30 results about "Mitochondrial respiration" patented technology

The invention relates to an in vitro method for classifying a subject afflicted with a cancer as suffering from a cancer with (at risk of) a metabolic reprograming towards fatty acids oxidation including a step of assaying the activation of RelB in a tumor sample form said cancer. The inventor indeed identified the pivotal role of RelB in energy metabolism and more particularly mitochondrial respiration and fatty acid oxidation. Accordingly, the invention also relates to inhibitors of RelB activity or expression, as well as of lipid metabolism for use in the treatment of cancers showing an activated RelB.

The invention discloses an application of a compound in preparation of a product for enhancing the metabolic activity of hematopoietic stem cells and treating metachromatic white matter dystrophy. The compound comprises Azoramide. Azoramide is adopted to treat transfected hematopoietic stem cells, and cell apoptosis, cell necrosis and mitochondrial respiration conditions of the hematopoietic stem cells are obviously improved, so that the hematopoietic stem cells are expected to be applied to enhancement of transfection efficiency and metabolic activity of the hematopoietic stem cells transfected by the ARSA gene and reduction of ROS generation, and the effectiveness of the hematopoietic stem cells in treatment of MLD diseases is enhanced.

The present invention relates to an in vitro method for predicting the response to immunotherapy treatment of hepatocellular carcinoma in a subject, comprising the following steps: 1) A step of determining the energy metabolic state of a liver tissue sample from a subject, wherein the sample comprises pathological tissue and optionally non-pathological tissue, 2) A step of detecting the presence or absence of energy conversion resulting from a reduction in mitochondrial respiration in the pathological tissue by comparing it with a liver tissue sample of the subject or a non-pathological tissue from a standard non-pathological liver sample, Here: - If mitochondrial respiration is reduced in pathological tissue, the subject is less likely to respond to immunotherapy treatment, and - If mitochondrial respiration is not reduced in the pathological tissue, the subject is highly likely to respond to immunotherapy treatment.

The application belongs to the technical field of pesticide mite-killing, and discloses a mite-killing composition and application thereof, wherein the mite-killing composition comprises active ingredient A and active ingredient B; the active ingredient A is a compound shown in formula I; and the active ingredient B is selected from any one of a mitochondrial respiration inhibitor mite-killing agent, a growth inhibitor mite-killing agent, a neurotoxin mite-killing agent and other mite-killing agents. The mite-killing composition has obvious synergistic effect, has good control effect on common leaf mite family harmful mites of crops, can effectively control the harm of mite pests, reduces the use dose of pesticides and reduces the cost of agricultural production.

The application discloses a bZIP transcription factor mediating sensitivity change of Magnaporthe oryzae to mitochondrial respiratory inhibitors and high expression in mitochondrial dysfunction, and enhancing mtDNA replication in mitochondria PoATFS1 . PoATFS1 The overexpression transformant is sensitive to various respiratory inhibitors, and the knockout transformant is sensitive to various respiratory inhibitors. Meanwhile, PoATFS1 The mtDNA content in the overexpression transformant increases, and the mtDNA content in the knockout transformant decreases, which indicates that PoATFS1 The gene is involved in regulating mitochondrial homeostasis. The application provides a synergistic agent screening candidate target for restoring the sensitivity of resistant plant pathogens to respiratory inhibitors, and is favorable for the management of drug resistance of plant pathogens and the improvement of the activity of the existing respiratory inhibitors.

The present invention relates to a non-therapeutic cosmetic composition for increasing the cellular mitochondrial respiration of keratinocytes underlying the stratum corneum of the epidermis, comprising an active complex: extracts of Melaleuca alternifolia, extracts of Lavandula hybrida, and melatonin. The invention also relates to the use of this non-therapeutic cosmetic composition for increasing the cellular mitochondrial respiration of keratinocytes underlying the stratum corneum of the epidermis.

The present invention addresses the problem of developing a drug for inhibiting the DNA damage restoration mechanism in a cancer which does not have a mutation in BRCA 1 / 2 and in which homologous recombination repair functions normally.　The inventors of the present invention have clarified that cell death can be induced by inhibiting PARP functions and mitochondrial respiration functions in cells, and indicated that the problem can be solved. In other words, the present invention provides: a method for inducing cell death by inhibiting PARP functions and mitochondrial respiration functions in cells; and a pharmaceutical composition for treating cancer, the pharmaceutical composition containing a PARP inhibitor and a mitochondrial respiration inhibitor.

