administering to a melanoma tumor an effective amount of an agent to reduce angiogenesis and cell proliferation. Also disclosed herein is a method for treating a melanoma in a mammal comprising: administering to a melanoma tumor in a mammal an effective amount of an agent that reduces Akt3 activity; administering to a melanoma tumor in a mammal an effective amount of an agent that reduces V599E B-Raf activity, thereby treating a melanoma tumor. In another aspect, the invention provides a pharmaceutical composition for treating a melanoma tumor comprising: an agent that reduces Akt3 activity; and a carrier.

The compounds according to formula VIII, their pharmaceutically acceptable acid or base addition salts, and the uses thereof is disclosed. These compounds and their pharmaceutically acceptable acid or base addition salts can be used for the preparing a medicament for modulating estrogen related receptor (ERR), and treating metabolic diseases, such as high blood fat, fatty liver, hyperglycemia, diabetes, obesity, etc. The definition of the groups of the formula is defined as the description.

The invention belongs to the production technology for antitumor drugs, and discloses uses of sorafenib and sorafenib salts in preparing drugs for reversing BCRP protein-mediated multidrug resistance of tumors. According to the present invention, the sorafenib and the sorafenib salts are combined with antitumor drugs, such that the sensitivity of multidrug resistant tumor cells to the antitumor drugs are recovered; the prepared drugs are applicable for providing combination chemotherapy for the clinical chemotherapy resistant patients or preventing the drug resistance of the tumor cells from generation.

This invention describes a relevant etiology of cancer and a novel anti-cancer therapeutic strategy, based on the discovery that a protein named serine protease inhibitor (SPIK / SPINK / PSTI) was up-regulated by hepatitis B and C virus infections consequently suppressing the cell apoptosis. Accordingly, this invention provides an inhibitor of SPIK and / or a technology of suppression of over-expression of SPIK in cells. The inhibitors include: 1) chemical compounds, which can inhibit SPIK transcripts, protein activity, and gene expression, 2) SPIK siRNA (RNAi gene silence or dsRNA of SPIK, 3) DNA anti-sense and anti-SPIK antibody. Further, this invention provides a method of using the inhibitor as an anti-cancer agent to re-instate cancer cell apoptosis (e.g., serine protease dependent cell apoptosis).

The present invention relates generally to the fields of molecular biology and growth factor regulation. More specifically, the invention relates to therapies for the treatment of pathological conditions, such as cancer.

The invention relates to the field of microorganisms, and discloses lactobacillus fermentum with a weight reducing function and an application of the lactobacillus fermentum. The lactobacillus fermentum is named as WHH3906, is separated from butter collected in Tibet Autonomous Region in China, is preserved in China General Microbiological Culture Collection Center on March 13, 2020, has a preservation number of CGMCC NO.19472, and is classified and named as lactobacillus fermentum. The lactobacillus fermentum strain can effectively reduce serum leptin level to recover leptin sensitivity of anorganism, effectively prevent and treat obesity, relieve non-alcoholic fatty liver and relieve chronic inflammation. After being compounded with lactobacillus plantarum 1701, the lactobacillus fermentum can synergistically relieve chronic inflammation.

The present invention provides methods for treating cancer and other pathological proliferating conditions by inhibiting mitosis using at least one pyrrolo[2,3-d]pyrimidine having the general formula (16): where X is selected from the group consisting of lower alkyls, heteroalkyls, substituted or unsubstituted aryls or heteroaryls, arylalkyls, and heteroarylalkyls; where R1 is selected from the group consisting of hydrogen, lower alkyls, heteroalkyls, substituted or unsubstituted aryls or heteroaryls, arylalkyls, and heteroarylalkyls; where R2 is selected from the group consisting of hydrogen, lower alkyls, heteroalkyls, alkoxys, substituted or unsubstituted aryls or heteroaryls; where R3 is selected from the group consisting of zero, lower alkyls, heteroalkyls, alkenyls, and heteroalkenyls; and where R4 is selected from the group consisting of substituted or unsubstituted aryls or heteroaryls, arylalkyls, heteroarylalkyls, and hydrogen. The compound may inhibit mitosis in cells that have developed multidrug resistance due to P-glycoprotein and MRP1, and facilitate the reversal of P-glycoprotein mediated resistance.

