152 results about "Liver failure" patented technology

A test indicator for quantifying remaining liver function is provided. A novel liver receptor imaging agent with liver targeting property is utilized to develop a method for quantifying remaining liver function to serve as test indicator for judging the liver failure outcome in clinic, particularly for judging the necessity of liver transplantation for patients with liver failure or liver disease. The radioactivity uptake of the test indicator was negatively correlated with the extent of liver reserve. The cutoff value of liver reserve for liver transplantation is also disclosed.

Methods and compositions comprising peroxisomal and/or mitochondrial beta oxidation stimulating agents to reverse or resolve, slow the progression of, treat or prevent the development of fatty liver and conditions stemming from fatty liver, such as NASH, liver inflammation, cirrhosis and liver failure. An active agent that by itself is associated with an increased risk of fatty liver development and conditions stemming from fatty liver, such as NASH, liver inflammation, cirrhosis and liver failure, may be administered in combination with peroxisomal and/or mitochondrial beta oxidation stimulating agents. A combination regimen involving such agents, as simultaneous or concomitant therapy, or as a fixed dosage form, is also provided.

The invention discloses application of fructus forsythiae aglycone in preparing a medicament for preventing or treating liver injury or liver failure, and belongs to the medical field. The fructus forsythiae aglycone is a traditional Chinese medicine monomer obtained by extracting from the conventional fructus forsythiae, and is shown to have better treatment effect for the liver injury caused by acetaminopben, the livery injury caused by anti-tumor drug cis-platinum, acute or chronic livery injury caused by carbon tetrachloride, the livery injury caused by D-galactosamine and the liver failure caused by the D-galactosamine and lipopolysaccharide according to an animal test, has effect, which is better than that of fructus forsythiae and fructus forsythiae aglycone, in treating liver injury or liver failure. The fructus forsythiae aglycone is exact in curative effect and low in side effect for treating the liver injury and the liver failure, and has wide medical application prospect.

The invention discloses pediococcus pentosaceus and application thereof. The Latin name of the pediococcus pentosaceus is Pediococcus pentosaceus LI05, and the pediococcus pentosaceus is preserved in the China General Microbiological Culture Collection Center and has a preservation number of CGMCC No.7049. The pediococcus pentosaceus disclosed by the invention has the morphological characteristics that the thallus is rod-shaped, dose not generate spores, does not have motility, and has masculine Gram staining. The whole-cell fatty acid of the pediococcus pentosaceus disclosed by the invention comprises the following main components in percentage by weight: about 1.45% of 14:0, about 3.26% of 16:1w7c/16:1w6c, about 31.25% of 16:0, about 6.31% of 18:1w9c, about 38.59% of 18:1w7c, about 1.37% of 18:0 and about 14.59% of un18.846/19:1w6c. The invention also discloses a complete sequence of 16S ribosome DNA (16SrDNA) of the pediococcus pentosaceus. The pediococcus pentosaceus and a preparation thereof disclosed by the invention can be used for adjusting the micro-ecological balance of intestinal tracts of human or animals, promoting digestive absorption and slowing down the happening and development of liver failure of experimental animals.

The invention provides a GSTM3 (Glutathione S-Transferase M3) gene methylation quantitative detection method for hepatic failure prognosis and a kit, and provides a method and a device for quantitatively detecting the methylation degree of a glutathione S-transferase M3 promoter. The kit is internally provided with a reagent for extracting peripheral blood genome DNA (Deoxyribose Nucleic Acid), a reagent for modifying the genome DNA, a 5*premixing PCR (Polymerase Chain Reaction) system, a methylation specific primer pair and a Taqman fluorescence probe aiming at a target gene GSTM3 promoter, and a specific primer pair and a Taqman fluorescence probe of reference genes ALU-C4. According to the GSTM3 gene methylation quantitative detection method for the hepatic failure prognosis and the kit, the methylation specific primer pair and the probe of the target gene GSTM3 promoter and the specific primer pair and the probe of the reference genes can be used for carrying out a real-time quantitative polymerase chain reaction (PCR) on the peripheral blood genome DNA; a quantitative methylation specific PCR method is used for detecting a threshold value circulation value of the target gene GSTM3 and the reference genes ALU-C4 and calculating a gene GSTM3 methylation quantitative value, so as to be good for evaluating illness states, judging the prognosis and guiding the treatment.

