38 results about "Progeria" patented technology

This invention relates to the use of autologous stem / progenitor cells to restore or rejuvenate adult stem cell function in a mammal, wherein the restoration or rejuvenating extends lifespan and / or improves health of the mammal. In addition, the invention also relates to compositions containing one or more regulatory factors secreted or released from isolated mammalian stem / progenitor cells and use of such compositions to extend lifespan and / or improve health of a mammal. Also provided are methods of treating, delaying, preventing or reversing progeria or related syndromes in a mammal using isolated autologous or allogeneic stem / progenitor cells and / or regulatory factors secreted or released therefrom.

The invention discloses a genetic diagnosis kit which detects the early-aging syndromes of adults and belongs to the biotechnical field. A method which diagnoses the early-aging syndromes of the adults includes the following steps of: (1) gathering the blood, body fluid or tissue samples of individuals to be tested and extracting the DNA; (2) taking the DNA as a template and carrying out PRC reaction to PRC primers which are designed in accordance with the mutation sites of WRN genes to obtain products of the PRC reaction; (3) carrying out sequencing analysis to the obtained PRC products and comparing the obtained sample sequences with normal genetic sequences to determine whether mutation exists; and (4) judging whether the individuals to be tested have the early-aging syndromes caused by the mutation of the WRN genes according to the results. The invention has the advantages of providing the mutation of the WRN genes among the Chinese population for the first time and showing the correlation between the mutated genes and WS symptoms. The detection method is simple and low in cost, with direct and reliable results, and can be applied to the large-scale screening and diagnosis of the 2806insA mutation of WRN genes of Werner syndrome.

The invention relates to a mutant gene p53A1243G caused by the point mutation of a tumor suppressor gene p53, encoded protein p53N236S and functions thereof, and application thereof to tumor diagnosis. First, the important functions of p53N236S in an ALT tumor caused by progeria syndrome are disclosed. The invention can be applied to the tumor diagnosis with p53N236S as the target molecule, the screening of anticancer medicine and cancer treatment strategies, and has important significance in preventing tumors caused by aging.

This invention relates to the use of autologous stem / progenitor cells to restore or rejuvenate adult stem cell function in a mammal, wherein the restoration or rejuvenating extends lifespan and / or improves health of the mammal. In addition, the invention also relates to compositions containing one or more regulatory factors secreted or released from isolated mammalian stem / progenitor cells and use of such compositions to extend lifespan and / or improve health of a mammal. Also provided are methods of treating, delaying, preventing or reversing progeria or related syndromes in a mammal using isolated autologous or allogeneic stem / progenitor cells and / or regulatory factors secreted or released therefrom.

Disclosed herein are point mutations in the LMNA gene that cause HGPS. These mutations activate a cryptic splice site within the LMNA gene, which leads to deletion of part of exon 11 and generation of a mutant Lamin A protein product that is 50 amino acids shorter than the normal protein. In addition to the novel Lamin A variant protein and nucleic acids encoding this variant, methods of using these molecules in detecting biological conditions associated with a LMNA mutation in a subject (e.g., HGPS, arteriosclerosis, and other age-related diseases), methods of treating such conditions, methods of selecting treatments, methods of screening for compounds that influence Lamin A activity, and methods of influencing the expression of LMNA or LMNA variants are also described. Oligonucleotides and other compounds for use in examples of the described methods are also provided, as are protein-specific binding agents, such as antibodies, that bind specifically to at least one epitope of a Lamin A variant protein preferentially compared to wildtype Lamin A, and methods of using such antibodies in diagnosis, treatment, and screening. Also provided are kits for carrying out the methods described herein.

The invention relates to compounds in the treatment or prevention of disorders associated with Lamin A and / or Lamin C depletion or LMNA mutations, such as laminopathy, premature ageing disorders, normal ageing and cancer(such as a cancer characterised by low levels of LMNA expression).

Although it can be farnesylated, the mutant lamin A protein expressed in Hutchison Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and / or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression. Similarly, treatment with FTIs should improve disease status in progeria and other laminopathies. In addition, elements of atherosclerosis and aging in non-laminopathy individuals will improve after treatment with farnesyltransferase inhibitors.

A chimeric protein that is a fusion construct of a series of functional domains is used to deliver a therapeutic agent to a human subject suffering from disease. In some embodiments, the chimeric protein includes a therapeutic region and a transportation region. The transportation region allows the chimeric protein to be moved across a cellular membrane of an affected cell within the subject. The therapeutic region can be effective in the treatment of, for example, muscular dystrophy, diastrophic dysplasia, malignant melanoma, porphyria, alpha-1 antitrypsin deficiency, Aicardi-Goutieres syndrome, cystic fibrosis, progeria, Marfan syndrome, tuberous sclerosis, adrenoleukodystrophy, and the like.

