Skin: The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.Lettuce: Any of the various plants of the genus Lactuca, especially L. sativa, cultivated for its edible leaves. (From American Heritage Dictionary, 2d ed)Skin Aging: The process of aging due to changes in the structure and elasticity of the skin over time. It may be a part of physiological aging or it may be due to the effects of ultraviolet radiation, usually through exposure to sunlight.Tiopronin: Sulfhydryl acylated derivative of GLYCINE.Skin DiseasesSkin Neoplasms: Tumors or cancer of the SKIN.Diet: Regular course of eating and drinking adopted by a person or animal.Life Style: Typical way of life or manner of living characteristic of an individual or group. (From APA, Thesaurus of Psychological Index Terms, 8th ed)Hormesis: Biphasic dose responses of cells or organisms (including microorganisms) to an exogenous or intrinsic factor, in which the factor induces stimulatory or beneficial effects at low doses and inhibitory or adverse effects at high doses.Aging: The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.Physical Endurance: The time span between the beginning of physical activity by an individual and the termination because of exhaustion.Exercise: Physical activity which is usually regular and done with the intention of improving or maintaining PHYSICAL FITNESS or HEALTH. Contrast with PHYSICAL EXERTION which is concerned largely with the physiologic and metabolic response to energy expenditure.Physical Conditioning, Animal: Diet modification and physical exercise to improve the ability of animals to perform physical activities.DNA, Mitochondrial: Double-stranded DNA of MITOCHONDRIA. In eukaryotes, the mitochondrial GENOME is circular and codes for ribosomal RNAs, transfer RNAs, and about 10 proteins.Exercise Test: Controlled physical activity which is performed in order to allow assessment of physiological functions, particularly cardiovascular and pulmonary, but also aerobic capacity. Maximal (most intense) exercise is usually required but submaximal exercise is also used.Exercise Therapy: A regimen or plan of physical activities designed and prescribed for specific therapeutic goals. Its purpose is to restore normal musculoskeletal function or to reduce pain caused by diseases or injuries.Muscle, Skeletal: A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.Oxygen Consumption: The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)Physical Education and Training: Instructional programs in the care and development of the body, often in schools. The concept does not include prescribed exercises, which is EXERCISE THERAPY.Exercise Tolerance: The exercise capacity of an individual as measured by endurance (maximal exercise duration and/or maximal attained work load) during an EXERCISE TEST.Progeria: An abnormal congenital condition, associated with defects in the LAMIN TYPE A gene, which is characterized by premature aging in children, where all the changes of cell senescence occur. It is manifested by premature greying; hair loss; hearing loss (DEAFNESS); cataracts (CATARACT); ARTHRITIS; OSTEOPOROSIS; DIABETES MELLITUS; atrophy of subcutaneous fat; skeletal hypoplasia; elevated urinary HYALURONIC ACID; and accelerated ATHEROSCLEROSIS. Many affected individuals develop malignant tumors, especially SARCOMA.Polynesia: The collective name for the islands of the central Pacific Ocean, including the Austral Islands, Cook Islands, Easter Island, HAWAII; NEW ZEALAND; Phoenix Islands, PITCAIRN ISLAND; SAMOA; TONGA; Tuamotu Archipelago, Wake Island, and Wallis and Futuna Islands. Polynesians are of the Caucasoid race, but many are of mixed origin. Polynesia is from the Greek poly, many + nesos, island, with reference to the many islands in the group. (From Webster's New Geographical Dictionary, 1988, p966 & Room, Brewer's Dictionary of Names, 1992, p426)Lamin Type A: A subclass of developmentally regulated lamins having a neutral isoelectric point. They are found to disassociate from nuclear membranes during mitosis.Aging, Premature: Changes in the organism associated with senescence, occurring at an accelerated rate.Farnesyltranstransferase: An enzyme that catalyzes the synthesis of geranylgeranyl diphosphate from trans, trans-farnesyl diphosphate and isopentenyl diphosphate.ChileCell Nucleus Shape: The quality of surface form or outline of the CELL NUCLEUS.Protein PrecursorsNuclear Lamina: A lattice of fibrils which covers the entire inner surface of the nuclear envelope and interlinks nuclear pores (NUCLEAR PORE).Prenylation: Attachment of isoprenoids (TERPENES) to other compounds, especially PROTEINS and FLAVONOIDS.Postural Balance: A POSTURE in which an ideal body mass distribution is achieved. Postural balance provides the body carriage stability and conditions for normal functions in stationary position or in movement, such as sitting, standing, or walking.Vestibular Diseases: Pathological processes of the VESTIBULAR LABYRINTH which contains part of the balancing apparatus. Patients with vestibular diseases show instability and are at risk of frequent falls.Sensation Disorders: Disorders of the special senses (i.e., VISION; HEARING; TASTE; and SMELL) or somatosensory system (i.e., afferent components of the PERIPHERAL NERVOUS SYSTEM).Adenosine Triphosphate: An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.Solitary Pulmonary Nodule: A single lung lesion that is characterized by a small round mass of tissue, usually less than 1 cm in diameter, and can be detected by chest radiography. A solitary pulmonary nodule can be associated with neoplasm, tuberculosis, cyst, or other anomalies in the lung, the CHEST WALL, or the PLEURA.Autonomic Fibers, Preganglionic: NERVE FIBERS which project from the central nervous system to AUTONOMIC GANGLIA. In the sympathetic division most preganglionic fibers originate with neurons in the intermediolateral column of the SPINAL CORD, exit via ventral roots from upper thoracic through lower lumbar segments, and project to the paravertebral ganglia; there they either terminate in SYNAPSES or continue through the SPLANCHNIC NERVES to the prevertebral ganglia. In the parasympathetic division the fibers originate in neurons of the BRAIN STEM and sacral spinal cord. In both divisions the principal transmitter is ACETYLCHOLINE but peptide cotransmitters may also be released.Adrenergic Fibers: Nerve fibers liberating catecholamines at a synapse after an impulse.Anion Transport Proteins: Membrane proteins whose primary function is to facilitate the transport of negatively charged molecules (anions) across a biological membrane.Lymphocytes, Null: A class of lymphocytes characterized by the lack of surface markers specific for either T or B lymphocytes.Sphingosine: An amino alcohol with a long unsaturated hydrocarbon chain. Sphingosine and its derivative sphinganine are the major bases of the sphingolipids in mammals. (Dorland, 28th ed)Stevens-Johnson Syndrome: Rare cutaneous eruption characterized by extensive KERATINOCYTE apoptosis resulting in skin detachment with mucosal involvement. It is often provoked by the use of drugs (e.g., antibiotics and anticonvulsants) or associated with PNEUMONIA, MYCOPLASMA. It is considered a continuum of Toxic Epidermal Necrolysis.Faculty, Medical: The teaching staff and members of the administrative staff having academic rank in a medical school.Proteins: Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.Sister Mary Joseph's Nodule: Metastatic lesion of the UMBILICUS associated with intra-abdominal neoplasms especially of the GASTROINTESTINAL TRACT or OVARY.Biology: One of the BIOLOGICAL SCIENCE DISCIPLINES concerned with the origin, structure, development, growth, function, genetics, and reproduction of animals, plants, and microorganisms.Cell Biology: The study of the structure, behavior, growth, reproduction, and pathology of cells; and the function and chemistry of cellular components.Umbilicus: The pit in the center of the ABDOMINAL WALL marking the point where the UMBILICAL CORD entered in the FETUS.History, 21st Century: Time period from 2001 through 2100 of the common era.