The present invention relates to isolated liver progenitor stem cells, and cell population thereof, wherein said progenitor stem cells originate from adult liver, esp. of human. The present invention also relates to the use of said isolated progenitor stem cells in medicine, hepatology, inborn errors of liver metabolism, transplantation, infectious diseases, liver failure. The present invention also relates to methods of isolating these cells, their culture, characterization before and after differentiation, and their use for transplantation, animal models of human disease, toxicology and pharmacology.

Isolated liver progenitor stem cells and cell populations of isolated liver progenitor stem cells are disclosed. The progenitor stem cells originate from adult liver, especially human adult liver. The isolated progenitor stem cells have uses in medicine, hepatology, inborn errors of liver metabolism transplantation, infectious diseases and liver failure. Methods of isolating these cells and their culture is described. The isolated cells are characterized before and after differentiation. Their use for transplantation and as animal models of human disease, toxicology and pharmacology is disclosed.

The invention relates to a whole blood perfusion bioartificial liver system which comprises a blood circulation part and a bioartificial liver circulation part. The blood circulation part comprises a blood input port, a blood pump, a hollow fiber column and a blood feedback port which are sequentially connected. The bioartificial liver circulation part comprises a circulation pump, a constant temperature heater, an oxygenator and a bioreactor which are sequentially connected. An inlet of the circulation pump is connected with an outlet of an outer cavity of the hollow fiber column. A liquid outlet of the bioreactor is connected with an inlet of the outer cavity of the hollow fiber column. The bioartificial liver circulation part is further provided with two bypass pipelines. The whole blood perfusion bioartificial liver system further comprises a liquid input part and a dialyzate drainage part. The whole blood perfusion bioartificial liver system is safe, reliable and efficient, achieves continuous treatment, combines the venous transfusion and part kidney dialysis functions, is comprehensive, and provides effective support for hepatic failure patients.

The invention discloses a hepatic failure serum glycoprotein N-glycome map model establishing method, wherein a serum glycoprotein N-glycome map is detected by using a G-Test detection method, the N-glycome map model having significant difference between hepatic failure patients and normal control people is established, and the NA2 having significant expression difference between the hepatic failure group and the normal control group is screened. According to the present invention, the hepatic failure detection sensitivity and the hepatic failure detection specificity of the N-glycome map model constructed based on the method of the present invention respectively are 100.0% and 97.6%; in the subsequent applications, by comparing the peak value of the single-peak NA2 in the serum glycoprotein N-glycome map of the person to be detected and in the map model established by the method of the present invention, the hepatic failure degree of the person to be detected can be detected; and baseon the method of the present invention, a large number of hepatic failure patients can be subjected to conventional and non-invasive detection so as to help doctors and patients timely monitor the occurrence and the progression of hepatic failure, such that the method is expected to be popularized in clinical practice.

The invention provides a quantitative detection method and a reagent kit GSTP1 (Glutathione S-Transferase P1) methylation for predicting hepatic failure prognosis. The invention relates to quantitative detection for gene methylation, and in particular relates to a quantitative detection method and a reagent kit f GSTP1 (Glutathione S-Transferase P1) methylation for predicting hepatic failure prognosis. The reagent kit contains a reagent for extracting genomic DNA (Deoxyribonucleic Acid), a reagent for modifying the genomic DNA, a 5x premixing PCR (Polymerase Chain Reaction) system, a standard substance, positive and negative control, a methylation-specific primer pair aiming at a target gene GSTP1 promoter, a specific primer pair of a reference gene ALU-C4, and a corresponding Taqman fluorescent probe. By extracting peripheral blood genomic DNA and carrying out real-time fluorescence quantitative PCR, a quantitative value of the gene GSTP1 methylation is obtained through calculation. The reagent kit provided by the invention can help doctors to determine the pathogenetic condition and prognosis of hepatic failure patients so as to make effective treatment plans.