The invention relates to a traditional Chinese medicine product for eliminating cigarette poison, restoring functions and reducing and controlling cigarette. The traditional Chinese medicine product mainly comprises, by weight, 50-70 parts of cordate houttuynia, 20-40 parts of sow thistle, 20-40 parts of liquorice, 50-70 parts of ageratum, 10-30 parts of the semen plantaginis, 22-40 parts of polygala, 20-40 parts of the pine needles, 20-40 parts of lily and 20-40 parts of dandelion. The invention further discloses preparation methods of various finished products, such as candy, gum, bagged tea and air fragrance, of the same formula. By the traditional Chinese medicine product worthy of protection, popularization of application, detoxification of smoking people, restoration of bodies poisoned by smoking for a long time and cigarette reducing and controlling of the smoking people are paid equal attention to, and great social significance is achieved.

Microbial type rhodopsins, such as the light-gated cation-selective membrane channel, channelrhodopsin-2 (Chop2 / ChR2) or the ion pump halorhodopsin (HaloR) are expressed in retinal ganglion cells upon transduction using recombinant AAV vectors. Selective targeting of these transgenes for expression in discrete subcellular regions or sites is achieved by including a sorting motif in the vector that can target either the central area or surround (off-center) area of these cells. Nucleic acid molecules comprising nucleotide sequences encoding such rhodopsins and sorting motifs and their use in methods of differential expression of the transgene are disclosed. These compositions and methods provide significant improvements for restoring visual perception and various aspects of vision, particular in patients with retinal disease.

The invention relates to the technical field of nano-selenium preparation, and particularly discloses layered bimetal hydroxide / selenium nanocomposite and application thereof. The layered bimetal hydroxide / selenium nanocomposite is prepared through the following steps that selenium salt solution is dropwise added into layered bimetal hydroxide LDH hydration solution, stirring is conducted, then reducing agent is added, stirring is conducted continuously until the reaction liquid turns into crimson, then centrifugation, washing and drying are conducted on the product, and the layered bimetal hydroxide / selenium nanocomposite Se@LDH is obtained. The selenium nanocomposite can be used as a transmitting system for siRNA to promote the orderly release of the siRNA, and at the same time, the concentration of intracellular drug is increased, so that the sensibility of a drug-resistant cell to taxol is recovered.

Microbial type rhodopsins, such as the light-gated cation-selective membrane channel, channel-rhodopsin-2 (Chop2 / ChR2) or the ion pump halorhodopsin (HaloR) are expressed in retinal ganglion cells upon transduction using recombinant AAV vectors. Selective targeting of these transgenes for expression in discrete subcellular regions or sites is achieved by including a sorting motif in the vector that can target either the central area or surround (off-center) area of these cells. Nucleic acid molecules comprising nucleotide sequences encoding such rhodopsins and sorting motifs and their use in methods of differential expression of the transgene are disclosed. These compositions and methods provide significant improvements for restoring visual perception and various aspects of vision, particular in patients with retinal disease.

It has now been found that N-L-alpha-aspartyl-L-phenylalanine 1-methyl ester (APM) and / or one of its lower alkyl derivatives can be used to treat allergic contact dermatitis associated with irritating oils such as catechol-containing plant-derived antigens such as poison ivy, poison oak, poison sumac and Asian lacquer tree and oils containing capsaicin. Topical application of APM and / or derivative can reduce or alleviate the symptoms associated with irritation of the skin and / or mucous membranes caused by contact or inhalation of these oils or fumes from burning vegetation containing these oils.

This invention relates to the combination of vemurafenib and the heat shock protein 90 (HSP90) inhibitor XL888 to treat melanoma, particularly BRAF V600 mutant melanoma in patients in need of such treatment.

Provided is a glucagon-like peptide-1 (GLP-1) analog shown as the following formula, wherein X is selected from glycine and glycinamide. The GLP-1 analog has a non-proteogenic amino acid residue in position 8 relative to the sequence GLP-1, and is acylated with a moiety comprising two acidic groups to the lysine residue in position 26. The GLP-1 analog is resistant to dipeptidyl peptidase IV so as to have an extended half-life in vivo. Also provided is a use of the GLP-1 analog in conquering blood sugar.