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.History, 19th Century: Time period from 1801 through 1900 of the common era.Telomere: A terminal section of a chromosome which has a specialized structure and which is involved in chromosomal replication and stability. Its length is believed to be a few hundred base pairs.G-Quadruplexes: Higher-order DNA and RNA structures formed from guanine-rich sequences. They are formed around a core of at least 2 stacked tetrads of hydrogen-bonded GUANINE bases. They can be formed from one two or four separate strands of DNA (or RNA) and can display a wide variety of topologies, which are a consequence of various combinations of strand direction, length, and sequence. (From Nucleic Acids Res. 2006;34(19):5402-15)Telomerase: An essential ribonucleoprotein reverse transcriptase that adds telomeric DNA to the ends of eukaryotic CHROMOSOMES.Cell Aging: The decrease in the cell's ability to proliferate with the passing of time. Each cell is programmed for a certain number of cell divisions and at the end of that time proliferation halts. The cell enters a quiescent state after which it experiences CELL DEATH via the process of APOPTOSIS.Telomere-Binding Proteins: Proteins that specifically bind to TELOMERES. Proteins in this class include those that perform functions such as telomere capping, telomere maintenance and telomere stabilization.Telomeric Repeat Binding Protein 2: A ubiquitously expressed telomere-binding protein that is present at TELOMERES throughout the cell cycle. It is a suppressor of telomere elongation and may be involved in stabilization of telomere length. It is structurally different from TELOMERIC REPEAT BINDING PROTEIN 1 in that it contains basic N-terminal amino acid residues.Recombination, Genetic: Production of new arrangements of DNA by various mechanisms such as assortment and segregation, CROSSING OVER; GENE CONVERSION; GENETIC TRANSFORMATION; GENETIC CONJUGATION; GENETIC TRANSDUCTION; or mixed infection of viruses.DNA Breaks, Double-Stranded: Interruptions in the sugar-phosphate backbone of DNA, across both strands adjacently.Telomere Homeostasis: Maintenance of TELOMERE length. During DNA REPLICATION, chromosome ends loose some of their telomere sequence (TELOMERE SHORTENING.) Various cellular mechanism are involved in repairing, extending, and recapping the telomere ends.DNA Repair: The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.Cataloging: Activities performed in the preparation of bibliographic records for CATALOGS. It is carried out according to a set of rules and contains information enabling the user to know what is available and where items can be found.Catalogs, LibraryBook Classification: A general term covering bibliographical and bibliothecal classifications. It mostly refers to library CLASSIFICATION for arrangement of books and documents on the shelves. (Harrod's Librarians' Glossary, 7th ed, p85)Weight Gain: Increase in BODY WEIGHT over existing weight.Energy Metabolism: The chemical reactions involved in the production and utilization of various forms of energy in cells.Cell Transformation, Neoplastic: Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.Body Weight: The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.Transformation, Genetic: Change brought about to an organisms genetic composition by unidirectional transfer (TRANSFECTION; TRANSDUCTION, GENETIC; CONJUGATION, GENETIC, etc.) and incorporation of foreign DNA into prokaryotic or eukaryotic cells by recombination of part or all of that DNA into the cell's genome.MicrofilmingLibrary Technical Services: Acquisition, organization, and preparation of library materials for use, including selection, weeding, cataloging, classification, and preservation.Vitamin A: Retinol and derivatives of retinol that play an essential role in metabolic functioning of the retina, the growth of and differentiation of epithelial tissue, the growth of bone, reproduction, and the immune response. Dietary vitamin A is derived from a variety of CAROTENOIDS found in plants. It is enriched in the liver, egg yolks, and the fat component of dairy products.Vitamins: Organic substances that are required in small amounts for maintenance and growth, but which cannot be manufactured by the human body.Vitamin E: A generic descriptor for all TOCOPHEROLS and TOCOTRIENOLS that exhibit ALPHA-TOCOPHEROL activity. By virtue of the phenolic hydrogen on the 2H-1-benzopyran-6-ol nucleus, these compounds exhibit varying degree of antioxidant activity, depending on the site and number of methyl groups and the type of ISOPRENOIDS.Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant.Vitamin D: A vitamin that includes both CHOLECALCIFEROLS and ERGOCALCIFEROLS, which have the common effect of preventing or curing RICKETS in animals. It can also be viewed as a hormone since it can be formed in SKIN by action of ULTRAVIOLET RAYS upon the precursors, 7-dehydrocholesterol and ERGOSTEROL, and acts on VITAMIN D RECEPTORS to regulate CALCIUM in opposition to PARATHYROID HORMONE.Vitamin B 12: A cobalt-containing coordination compound produced by intestinal micro-organisms and found also in soil and water. Higher plants do not concentrate vitamin B 12 from the soil and so are a poor source of the substance as compared with animal tissues. INTRINSIC FACTOR is important for the assimilation of vitamin B 12.Vitamin A Deficiency: A nutritional condition produced by a deficiency of VITAMIN A in the diet, characterized by NIGHT BLINDNESS and other ocular manifestations such as dryness of the conjunctiva and later of the cornea (XEROPHTHALMIA). Vitamin A deficiency is a very common problem worldwide, particularly in developing countries as a consequence of famine or shortages of vitamin A-rich foods. In the United States it is found among the urban poor, the elderly, alcoholics, and patients with malabsorption. (From Cecil Textbook of Medicine, 19th ed, p1179)Arteriosclerosis Obliterans: Common occlusive arterial disease which is caused by ATHEROSCLEROSIS. It is characterized by lesions in the innermost layer (ARTERIAL INTIMA) of arteries including the AORTA and its branches to the extremities. Risk factors include smoking, HYPERLIPIDEMIA, and HYPERTENSION.Vitamin D Deficiency: A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)Sodium-Coupled Vitamin C Transporters: Membrane transport proteins that actively co-transport ASCORBIC ACID and sodium ions across the CELL MEMBRANE. Dietary absorption of VITAMIN C is highly dependent upon this class of transporters and a subset of SODIUM GLUCOSE TRANSPORTERS which transport the oxidized form of vitamin C, DEHYDROASCORBIC ACID.American Recovery and Reinvestment Act: Public Law No: 111-5, enacted February 2009, makes supplemental appropriations for job preservation and creation, infrastructure investment, energy efficiency and science, assistance to the unemployed, and State and local fiscal stabilization, for fiscal year ending September 30, 2009.Research Support, American Recovery and Reinvestment ActScience: The study of natural phenomena by observation, measurement, and experimentation.Research Support as Topic: Financial support of research activities.United StatesResearch: Critical and exhaustive investigation or experimentation, having for its aim the discovery of new facts and their correct interpretation, the revision of accepted conclusions, theories, or laws in the light of newly discovered facts, or the practical application of such new or revised conclusions, theories, or laws. (Webster, 3d ed)National Institutes of Health (U.S.): An operating division of the US Department of Health and Human Services. It is concerned with the overall planning, promoting, and administering of programs pertaining to health and medical research. Until 1995, it was an agency of the United States PUBLIC HEALTH SERVICE.Patient Care Team: Care of patients by a multidisciplinary team usually organized under the leadership of a physician; each member of the team has specific responsibilities and the whole team contributes to the care of the patient.Universities: Educational institutions providing facilities for teaching and research and authorized to grant academic degrees.Federal Government: The level of governmental organization and function at the national or country-wide level.Sunscreening Agents: Chemical or physical agents that protect the skin from sunburn and erythema by absorbing or blocking ultraviolet radiation.Ultraviolet Rays: That portion of the electromagnetic spectrum immediately below the visible range and extending into the x-ray frequencies. The longer wavelengths (near-UV or biotic or vital rays) are necessary for the endogenous synthesis of vitamin D and are also called antirachitic rays; the shorter, ionizing wavelengths (far-UV or abiotic or extravital rays) are viricidal, bactericidal, mutagenic, and carcinogenic and are used as disinfectants.Sunburn: An injury to the skin causing erythema, tenderness, and sometimes blistering and resulting from excessive exposure to the sun. The reaction is produced by the ultraviolet radiation in sunlight.Sunlight: Irradiation directly from the sun.Sun Protection Factor: A measure of relative protection provided by SUNSCREENING AGENTS against burns due to ultraviolet (UV) radiation from a light source.Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes.Sulfadoxine: A long acting sulfonamide that is used, usually in combination with other drugs, for respiratory, urinary tract, and malarial infections.Pyrimethamine: One of the FOLIC ACID ANTAGONISTS that is used as an antimalarial or with a sulfonamide to treat toxoplasmosis.Photosensitivity Disorders: Abnormal responses to sunlight or artificial light due to extreme reactivity of light-absorbing molecules in tissues. It refers almost exclusively to skin photosensitivity, including sunburn, reactions due to repeated prolonged exposure in the absence of photosensitizing factors, and reactions requiring photosensitizing factors such as photosensitizing agents and certain diseases. With restricted reference to skin tissue, it does not include photosensitivity of the eye to light, as in photophobia or photosensitive epilepsy.