The present invention includes compositions and methods for treating diseases or disorders associated with pathological calcification or pathological ossification. In certain embodiments, the diseases or disorders are selected from the group consisting of Generalized Arterial Calcification of Infancy (GACI), Idiopathic Infantile Arterial Calcification (IIAC), Ossification of the Posterior Longitudinal Ligament (OPLL), hypophosphatemic rickets, osteoarthritis, calcification of atherosclerotic plaques, PXE, hereditary and non-hereditary forms of osteoarthritis, ankylosing spondylitis, hardening of the arteries occurring with aging, calciphylaxis resulting from end stage renal disease and progeria.

The invention discloses a synthesizing method of image agent to diagnoze early senile dementia, which is synthesized by right-row technical path.

Although it can be farnesylated, the mutant lamin A protein expressed in Hutchinson Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and / or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression. Similarly, treatment with FTIs should improve disease status in progeria and other laminopathies. In addition, elements of atherosclerosis and aging in non-laminopathy individuals will improve after treatment with farnesyltransferase inhibitors.

The invention discloses a method for down-regulating a zebra fish lmna gene by using morpholino and an established progeria disease model; a morpholino oligonucleotide recombinant plasmid lmna-MO aiming at the zebra fish lmna gene and a lmna-EGFP-pCS<2+> recombinant plasmid for specific instruction of the expression quantity of the lmna gene are respectively designed and constructed; the two recombinant plasmids are co-injected into zebra fish embryos by a microinjection way, and the expression quantity of green fluorescent proteins is used as a lmna expression down-regulation mark, so that the zebra fish animal model with down-regulated lmna gene expression is established. The zebra fish animal model with down-regulated lmna gene expression is established, and can provide an animal model for deep research of laminopathy.

The present invention includes compositions and methods for treating diseases or disorders associated with pathological calcification or pathological ossification. In certain embodiments, the diseases or disorders are selected from the group consisting of Generalized Arterial Calcification of Infancy (GACI), Idiopathic Infantile Arterial Calcification (IIAC), Ossification of the Posterior Longitudinal Ligament (OPLL), hypophosphatemic rickets, osteoarthritis, calcification of atherosclerotic plaques, PXE, hereditary and non-hereditary forms of osteoarthritis, ankylosing spondylitis, hardening of the arteries occurring with aging, calciphylaxis resulting from end stage renal disease and progeria.

The invention discloses a peanut senescence gene for regulating programmed cell death, a coding sequence and application. RNA (ribonucleic acid) is extracted from root tip of peanut, and is cloned to a peanut senescence gene AhSAG, and the ORF (open read frame) of the peanut senescence gene is a cDNA (complementary deoxyribonucleic acid) sequence with coding sequence of 474bp and codes of 157aa; the AhSAG comes from a peanut root tip meristematic tissue of aluminum-induced peanut root tip generating programmed cell death, and is a senescence induction enhanced gene to induce, activate and promote progeria of plants. The peanut senescence disclosed by the invention can be expressed in tobacco, and can be used for regulating the adaptability of plant cells to environment changes and maintaining environmental stability and synthesis capacity in the cell.

The invention discloses a yellow dog penis extractive with resistance to ovarian function progeria as well as a preparation method and applications thereof. The extractive is prepared by using the preparation method comprising the following steps: taking yellow dog penis slices firstly, soaking the yellow dog penis slices in ethanol with the concentration of 90-95 percent for 2-4h; then, extracting with supercritical CO2 fluid to obtain an extract; and drying in vacuum to obtain a yellow dog penis extractive, wherein the supercritical CO2 fluid is prepared under the extraction conditions: theextraction pressure is 25MPa, the extraction temperature is 65 DEG C, a separation kettle I has the pressure of 5 MPa and the temperature of 40 DEG C; a separation kettle II has the pressure of 5 MPaand the temperature of 35 DEG C; the entrainer is 95% ethanol; and the extraction time is 2h. The yellow dog penis extractive provided by the invention has high active ingredient content and less inactive large-polarity compounds and determines the optimal process with highest active ingredient extraction efficiency by inspecting the extraction pressure, the extraction temperature and the extraction time of the supercritical CO2, the entrainer and the dosage thereof. Shown by experimental results and compared with a traditional aqueous extract or an alcohol extract, the supercritical CO2 extract has better resistance to the ovarian function progeria.

The present disclosure relates to the treatment of Hutchinson-Gilford Progeria Syndrome (HGPS) and diseases related to vascular ageing and in the treatment of smooth muscle cells diseases, in particular an inhibitor of a metalloprotease the treatment of smooth muscle cells diseases. The disclosure subject matter describes a more effective therapies for the treatment of Hutchinson-Gilford Progeria Syndrome and diseases related to vascular ageing, or namely by the use of an inhibitor of a metalloprotease.

The present invention relates to a novel decursin derivative and a composition for preventing or treating aging-related diseases containing the same as an active ingredient. The novel decursin derivative has exhibited an excellent effect of inhibiting progerin expression and an excellent effect of inhibiting binding between progerin and lamin A, and it has been confirmed that the novel decursin derivative prolongs the survival period of animal models in which progeria is induced. Therefore, a compound of the present invention can be effectively used for the prevention or treatment of aging-related diseases such as progeria, etc.