The invention relates to a composite microsphere for co-loading adriamycin nanoparticles and ginsenoside rh2 and a preparation method thereof, wherein the preparation method comprises the following steps: (1) preparing adriamycin hydrochloride and a nanoparticle carrier material into doxorubicin polyelectrolyte nanoparticles; (2) dispersing the adriamycin polyelectrolyte nanoparticles in water toform a nano-particle suspension, and dispersing the nano-particle suspension in an organic solution containingginsenoside rh2 and a high-molecular polymer to prepare S / W1 / O colostrum; (3) adding the S / W1 / O colostrum into an aqueous solution containing an emulsifier to prepare S / W1 / O / W2 complex milk; (4) solidifying the S / W1 / O / W2 complex emulsion into microspheres, collecting the microspheres, washing and drying. The microsphere prepared by the method can achieve the sequential release, slow release of doxorubicin hydrochloride and ginsenoside rh2,and has the advantages of low burst release rate and high encapsulation rate.

An analytical system and method for detecting volatile organic chemicals in water including a coated SAW detector that provides for improved reduction of moisture at the coating of the SAW detector. A stabilized SAW sensitivity and long lasting calibration is achieved. The analytical system further includes an improved sample vessel and sparger that allow for easy grab sample analysis, while also providing efficient purging of the volatile organic compounds from the water sample. In addition, an improved preconcentrator provides a stabilized sorbent bed.

The invention discloses application of an AR-V7 variable shearing sequence in resisting castration resistant tumors, and specifically the variable shearing sequence is as shown in SEQ ID NO.7. The invention also discloses CYTOR capable of controlling expression of the AR-V7, and discloses CYTOR which can be used for treating castration resistance, relapse and metastasis after hormone castration treatment of androgen receptor associated tumors. The invention also discloses antisense oligonucleotide capable of controlling AR-V7 expression, and provides a novel treatment way for castration resistance, relapse and metastasis after hormone castration treatment of androgen receptor associated tumors.

An analytical system and method for detecting volatile organic chemicals in water including a coated SAW detector that provides for improved reduction of moisture at the coating of the SAW detector. A stabilized SAW sensitivity and long lasting calibration is achieved. The analytical system further includes an improved sample vessel and sparger that allow for easy grab sample analysis, while also providing efficient purging of the volatile organic compounds from the water sample. In addition, an improved preconcentrator provides a stabilized sorbent bed.

The invention relates to the medical field of sensitizing antitumor medicaments and reversing tumor multi-drug resistance, in particular to inhibiting effect of nitric oxide (NO) donor-type alkoxy biphenyl carboxylic acid compounds on P-glycoprotein, and application thereof in reversing tumor multi-drug resistance. The characteristics of the invention are summarized as follows: NO donor-type alkoxy biphenyl compounds are characterized in that the compounds have alkoxy biphenyl carboxylic acid parent framework and furazan nitrogen oxide type NO donor radicals, are formed by connected amino acids unequal in length with radicals, can be taken as P-gp inhibitors and tumor multi-drug resistance reversal agents, can remarkably increase the cell uptake amount of P-gp substrates, reduce substrate efflux, regulate the expression of P-gp down, can be used in combination with the antitumor medicaments to increase the concentration of the compounds in multi-drug resistance tumor cells, have a drug-resistance reversal multiple up to hundreds of times, enable multi-drug resistance cell strains to recover sensibility to chemotherapeutic medicaments, and have extensive application prospects.

The invention provides a beta-lactam compound antibiotic composition, which contains cefuroxime and a tazobactam sodium monohydrate, or cefuroxime salts and the tazobactam sodium monohydrate, wherein the weight ratio of the cefuroxime salts counted according to the cefuroxime to the tazobactam sodium monohydrate counted according to the tazobactam is (1-8):1. The beta-lactam compound antibiotic composition disclosed by the invention is used for being prepared into a clinically-acceptable medicinal preparation with the cefuroxime and salts thereof as well as the tazobactam sodium monohydrate as active components. According to the beta-lactam compound antibiotic composition, the tazobactam sodium monohydrate is mixed with the cefuroxime and salts thereof so as to improve the flowability of composition powder, enable the uniformity of the medicament to be better in the production process and improve the yield of the product; and the beta-lactam compound antibiotic composition has saved production cost and is especially suitable for popularization and application.