Physical and functional interaction between p53 and the Werner's syndrome protein. (1/201)

Werner's syndrome is a human autosomal recessive disorder leading to premature aging. The mutations responsible for this disorder have recently been localized to a gene (WRN) encoding a protein that possesses DNA helicase and exonuclease activities. Patients carrying WRN gene mutations exhibit an elevated rate of cancer, accompanied by increased genomic instability. The latter features are also characteristic of the loss of function of p53, a tumor suppressor that is very frequently inactivated in human cancer. Moreover, changes in the activity of p53 have been implicated in the onset of cellular replicative senescence. We report here that the WRN protein can form a specific physical interaction with p53. This interaction involves the carboxyl-terminal part of WRN and the extreme carboxyl terminus of p53, a region that plays an important role in regulating the functional state of p53. A small fraction of WRN can be found in complex with endogenous p53 in nontransfected cells. Overexpression of WRN leads to augmented p53-dependent transcriptional activity and induction of p21(Waf1) protein expression. These findings support the existence of a cross-talk between WRN and p53, which may be important for maintaining genomic integrity and for preventing the accumulation of aberrations that can give rise to premature senescence and cancer.  (+info)

Unique mutations in mitochondrial DNA of senescence-accelerated mouse (SAM) strains. (2/201)

Mitochondrial DNA (mtDNA) is exclusively inherited maternally and hence could offer a good method for tracing the lineage of mouse strains. We examined the mtDNA sequence of senescence-accelerated mouse (SAM) strains as well as other laboratory strains of inbred mice to deduce the ancestral strain of SAM. Four unique mutations were identified at bases 2256, 10,847, 11,181, and 13,053 in SAM strains. The mutations were not found in other mouse strains including AKR/J, one of the parental strains of SAM. Comparison of the mtDNA sequences also led to the consensus mtDNA sequence of laboratory strains of inbred mice. The seven laboratory strains of common inbred mice showed polymorphisms at base 9348, thymine repeat from base 9818, and adenine repeat from base 9821, and could be classified into five types by combination of the differences. Although we could not identify mouse strains with the same type of mtDNA as SAM in this study, the polymorphisms would provide a promising clue to ascertain the ancestral strain(s) of SAM. The polymorphism in mtDNA could be used to ascertain the genealogy of other mouse strains as well.  (+info)

Antioxidant systems in tissues of senescence accelerated mice. (3/201)