The invention belongs to the technical field of cell treating, relates to a method for treating progeria or Hutchinson-Gilford progeria syndrome, in particular to a treating agent for restoring body function aging and delaying recession of organ functions and comprising GD2+ stroma cells and KDR+ hematopoietic stem cells and further relates to application, in preparation of the treating agent for treating progeria or Hutchinson-Gilford progeria syndrome or for restoring body function aging and delaying recession of the organ functions, of the combination of the GD2+ stroma cells and the KDR+ hematopoietic stem cells. It has been found that the treating agent can be effectively used for treating progeria or Hutchinson-Gilford progeria syndrome, especially for restoring body function aging and delaying recession of the organ functions.

The present invention discloses a grape seed purple sweet potato starch which consists of the following raw materials in parts by weight: 950-980 parts of fresh purple sweet potatoes, 20-25 parts of Chinese wolfberry fruits, 40-50 parts of grape seeds, 60-70 parts of red dates, 35-40 parts of honey, 6-8 parts of semen coicis, 6-8 parts of ginsengs, etc. The purple sweet potato starch is high in purity and rich in anthocyanins, does not lead to a waste of anthocyanins, and can fully utilize purple sweet potato raw materials. The added grape seeds and lycium barbarum polysaccharides can eliminate free radicals, protect skin, prevent progeria, and enhance immunity. The red dates and honey improve the taste of starch. The added extracts of semen coicis, ginsengs, pearls, ganoderma lucidum, gentiana scabra, etc. can enable the grape seed purple sweet potato starch to have certain effects of tonifying life and whitening skin.

The invention discloses a pluripotent stem cell carrying a human progeria gene mutation, a mesenchymal stem cell and a preparation method. The method comprises: (1) taking human pluripotent stem cells cultured in vitro, mutating the human adult progeria gene WRN in the human pluripotent stem cells, making the WRN function inoperative, and obtaining human pluripotent stem cells in which the WRN function is lost (2) performing directional induction and differentiation on the human pluripotent stem cells with loss of WRN function to obtain mesenchymal stem cells with loss of WRN function. The mesenchymal stem cells derived from pluripotent stem cells provided by the present invention can be used to establish a drug screening platform for screening WS therapeutic drugs, and also provide more clues for delaying the natural aging process.

The invention provides a biochemical marker-assisted selection method for the trait of premature senescence and non-premature senescence of short-season cotton. The biochemical markers involved in the invention are superoxide dismutase (SOD), peroxidase (POD), catalase (CAT) and malondialdehyde (MDA) content, and the selection method is to select precocious and non-premature aging parents Hybridization, using the relative activity of the three enzymes SOD, POD, and CAT in the critical period as selection markers, the population of hybrid offspring was selected from the F2 generation, and combined with conventional breeding techniques, a precocious, non-premature senescence, green branches and green leaves were bred. The short-season cotton series of white catkins are Zhongmian 16, 24, 27 and 36. This technology overcomes the disadvantages of conventional breeding, such as long selection period, great influence by environmental conditions, time-consuming and laborious, and low selection efficiency. Effectively alleviate the genetic positive correlation between precocity and premature aging, and the negative genetic correlation between early maturity and high quality and disease resistance, integrating precocious maturity without premature aging, high quality, high yield and disease resistance.

The present invention includes compositions and methods for treating diseases or disorders associated with pathological calcification or pathological ossification. In certain embodiments, the diseases or disorders are selected from the group consisting of Generalized Arterial Calcification of Infancy (GACI), Idiopathic Infantile Arterial Calcification (IIAC), Ossification of the Posterior Longitudinal Ligament (OPLL), hypophosphatemic rickets, osteoarthritis, calcification of atherosclerotic plaques, PXE, hereditary and non-hereditary forms of osteoarthritis, ankylosing spondylitis, hardening of the arteries occurring with aging, calciphylaxis resulting from end stage renal disease and progeria.

The invention relates to a mutant gene p53A1243G caused by the point mutation of a tumor suppressor gene p53, encoded protein p53N236S and functions thereof, and application thereof to tumor diagnosis. First, the important functions of p53N236S in an ALT tumor caused by progeria syndrome are disclosed. The invention can be applied to the tumor diagnosis with p53N236S as the target molecule, the screening of anticancer medicine and cancer treatment strategies, and has important significance in preventing tumors caused by aging.

Use of endothelial progenitor cells in the manufacture of a medicament for rejuvenating neovascularization capacity, ameliorating aging features, preventing aging, extending lifespan, and / or treating progeria and / or age-related diseases. A method for rejuvenating neovascularization capacity, ameliorating aging features, preventing aging, extending lifespan, and / or treating progeria and / or age-related diseases, includes: administering a pharmaceutically effective amount of EPCs to a subject in need thereof.