6 results about "Mitochondrial respiration" patented technology

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.

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 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 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.

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.