Significant decrease in the level of lipid antioxidants (measured from the kinetics of the induced chemiluminescence in brain homogenate) and of the hydrophilic antioxidant carnosine as well was observed in the brain of 14-16-month-old mice of SAMP1 line, which is characterized by accelerated accumulation of senile features, in comparison with the control line SAMR1. In the brain of SAMP1 animals the activity of cytosolic Cu/Zn-containing superoxide dismutase (SOD) was reduced, while the activity of membrane-bound Mn-SOD was at an extremely low level. The activity of glutathione-dependent enzymes (glutathione peroxidase, glutathione reductase, and glutathione transferase) did not differ in the brain of SAMP1 and SAMR1 animals, and catalase activity was similarly low in both cases. At the same time, excess concentration of excitotoxic compounds, significantly exceeding that for the control line, was determined in the brain and blood of SAMP1 animals. The activity of glutathione enzymes in liver and heart as well as the activity of cytosolic Cu/Zn-SOD in liver did not differ in the two studied lines, while the activity of erythrocyte glutathione peroxidase was slightly increased, and the activity of liver catalase and erythrocyte Cu/Zn-SOD was significantly decreased for SAMP1 compared with SAMR1. The results demonstrate that the accelerated ageing of SAMP1 animals is connected to a significant extent with the decreased efficiency of the systems utilizing reactive oxygen species (ROS) in tissues.  (+info)

Association of human aging with a functional variant of klotho. (4/201)

Mice deficient in Klotho gene expression exhibit a syndrome resembling premature human aging. To determine whether variation in the human KLOTHO locus contributes to survival, we applied two newly characterized polymorphic microsatellite markers flanking the gene in a population-based association study. In a cohort chosen for its homogeneity, Bohemian Czechs, we demonstrated significant differences in selected marker allele frequencies between newborn and elderly individuals (P < 0.05). These results precipitated a search for functional variants of klotho. We identified an allele, termed KL-VS, containing six sequence variants in complete linkage disequilibrium, two of which result in amino acid substitutions F352V and C370S. Homozygous elderly individuals were underrepresented in three distinct populations: Bohemian Czechs, Baltimore Caucasians, and Baltimore African-Americans [combined odds ratio (OR) = 2.59, P < 0.0023]. In a transient transfection assay, secreted levels of klotho harboring V352 are reduced 6-fold, whereas extracellular levels of the S370 form are increased 2.9-fold. The V352/S370 double mutant exhibits an intermediate phenotype (1.6-fold increase), providing a rare example of intragenic complementation in cis by human single nucleotide polymorphisms. The remarkable conservation of F352 among homologous proteins suggests that it is functionally important. The corresponding substitution, F289V, in the closest human klotho paralog with a known substrate, cBGL1, completely eliminates its ability to cleave p-nitrophenyl-beta-D-glucoside. These results suggest that the KL-VS allele influences the trafficking and catalytic activity of klotho, and that variation in klotho function contributes to heterogeneity in the onset and severity of human age-related phenotypes.  (+info)

Life span and renal morphological characterization of the SAMP1//Ka mouse. (5/201)

The senescence-accelerated-mouse prone 1 (SAMP1) is considered to be a model of accelerated senility and it also develops severe kidney damage. The SAMP1//Ka mouse is a specific pathogen free (SPF) subline of SAMP1. The present study examined the life span of the SAMP1//Ka mouse and morphologically investigated the kidneys of this animal at 3, 4, 5, 9, 12, 15, 18 and 24 months of age. Males survived for an average of 25 months and females for 28 months. The median lifespan was 18 months for males and 20 for females. Focal cell infiltration and thickening of the basement membrane in the glomerular capsules or tubules appeared from 4 months of age. At 12 months old, glomerular lesions with expansion of the mesangial matrix and thickening of the basement membrane as well as scar lesions in the outer cortex appeared, and amyloid was deposited in the interstitium or glomeruli from 18 months of age. Morphometrically, although the area of the kidney sections was increased at 24 months of age, the diameter of the renal corpuscles, the number of nuclei of the proximal convoluted tubules and the percentage of renal corpuscles with a cuboidal glomerular capsule did not change with age. The results of the present study indicate that the life span of the SAMP1//Ka is increased and that their age-related renal changes differ from those of the original SAMP1.  (+info)

Premature aging in mice deficient in DNA repair and transcription. (6/201)

One of the factors postulated to drive the aging process is the accumulation of DNA damage. Here, we provide strong support for this hypothesis by describing studies of mice with a mutation in XPD, a gene encoding a DNA helicase that functions in both repair and transcription and that is mutated in the human disorder trichothiodystrophy (TTD). TTD mice were found to exhibit many symptoms of premature aging, including osteoporosis and kyphosis, osteosclerosis, early greying, cachexia, infertility, and reduced life-span. TTD mice carrying an additional mutation in XPA, which enhances the DNA repair defect, showed a greatly accelerated aging phenotype, which correlated with an increased cellular sensitivity to oxidative DNA damage. We hypothesize that aging in TTD mice is caused by unrepaired DNA damage that compromises transcription, leading to functional inactivation of critical genes and enhanced apoptosis.  (+info)

Ageing: repair and transcription keep us from premature ageing. (7/201)

Trichothiodystrophy (TTD) is a complex disorder caused by mutations in the XPD gene which affect both DNA repair and transcription. A mouse with a TTD mutation has now been found to display remarkable signs of premature ageing.  (+info)

Insufficient interleukin-2 production from splenic CD4+ T cells causes impaired cell proliferation and early apoptosis in SAMP1, a strain of senescence-accelerated mouse. (8/201)

We examined the proliferative and cytokine-producing activities of CD4+ T cells from young mice of the senescence-accelerated mouse strain SAMP1, which had shown markedly low T-dependent antibody-producing responses. When splenic T cells were cultured with concanavalin A (Con A), the percentage of CD4+ cells decreased earlier in SAMP1 than in C3H/He mice. At 40 hr of culture, the percentage of BrdU-labelled proliferating CD4+ cells increased strongly in C3H/He, but only slightly in SAMP1. When purified CD4+ T cells were cultured with Con A, the percentage of 5-bromo-2'-deoxyuridine (BrdU)-labelled cells peaked at around 48 hr of culture in both strains, but decreased significantly at 64 hr in SAMP1. The production of interleukin (IL)-2 but not IL-4 or interferon-gamma (IFN-gamma) was significantly lower in SAMP1 than in C3H/He at 48 hr of culture. IL-2 production was also markedly low in SAMP1, even under the stimulation of anti-CD3 with anti-CD28 antibodies. The frequency of cells producing IL-2 was significantly lower in SAMP1 than in C3H/He at 6-24 hr of culture with Con A. The percentage of annexin-positive and propidium iodide (PI)-negative apoptotic cells was significantly higher in SAMP1 than in C3H/He at 96 hr of culture. Exogenous IL-2 prevented the decrease in BrdU-labelled cells and the increase in apoptotic cells in the SAMP1 cell culture. These results indicate that SAMP1 CD4+ T cells cannot produce IL-2 at levels sufficient to support cell proliferation and survival. This may account for the weak T-dependent antibody response in SAMP1 mice.  (+info)

*Coal mining in Brazil

... premature aging; prooxidant and antioxidant alterations that lead to cellular damage; cardiopulmonary disease; hypertension; ...