The invention discloses a tissue engineering microencapsulated hepatocyte and a preparation method thereof, belonging to the field of animal cell tissue engineering. The preparation method comprises the following steps of: adding hepatocytes and vascular endothelial cells in the quantity ratio of 1: (0.5-1) into water solution of sodium alginate for mixing to prepare a cell suspension, wherein the mass percentage concentration of the water solution of sodium alginate is 1.5-2; and then preparing sodium alginate-polylysine-sodium alginate microencapsulated hepatocyte by adopting a high-voltage static microcapsule generator. The invention also discloses the application of the tissue engineering microencapsulated hepatocyte in preparing hepatic failure medicaments; the prepared microencapsulated hepatocyte has the characteristics of small volume, high biocompatibility and favorable permeability, is suitably used as a vector for cell transplantation, and can exert in a host body for a long term so as to avoid the side effects caused by repeatedly using chemical medicaments; in addition, the microencapsulated hepatocyte has simple preparation process, thereby being suitable for large-batch production.

Disclosed are methods for treating liver failure in a subject comprising transplanting hepatocytes or stem or progenitor cells in an extrahepatic site in the subject in an amount sufficient to provide liver support and/or induce liver regeneration, where the transplanted hepatocytes or stem or progenitor cells are used along with extracellular matrix-coated microcarriers.

Disclosed are methods of inducing formation of a liver organoid from precursor cells, such as iPSC cells. The disclosed liver organoids may be used for screening for a serious adverse event (SAE), such as liver failure and/or drug induced liver injury (DILI), and/or drug toxicity. The disclosed liver organoids may also be used to treat an individual having liver damage, or for identifying a preferred therapeutic agent.

Disclosed are methods of inducing formation of a liver organoid from precursor cells, such as iPSC cells. The disclosed liver organoids may be used for screening for a serious adverse event (SAE), such as liver failure and/or drug induced liver injury (DILL), and/or drug toxicity. The disclosed liver organoids may also be used to treat an individual having liver damage, or for identifying a preferred therapeutic agent.

Hepatic cirrhosis is considered a severe health problem in Mexico, since it is the third mortality cause in working-age people and there is no 100% effective treatment. Cirrhosis is characterized by an exacerbated increase of collagen in liver parenchyma, replacing the hepatocytes and thus provoking liver failure. This is one of the reasons why we have used a gene therapy through specific delivery to cirrhotic livers of the gene of human urokinase plasminogen activator (huPA), which activates mechanisms that induce the degradation of excess cellular matrix and stimulate hepatocyte proliferation, obtaining thus a fast re-establishment of the liver function. In the instant invention, the modified human uPA gene was inserted in the adenoviral vector (pAd-DeltahuPA), because it is not secreted and does not provoke hypercoagulation or spontaneous internal bleedings. Moreover, data from the bio-distribution essay with an adenoviral vector with reporter gene beta-gal have shown liver specificity as the target organ of the vector. Using ELISA, huPa protein was detected in liver homogenates (4500 pg/ml) in animals treated with pAd-DeltahuPA and was also intracellularly detected through immunochemistry in liver cuts (80% positive cells). huPa induced a dramatic fibrosis reduction (85%) on day 10 of vector administration, compared to control cirrhotic rats and 55% hepatocyte proliferation increase. Liver function tests (ALT, AST, alkaline phosphatase and bilirubin) dropped to nearly normal levels and hepatocyte proliferation was observed. Because of the two beneficial event cascades, gene therapy with modified huPA can be developed as a definite potential treatment for patients with liver cirrhosis.