The invention belongs to the technical field of pesticide mite killing, and discloses a mite killing composition and application thereof, the mite killing composition comprises an active component A and an active component B, the active ingredient A is a compound shown in a formula I: # imgabs0 #, and the active ingredient B is selected from any one of a mitochondrial respiration inhibitor acaricide, a growth inhibitor acaricide, a neurotoxin acaricide and other acaricides. The acaricidal composition disclosed by the invention is obvious in synergism, has a relatively good prevention and treatment effect on common tetranychidae pest mites of crops, and can effectively control the harm of mite pests, reduce the use dosage of pesticides and reduce the agricultural production cost.

The invention relates to the technical field of recombinant protein expression and cell culture, in particular to application of 7, 8-DHF to improvement of CHO cell line recombinant protein expression quantity. According to the invention, 7, 8-DHF is used as a serum-free culture medium additive, and compared with a traditional additive, the yield of recombinant protein can be more efficiently increased by improving the mitochondrial respiratory capacity and the redox steady state and inhibiting cell apoptosis under the condition of not influencing cell growth; therefore, the requirement of the production process of the produced product on the scale of a bioreactor and the consumption of a culture medium are reduced, the production efficiency is improved, the production cost of the biological product is finally reduced, the antibody aggregation can be reduced, and the immunogenicity risk caused by aggregation can be effectively reduced. And a new solution is provided for high-quality and high-efficiency production of CHO cell line recombinant protein.

This invention relates to an ex vivo method for predicting the response to immunotherapy for hepatocellular carcinoma in a subject, the method comprising the steps of: 1) determining the energy metabolic state of a liver tissue sample from the subject, the sample comprising pathological tissue and optionally non-pathological tissue; 2) detecting the presence or absence of energy transitions consisting of reduced mitochondrial respiration in the pathological tissue compared to non-pathological tissue from the subject's liver tissue sample or non-pathological tissue from a standard non-pathological liver sample, wherein: - if mitochondrial respiration is reduced in the pathological tissue, the subject is unlikely to respond to immunotherapy; - if mitochondrial respiration is not reduced in the pathological tissue, the subject is likely to respond to immunotherapy.

The compounds and methods of the present disclosure exhibit induce Ucp1 transcription, enhance of mitochondrial respiration, activate protein kinase A, increase lipolysis, and increase p38 MAPK phosphorylation in cells, particularly brown adipocytes and white adipocytes. They also protect primary cardiomyocytes against hypertrophy induced by adrenergic agonists. Such compounds and methods are useful in the treatment and prevention of conditions such as obesity and associated complex metabolic, endocrine, and hemodynamic changes, as well as related conditions as dyslipidemias, cardiovascular disease, and type 2 diabetes.

The invention relates to the technical field of biological medicines, and discloses application of methionine adenosine transferase 2A and related substances thereof in preparation of anti-aging products. The invention finds that methionine adenosine transferase 2A (MAT2A) can induce mitochondrial metabolism brittleness through HMGCS1-mediated ubiquinone synthesis, so that the methionine adenosine transferase 2A (MAT2A) plays an unreported metabolic part-time role in regulating cell senescence. The specific improvement of the expression quantity of the MAT2A gene in the pericyte is beneficial for improving the cell proliferation activity, the cell mitochondrial respiration level, the cell oxygen consumption rate, the cell total ATP level and the expression level of a nuclear morphological marker LamB1, and meanwhile, the senescence cell percentage and the expression level of a senescence marker P21 are reduced; related substances for improving expression of methionine adenylyltransferase 2A can be used for preparing anti-aging drugs.

The invention relates to the field of biological medicine, in particular to lncLRFIF and application of the lncLRFIF in preparation of medicine for treating laying hen fatty liver hemorrhagic syndrome. The invention provides lncLRFIF. It is found for the first time that lncLRFIF can be used for preparing a medicine for treating the fatty liver hemorrhagic syndrome of laying hens. According to the specific embodiment of the invention, lncLRFIF is knocked down through siRNA, so that the activities of ALT and AST in the chicken primary hepatocyte supernatant treated by FFAs are recovered, lipid droplet accumulation and the content of TG and T-CHO are remarkably reduced, lipid synthesis is increased, lipid transport is increased, the content of ATP and ROS in mitochondria is increased, and mitochondrial respiration and functions are recovered. It can be seen that lncLRFIF can improve liver cell damage caused by FFAs and regulate lipid metabolism. The invention enriches the pathogenesis of the fatty liver hemorrhagic syndrome of laying hens, and provides a new idea for improving the egg laying performance of poultry.

A method for treating low-level blast traumatic brain injury includes administering a phosphodiesterase-5 (PDE5) inhibitor, such as sildenafil, to a subject following exposure of the subject to one or more low-level blasts. Administration of the PDE5 inhibitor may prove useful with respect to improving the vascular integrity of a subject by increasing brain capillary respiration, mitochondrial respiration, mitochondrial density, mitochondrial biogenesis, astrocyte level or homeostasis, and / or tight junction protein expression in the brain of the subject and / or inducing positive metabolic change in the subject by increasing NAD+ / NADH metabolism. Methods for mitigating the effects of blast injury on the vascular integrity of a subject and inducing metabolic change are also provided.