*Sunstar Group

"Pigmentation and Premature Aging Woes? New Japanese Line Has You Covered". Monsters & Critics. Retrieved 13 March 2015. ...

*ZMPSTE24

"Genomic instability in laminopathy-based premature aging". Nat. Med. 11 (7): 780-5. doi:10.1038/nm1266. PMID 15980864. ZMPSTE24 ...

*LMNA

... may cause features of premature aging (see DNA damage theory of aging). LMNA has been shown to interact with: ALOX12 EMD NARF ... Sliwińska MA (2007). "[The role of lamins and mutations of LMNA gene in physiological and premature aging] Polish". Postepy ... Scaffidi P, Misteli T (April 2005). "Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford ... "Genomic instability in laminopathy-based premature aging". Nat. Med. 11 (7): 780-5. doi:10.1038/nm1266. PMID 15980864. Tang K, ...

*Laminopathy

Mutations in lamin A (LMNA) cause Hutchinson-Gilford progeria syndrome, a dramatic form of premature aging. Mouse cells ... premature aging). Most of these symptoms develop after birth, typically during childhood or adolescence. Some laminopathies ... "Genomic instability in laminopathy-based premature aging". Nat. Med. 11 (7): 780-5. doi:10.1038/nm1266. PMID 15980864. Chen L, ... adequately repair DNA damages when A-type lamins are defective is likely responsible for some of the aspects of premature aging ...

*Nuclear lamina

Premature aging Restrictive dermopathy - A disease associated with extremely tight skin and other severe neonatal abnormalities ... "Genomic instability in laminopathy-based premature aging". Nat. Med. 11 (7): 780-5. doi:10.1038/nm1266. PMID 15980864. Yozef ...

*Hypervitaminosis D

Keisala T, Minasyan A, Lou YR, Zou J, Kalueff AV, Pyykkö I, Tuohimaa P (July 2009). "Premature aging in vitamin D receptor ... Animal research suggests that both excess and deficiency of vitamin D appears to cause abnormal functioning and premature aging ... Tuohimaa P (March 2009). "Vitamin D and aging". The Journal of Steroid Biochemistry and Molecular Biology. 114 (1-2): 78-84. ... Tuohimaa P, Keisala T, Minasyan A, Cachat J, Kalueff A (December 2009). "Vitamin D, nervous system and aging". ...

*SHC1

"The endothelium abridges insulin resistance to premature aging". Journal of the American Heart Association. 2 (3): e000262. doi ...

*Samuel Lam

"Runner's Face Story: Premature Aging From Being HyperAthletic". YouTube. October 10, 2011. Retrieved June 19, 2013. "Dr. Lam ...

*Binge drinking

These EEG findings are similar to premature aging. According to one review of the literature, if the developmental stage of ... It has been estimated by some that if the age at which people started drinking could be delayed to age 20, there would be a 50 ... College students have been found to be more likely to binge drink than their same age peers who were not enrolled in college. ... When the survey results were separated into age groups the findings were that 13 percent of 15-year-old's and 22 percent of 17- ...

*Metageria

... is a cutaneous condition characterized by premature aging. Hutchinson-Gilford syndrome List of cutaneous conditions ...

*Light skin

This can contribute to premature aging and skin cancer. The strongly red appearance of lightly pigmented skin as a response to ... Individuals with lightly pigmented skin who are repeatedly exposed to strong UV radiation, experience faster aging of the skin ...

*ERCC2

... premature aging) symptoms (see DNA damage theory of aging). ERCC2 has been shown to interact with: ERCC5, GTF2H1, GTF2H2, and ... TTD and CS both display features of premature aging. These features may include sensorineural deafness, retinal degeneration, ... "Nucleotide excision repair disorders and the balance between cancer and aging". Cell Cycle. 5 (24): 2886-8. doi:10.4161/cc.5.24 ...

*Steven Rice

He retired at the premature age of 27. Rice came out of retirement in 2002, playing in the Ontario Hockey Association's Major ...

*TP63

Recently, two new functions have been attributed to TAp63 in heart development and premature aging. TP63 mutations underlie ... "TAp63 prevents premature aging by promoting adult stem cell maintenance". Cell Stem Cell. 5 (1): 64-75. doi:10.1016/j.stem. ...

*Progerin

Recently, rapamycin has been shown to prevent progerin aggregates in cells and hence delay premature aging. Progerin, which has ... "Anti-cancer Drugs May Hold Promise For Premature Aging Disorder". Retrieved 2008-07-15. Scaffidi P, Misteli T (April 2008). " ... Liu B, Zhou Z (June 2008). "Lamin A/C, laminopathies and premature ageing". Histol. Histopathol. 23 (6): 747-63. PMID 18366013 ... "Adult stem cell changes underlie rare genetic disease associated with accelerated aging". Retrieved 2008-07-15. Noda A, Mishima ...

*Atherosclerosis

Werner syndrome (WS) is a premature aging condition in humans. WS is caused by a genetic defect in a RecQ helicase that is ... The average age was calculated from the ages of 200 of the soldiers. No age was recorded in nearly 100 of the men. Li X, Fang P ... These findings link excessive unrepaired DNA damage to premature aging and early atherosclerotic plaque development (see DNA ... Aging is the most important risk factor for cardiovascular problems. The causative basis by which aging mediates its impact, ...

*Jackson's Whole

... died of premature aging when they were very young. Taura died of premature aging when she was around 30. A collective of clones ... Lilly Durona becomes the first human trial for an experimental rejuvenation technique when her extreme age causes her death to ...

*Laura Cereta

... died at the premature age of 30. Her cause of death is unknown. None of her writings from the later years of her ... At the age of seven, her teacher guided her courses in Latin grammar. She also taught her how to draw pictures utilizing a ... At the age of twelve, her father summoned her again to come home to take on various household responsibilities. Among them, ... After two years at the convent, her father requested that Cereta come home to take care her siblings at the age of nine. After ...

*DNA repair

2002). "Premature aging in mice deficient in DNA repair and transcription". Science. 296 (5571): 1276-9. doi:10.1126/science. ... Accelerated aging disease Aging DNA Cell cycle DNA damage (naturally occurring) DNA damage theory of aging DNA replication ... Inherited diseases associated with faulty DNA repair functioning result in premature aging, increased sensitivity to ... Other DNA repair disorders include: Werner's syndrome: premature aging and retarded growth Bloom's syndrome: sunlight ...

*Classification of Ehlers-Danlos syndrome

... premature aging of the skin of the hands and feet); early onset varicose veins; pneumothorax (collapse of a lung); recession of ... Myopathic EDS (mEDS) characterized by congenital muscle hypotonia, and/or muscle atrophy, that improves with age, Proximal ...

*Werner syndrome helicase

Researchers are still determining how these mutations cause the appearance of premature aging seen in Werner syndrome. WRN is ... Aging. 3 (3): 311-8. doi:10.18632/aging.100293. PMC 3091524 . PMID 21389352. Ding SL, Shen CY (2008). "Model of human aging: ... Lebel M (2001). "Werner syndrome: genetic and molecular basis of a premature aging disorder". Cell. Mol. Life Sci. 58 (7): 857- ... "Epigenetic inactivation of the premature aging Werner syndrome gene in human cancer". Proc. Natl. Acad. Sci. U.S.A. 103 (23): ...

*Non-small-cell lung carcinoma

"Epigenetic inactivation of the premature aging Werner syndrome gene in human cancer". Proc. Natl. Acad. Sci. U.S.A. 103 (23): ... age, response to chemotherapy, and other factors such as the likely side effects of the treatment. After full staging, the ...

*Cornelia de Lange Syndrome

... premature greying of hair and some changes to the skin of the face causing a more aged appearance compared to chronological age ... In particular, defective DNA repair may underlie the features of premature aging. The diagnosis of CdLS is primarily a clinical ... There is evidence for some features of premature aging including the early development of Barrett's esophagus, osteoporosis ... "Natural history of aging in Cornelia de Lange syndrome". Am J Med Genet C Semin Med Genet. 145C (3): 248-60. doi:10.1002/ajmg.c ...

*WRNIP1

Werner's syndrome is a rare autosomal recessive disorder characterized by premature aging. The protein encoded by this gene ... Studies in yeast suggest that this gene may influence the aging process. Two transcript variants encoding different isoforms ...