The present invention relates to a compound exhibiting inhibitory activity of at least one of malate dehydrogenases I (MDH1) and malate dehydrogenases 2 (MDH2), and a pharmaceutical composition for preventing or treating cancer comprising the same as an active ingredient. The inventors of the present invention have experimentally confirmed that the compound exhibiting the MDH1 and / or MDH2 inhibitory activity has an inhibitory effect on mitochondrial respiration in cancer cells, an excellent inhibitory effect on cancer cell growth, etc. Thus, the compound of the present invention is expected to be effectively used as a pharmaceutical composition for treating cancer.

The present invention relates to a computer-implemented method for determining the oxidative phosphorylation profile of a cell sample, the method comprising a) determining the expression level(s) of adenine nucleotide translocator (ANT) and optionally one or more further targets involved in the oxidative metabolic phosphorylation pathway in the cell sample; b) providing the expression level data obtained in step a) to a mathematical model for metabolic profiling; and c) determining the oxidative phosphorylation profile of the cell sample (representative of its mitochondrial respiration profile) by calculation. Furthermore, the invention is directed to a computer program product configured to execute the computer-implemented method according to the invention on a computer.

The present invention relates to a non-therapeutic cosmetic composition for increasing mitochondrial cellular respiration of keratinocytes underlying the stratum corneum of the epidermis, comprising a complex of active ingredients: extracts of Melaleuca Alternifolia, extracts of Lavandula Hybrida, and melatonin. The invention also relates to the use of this non-therapeutic cosmetic composition to increase mitochondrial cellular respiration of keratinocytes underlying the stratum corneum of the epidermis.

This application discloses the use of compounds, including azoramide, in the preparation of products for enhancing the metabolic activity of hematopoietic stem cells and treating metachromatic leukodystrophy. Azoramide treatment of transfected hematopoietic stem cells significantly improved apoptosis, necrosis, and mitochondrial respiration. Therefore, azoramide is expected to be used to enhance the transfection efficiency and metabolic activity of ARSA gene-transfected hematopoietic stem cells and reduce ROS generation, thereby enhancing its effectiveness in treating MLD.

To provide a method for producing in vitro functional beta-cells (functional pancreatic beta-cells) and populations of cells resulting from the differentiation of pluripotent stem cells.SOLUTION: A method of differentiating pancreatic endoderm cells into functional beta cells expressing PDX1, NKX6.1, MAFA, UCN3, and SLC2A1, comprises culturing immature pancreatic beta cells in a medium supplemented with (a) an effective amount of T3 and (b) an effective amount of 3-deazaneplanocin A (DEZA), thereby producing functional beta cells expressing insulin.SELECTED DRAWING: None

The present application relates to the application of mitochondrial transplantation preparation in the preparation of a drug for treating non-alcoholic fatty liver disease, wherein the mitochondrial transplantation preparation comprises active mitochondria isolated from healthy donor cells, and has normal membrane potential and mitochondrial respiratory function. In vivo experiments on a non-alcoholic fatty liver mouse model prove that tail vein injection of the mitochondrial transplantation preparation of the present application can effectively reduce the weight of the mouse, improve the fatty liver condition of the mouse, reduce the accumulation of fat in the liver tissue, and at the same time restore the abnormal liver function of the non-alcoholic fatty liver mouse.

The application discloses a dual-response co-delivery nano platform for enhancing the radiotherapy effect on tumors, a preparation method and application thereof. The nano platform is formed by coordination self-assembly of metformin and metal cations, can produce dual responses to the low pH and high glutathione (GSH) level unique in the tumor microenvironment, realizes specific release of copper ions and metformin. The released metformin realizes radiotherapy sensitization by regulating mitochondrial respiratory metabolism. Meanwhile, radiotherapy up-regulates the expression of copper death-related proteins FDX1 and LIAS, can synergistically enhance the copper death pathway mediated by copper ions, causes immunogenic death of tumors, and produces a strong immune activation effect to inhibit tumor growth and recurrence and metastasis. The application provides a safe and effective new strategy for overcoming tumor radiotherapy resistance and immunosuppression.