*Lazaros Kountouriotis

At the age of 14, Lazaros became involved in the commercial activities of his father, representing him in Hydra while the elder ... Although he was not one of the initial instigators of the revolution, which he considered premature, he supported it fully ...
Kubo KY, Kotachi M, Suzuki A, Iinuma M, Azuma K.. Chewing during prenatal stress prevents prenatal stress-induced suppression of neurogenesis, anxiety-like behavior and learning deficits in mouse offspring.. Int J Med Sci 15:849-58, 2018. Azuma K, Zhou Q, Kubo KY.. Morphological and molecular characterization of the senile osteoporosis in senescence-accelerated mouse prone 6 (SAMP6).. Med Mol Morphol 51:139-146, 2018. Azuma K, Toyama T, Katano M, Kajimoto K, Hayashi S, Suzuki A, Tsugane H, Iinuma M, Kubo KY.. Yokukansan ameliorates hippocampus-dependent learning impairment in senescence-accelerated mouse.. Biol Pharm Bull.41:1593-1599, 2018. Kizaki K, Uchida S, Yamashita F, Tsukamoto M, Azuma K.. Microstructure of osteophytes in medial knee osteoarthritis.. Clin Rheumatol. 37:2893-2896, 2018. Tsukamoto M, Wang KY, Tasaki T, Murata Y, Okada Y, Yamanaka Y, Nakamura E, Yamada S, Izumi H, Zhou Q, Azuma K, Sasaguri Y, Kohno K, Sakai A.. Findings as a starting point to unravel the underlying ...
As PS1 is an integral protein of the γ-secretase complex, its stoichiometry may play an important role in balanced processing of APP. A decrease in PS1 (Refolo et al., 1999) or inactivation by mutations (Sudoh et al., 1998) may be associated with increased Aβ42. We had previously noticed an increase in APP as well as Aβ1-42 with age in SAMP8 mice (Morley et al., 2000), suggesting that a decrease in PS1 may cause increased aberrantγ -secretase activity. Accumulation of Aβ is attributed to loss of memory, as reduction of APP expression reverses this loss (Kumar et al., 2000). Therefore, reduction in APP expression is one of the pharmaceutical approaches to counter age-dependent or neurodegenerative disorders like AD that involve memory loss. Being an essential component of γ-secretase, PS1 is another therapeutic target for reducing Aβ formation. As SAMP8 mice have been shown to exhibit memory loss at a relatively early age (Flood and Morley, 1998; Miyamoto, 1997), we have studied the ...
Principal Investigator:MATSUNAGA Shunji, Project Period (FY):1998 - 1999, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:Orthopaedic surgery
International Scholarly Research Notices is a peer-reviewed, Open Access journal covering a wide range of subjects in science, technology, and medicine. The journals Editorial Board as well as its Table of Contents are divided into 108 subject areas that are covered within the journals scope.
In 2000, Franceschi et al. coined the term "inflammaging" in order to refer to a low-grade pro-inflammatory status appearing during the aging process. They emphasized the role of macrophages as well as cellular stress and genetic factors in the generation of the inflammaging condition. In addition, they hypothesized that this inflammatory environment could predispose the organism to the development of several age-related diseases. During recent years, this scenario has been confirmed by a plethora of experimental evidence. ... Interestingly, the aging process is simultaneously accompanied by both the features accelerating inflammaging and the counteracting, so-called anti-inflammaging characteristics. It seems that the balance between these opposite forces controls the outcome of the aging process, either leading to frailty and degenerative diseases or a healthy old age and longevity. .... The aging process is associated with a decline in autophagic capacity which impairs cellular housekeeping, ...
PE859 is a potent inhibitor of both tau and Aβ aggregation with IC50 values of 0.66 and 1.2 μM, respectively. PE859 inhibits Amyloid-β and Tau Aggregation, and Ameliorates Cognitive Dysfunction in Senescence-Accelerated Mouse Prone 8. PE859 reduces aggregated tau and prevents onset and progression of neural dysfunction in vivo.
Mitotech S.A. - a clinical stage biotech - reported that a study demonstrated efficacy of SkQ1 in extending lifespan and health-span of mtDNA mutator mice.
Helps undo years of premature aging-like dark spots and discoloration-as it speeds up skins natural DNA repair process. Powerful enzymes accelerate recovery from everyday sun damage, while antioxidant vitamin C helps fade spots and even out skin tone. Use twice daily for brightening results equal to a photofacial ...
A main feature of the aging process is a chronic progressive increase in the proinflammatory status, which was originally called "inflamm-aging". Inflamm-aging is the expansion of the network theory of aging and the remodeling theory of aging. The network theory of aging posits that aging is indirectly controlled by the network of cellular and molecular defense mechanisms. The remodeling theory, which was put forward to explain immunosenescence, is the gradually adaptive net result of the process of the body fighting malignant damage and is a dynamic process of optimization of the trade-off in immunity. In the process of aging, some researchers pointed out that the phenomenon where adaptive immunity declines is called immunosenescence, while the phenomenon where innate immunity is activated, coupled with the rise of proinflammation, is called inflamm-aging. Some regard the chronic inflammatory process with age as inflamm-aging, while others proposed the oxidation-inflammation theory of aging. ...
While one might argue over whether an activity can be defined as one level or another, the important concept to grasp here is the level of student engagement. One might well measure progression along these levels by looking at who is asking the important questions. As one moves along the continuum, computer technology becomes more important in the classroom but at the same time becomes more invisibly woven into the demands of good teaching and learning ...
Hægt er að senda serum ef sýnið hefur verið meðhöndlað á ákveðinn hátt: Heilblóð er látið storkna við 37°C og síðan skilið við 37°C. Sermið tekið strax ofan af og sent til rannsóknastofunnar á venjulegan hátt. Vinsamlegast sendið upplýsingar með sýninu ef það hefur verið meðhöndlað á þennan hátt.. Tekið skal fram að serum úr blóði sem storknar við 37°C er ekki hægt að samnýta fyrir komplimentmælingar.. Cyclosporin: 2 ml EDTA glas. Allar mælingar á cyclosporin eru gerðar á heilblóði teknu í EDTA.. Deilitalning T-fruma (einkum fyrir HIV sjúklinga): 2 ml EDTA glas.. Hvítfrumuskann: 45-90 ml af blóði (fer eftir aðstæðum hverju sinni). Blóðið er tekið af starfsmanni ónæmisfræðideildar eða samkvæmt nánari fyrirmælum og alltaf í samráði við ónæmisfræðideildina. ...
Abstract: : Purpose: To determine the effect of orally administered genistein on the blue light damage of retina within the senescence-accelerated mouse(SAM)at 28 weeks of exposure Methods: The blue light exposure was set up according to Gottsch et al (Arch Ophthalmol 1993;111:126). Forty-eight SAM P8 mice were divided into four groups. Within each group, the mice were exposed to continuous blue light. One group received a normal, genistein-free diet, one a fatty diet, one a fat+genistein diet, and one a genistein-rich diet. The mice were treated in this fashion for 28 weeks, beginning 4 weeks after birth. The effect of genistein was evaluated using electron microscopy at this specific time. Results: After 28 weeks, using electron microscopy, P8 mice receiving constant blue light and a fatty diet showed a significant thickening of Bruchs membrane and an increase in RPE-deposits compared with the mice receiving the other diet groups. Those with the pure fat diet showed atrophy of the ...
The senescence-accelerated SAMP8 mouse model displays features of cognitive decline and Alzheimers disease. With the purpose of identifying potential epigenetic markers involved in aging and neurodegeneration, here we analyzed the expression of 84 mature miRNAs, the expression of histone-acetylation regulatory genes and the global histone acetylation in the hippocampus of 8-month-old SAMP8 mice, using SAMR1 mice as control. We also examined the modulation of these parameters by eight weeks of voluntary exercise. Twenty-one miRNAs were differentially expressed between sedentary SAMP8 and SAMR1 mice and seven miRNAs were responsive to exercise in both strains. SAMP8 mice showed alterations in genes involved in protein acetylation homeostasis such as Sirt1 and Hdac6 and modulation of Hdac3 and Hdac5 gene expression by exercise. Global histone H3 acetylation levels were reduced in SAMP8 compared with SAMR1 mice and reached control levels in response to exercise. In sum, data presented here provide new
by Dr. Diana Driscoll , Sep 25, 2019 , Inflammation, Science, Vagus Nerve. Inflammaging How can we be proactive in our health and age more gracefully? Its all about controlling inflammaging! What is Inflammaging? By Dr. Diana Driscoll The aging process involves many changes in your body! Some changes are good - wisdom, maturity, and ...