Aging progresses at different rates among individuals, underscoring the need for better indicators of functional decline. The inventors showed that the T cell energy metabolism in the elderly reveals that high mitochondrial oxidative phosphorylation, especially in CD4 T regulatory cells, is associated with a reduced probability of being frail / prefrail, independent of age, sex, or comorbidities. When mitochondrial respiration drops below a critical threshold, it adversely affects intrinsic capacity. Furthermore, a low level of oxidative phosphorylation in CD4 T helper cells, particularly in central and effector memory subsets, was significantly associated with a faster decline in intrinsic capacity over time, suggesting that T cell mitochondrial bioenergetics represents a key biomarker for managing functional decline in older adults. Accordingly, the present invention relates to a method for determining the risk of age-related functional decline in a subject comprising the step of measuring the mitochondrial dependency in a population of T cells wherein the mitochondrial dependency (MitoDep) correlates with the age-related functional decline.

The present application relates to the field of biological medicine, and particularly relates to lncLRFIF and application thereof in preparation of a medicine for treating laying hen fatty liver hemorrhagic syndrome.The present application provides lncLRFIF, and it is found for the first time that lncLRFIF can be used for preparation of a medicine for treating laying hen fatty liver hemorrhagic syndrome.In specific embodiments of the present application, lncLRFIF is knocked down by siRNA, so that the activities of ALT and AST in supernatant of chicken primary hepatocytes under FFAs treatment are recovered, lipid droplet accumulation and TG and T-CHO contents are significantly reduced, lipid synthesis is increased, lipid transport is increased, mitochondrial ATP and ROS contents are increased, and mitochondrial respiration and function are recovered.It can be seen that lncLRFIF can improve liver cell damage caused by FFAs and regulate lipid metabolism.The present application enriches the pathogenesis of laying hen fatty liver hemorrhagic syndrome, and provides a new idea for improving poultry egg production performance.

The invention discloses a preparation method of a carrier-free nano-drug delivery system CSCN and an application of the carrier-free nano-drug delivery system CSCN in breast cancer treatment. According to the system, a common photosensitizer Ce6 is chemically modified and reacts with 2-hydroxyethyl disulfide to obtain a new photosensitizer Ce6-SS, and Ce6-SS and Cel are self-assembled to form the carrier-free nano-particle CSCN. The nanoparticles are of a spherical structure with good dispersity, and the system has a relatively strong cell inhibition effect under near-infrared light, can be effectively internalized into 4T1 cells and presents time dependence. The system can also generate lysosome escape, and can significantly reduce the mitochondrial membrane potential of 4T1 cells and damage the mitochondrial function under near-infrared illumination, thereby inhibiting mitochondrial respiration, relieving tumor hypoxia and enhancing the PDT curative effect. The results prove that the nano system can play a good synergistic PDT treatment effect, and has a good application prospect in the anti-tumor field.

A method of increasing mitochondrial respiration in a cell makes use of a compound having the structure of formula (I) or formula (II).

The invention discloses a bZIP transcription factor PoATFS1 which is capable of mediating sensitivity change of magnaporthe oryzae to a mitochondrial respiration inhibitor, is highly expressed when mitochondrial dysfunction occurs and is capable of enhancing mtDNA replication in mitochondria. The sensitivity of a PoATFS1 overexpression transformant to a plurality of respiratory inhibitors is reduced, and the sensitivity of a knockout transformant to a plurality of respiratory inhibitors is improved. Meanwhile, the content of mtDNA in a PoATFS1 overexpression transformant is increased, and the content of mtDNA in a knockout transformant is reduced, which indicates that the PoATFS1 gene participates in regulation and control of the mitochondrial homeostasis. According to the invention, a synergist screening candidate target is provided for sensitivity recovery of the resistant phytopathogen to the respiration inhibitor, and drug resistance treatment of the phytopathogen and activity improvement of the existing respiration inhibitor are facilitated.

To provide a method for enhancing metabolic efficiency of the heart SOLUTION: Compositions and methods for increasing metabolic efficiency of the heart are provided. The present invention provides compositions that stimulate cardiac glucose oxidation and mitochondrial respiration. The composition comprises a compound that shifts cardiac metabolism from fatty acid oxidation to glucose oxidation, such as trimetazidine, and a compound that promotes mitochondrial respiration, such as succinate. The compositions may also include molecules such as nicotinic acid, which serves as a precursor for nicotinamide adenine dinucleotide (NAD +) synthesis and also facilitates mitochondrial respiration. Preferably, the composition comprises a compound in which the trimetazidine derivative, the succinate and optionally the NAD + precursor are covalently linked in a single molecule.SELECTED DRAWING: Figure 1

Disclosed are methods of treating a subject in need thereof comprising applying an alternating electric field to a target site of the subject in need thereof; and administering one or more CD137 agonists to the subject in need thereof. Disclosed are methods of promoting an effector T (Teff) cell immune response, decreasing immune suppression, decreasing mitochondrial respiration of regulatory T (Treg) cells, and reducing expansion of Treg cells in a subject in need thereof comprising applying an alternating electric field to a target site of the subject in need thereof; and administering one or more CD137 agonists to the subject in need thereof.