Aging is the single most important prognostic factor associated with the development of many diseases including cancer (1). The results described here demonstrate that aging-associated increases in inflammation negatively impact the development and function of B progenitor cells, including reductions in key indicators of cell fitness. Importantly, using two different, naturally occurring molecules to reduce inflammation in old mice, we show that preventing aging-associated reductions in B progenitor fitness abrogates selection for NRASV12-initiated progenitors. These studies highlight how inflammation-induced alterations in the adaptive landscape in old age govern the selection of oncogenically initiated cells and, ultimately, leukemogenesis within hematopoietic progenitor cell populations (Figure 8D).. In recent years, there has been growing interest in identifying factors that regulate the aging process (8, 52, 53). We observed aging-associated increases in TNF-α, IL-6, and IL-1β levels in ...
Laboratoires Sérobiologiques, now part of BASF Beauty Care Solutions, has introduced its bark extract that fights inflammation to reduce the signs of aging.
Diagnosis of progeria is based on clinical examination of the child and can be confirmed with a genetic test. Signs of progeria include hair loss, wrinkles, missing teeth, delayed growth, lack of weight gain, dry scaly skin, vision loss, fragile bodies, pinched nose, and a small jaw. As the child ages, signs of progeria become more advanced. Interestingly, cognitive impairment is usually intact despite the increased risk of cognitive impairment in the normal aging population. Motor functioning is usually also preserved. Most children with the condition only live until 12 years of age. The main cause of death is atherosclerosis (hardening of the arteries), which can lead to a heart attack or stroke. Ninety percent of children with progeria die from one of these two causes ...
... , causes. Progeria disease is a genetic disorder characterized by rapid aging in children
Children with Progeria rarely live past the age of 14, often suffering from ailments that affect the elderly, such as heart disease and stroke.
Copyright © 2017 by Soderstrom Skin Institute, Peoria IL. Skin Dimensions is a registered trademark of Soderstrom Dermatology Center, SC. All other product and company names are trademarks™ or registered® trademarks of their respective holders and used with permission under license agreement. Unless otherwise noted, persons depicted on this Website are models. *Individual results may vary. ...
Hutchinson-Gilford Progeria Syndrome (HGPS) is an exceedingly rare genetic condition with striking features reminiscent of marked premature ageing. HGPS is commonly caused by a classic mutation in the A-type lamin gene, LMNA (G608G). This leads to the expression of an aberrant truncated lamin A protein, progerin. The nuclear lamina is known to anchor chromosomes, stabilising and regulating the genome. Interphase chromosomes are non-randomly positioned in the nuclei of cells and they occupy specific locations with respect to a radial distribution, gene-poor chromosomes are positioned at the nuclear periphery and gene-rich chromosomes are positioned towards the nuclear interior. The findings indicated that FTI-277, pravastatin, Zoledronic acid, N-acetyl-L-cysteine and all three combination treatments; FG, PZ, FPZ, have a positive effect on anchoring the genome to the nuclear matrix in AG01972 cell line. Furthermore, it was shown that in terms of positiong of chromosomes 18 and X, treatment of ...
the Hutchinson-Gilford progeria syndrome is a rare genetic condition that affects an estimated 1 in 8 million children. It is characterized by excessive
Hutchinson-Gilford Progeria Syndrome is a very rare genetic condition, causing greatly accelerated ageing. There is a genetic test, but, as of May 2013, no cure.
TY - JOUR. T1 - Oligonol Alleviates Sarcopenia by Regulation of Signaling Pathways Involved in Protein Turnover and Mitochondrial Quality. AU - Chang, Yun Ching. AU - Chen, Yi Tien. AU - Liu, Hung Wen. AU - Chan, Yin Ching. AU - Liu, Ming Yi. AU - Hu, Shu Hui. AU - Tseng, Wei Tai. AU - Wu, Hsin Ling. AU - Wang, Ming Fu. AU - Chang, Sue Joan. PY - 2019/1/1. Y1 - 2019/1/1. N2 - Scope: Oligonol has been shown to moderate mitochondrial biogenesis, protein synthesis, and protein degradation in diabetic mice in a previous study. It is therefore hypothesized that oligonol alleviated sarcopenia by regulating pathways involved in protein turnover and mitochondrial quality. Methods and results: The 32-week-old senescence-accelerated mouse prone 8 (SAMP8) mice are fed with chow diet containing 200 mg kg −1 oligonol for 8 weeks. Oligonol supplementation increased skeletal muscle mass, cross-sectional areas, and grip strength in SAMP8 mice. Oligonol increased phosphorylation of AKT/mTOR/p70sk6, inhibited ...
Genetic Causes of Progeria Syndrome. There is a protein called the Lamin A which is produced by the LMNA gene. The Lamin A protein influences the shapes nucleus in body cells. When genetic mutations cause abnormal production of the Lamin A protein, it causes the membrane enveloping the cell nucleus to become unstable and this development damages cell nucleus and kills them off faster than is normal. This ultimately leads to an embryo within the womb to develop progeria genes and cells, and the condition sets in the moment the child is born, until he/she passes away during the teenage years.. ...
Hutchinson-Gilford progeria syndrome (HGPS) is an extremely rare hereditary disease that affects the skin, musculoskeletal system, and vasculature. HGPS is characterized by signs of premature aging.
Children with Progeria are genetically predisposed to premature, progressive heart disease. Death occurs almost exclusively due to widespread heart disease, the leading cause of death worldwide. As with any person suffering from heart disease, the common events for Progeria children are high blood pressure, strokes, angina (chest pain due to poor blood flow to the heart itself), enlarged heart, and heart failure, all conditions associated with aging.. Thus, there is clearly a tremendous need for research in Progeria. Finding a cure for Progeria will not only help these children, but may provide keys for treating millions of adults with heart disease and stroke associated with the natural aging process.. Hutchinson-Gilford Progeria Syndrome ("Progeria", or "HGPS") is caused by a mutation in the gene called LMNA (pronounced, lamin - a). The LMNA gene produces the Lamin A protein, which is the structural scaffolding that holds the nucleus of a cell together. Researchers now believe that the ...
Hi, Im Harry Crowther, Im 18 years old and I have an extremely rare genetic disorder known as Atypical Progeria Syndrome (Non Classical Progeria) whereby I have a defect with the LAMIN A/C gene (LMNA). Though not to be confused with the classical Hutchinson Guilford Progeria Syndrome (HGPS) - both are Premature Aging Disorders. I was diagnosed in the USA aged 7 years old. Together with my Mum I keep this blog. Hope you enjoy my story.. ...
Hi, Im Harry Crowther, Im 18 years old and I have an extremely rare genetic disorder known as Atypical Progeria Syndrome (Non Classical Progeria) whereby I have a defect with the LAMIN A/C gene (LMNA). Though not to be confused with the classical Hutchinson Guilford Progeria Syndrome (HGPS) - both are Premature Aging Disorders. I was diagnosed in the USA aged 7 years old. Together with my Mum I keep this blog. Hope you enjoy my story.. ...
Hi, Im Harry Crowther, Im 18 years old and I have an extremely rare genetic disorder known as Atypical Progeria Syndrome (Non Classical Progeria) whereby I have a defect with the LAMIN A/C gene (LMNA). Though not to be confused with the classical Hutchinson Guilford Progeria Syndrome (HGPS) - both are Premature Aging Disorders. I was diagnosed in the USA aged 7 years old. Together with my Mum I keep this blog. Hope you enjoy my story.. ...
Progeria is a rare genetic condition characterized by an appearance of accelerated aging in children. Its name is derived from the Greek and means prematurely old. The classic type is the Hutchinson-Gilford Progeria Syndrome which was first described in England in 1886 by Dr. Jonathan Hutchinson and again in 1886 and 1904 by Dr. Hastings Gilford.
LMNA encodes both lamin A and C (lamin A/C), two components of the lamina, a layer of the inner nuclear membrane that may interact with chromatin [174]. Hutchinson-Gilfords progeroid syndrome, caused by a mutation in LMNA, is characterized by features resembling accelerated ageing [17]. Cells from Hutchinson-Gilfords progeroid syndrome patients are characterised by accumulation of abnormally shaped nuclei, accumulation of DNA damage and premature senescence [4328]. LMNA mutations (such as the G608G mutation) generate more accessible splicing donor sites and lead to the production of an alternatively spliced product of LMNA called progerin, normally found in ageing cells. Progerin binds directly to lamin A/C and induces profound nuclear aberrations in human cells. Mice Lmna mutants containing the G690G mutation, which also display an increased ratio of progerin/Lamin A, have shorter lifespan compared to the wild-type ( ~40% in heterozygous mice, and ~83% in homozygous mice), while mice with ...
Two papers published online in Science (1) and Nature (2) describe the remarkable news that Hutchinson-Gilford Progeria Syndrome (HGPS), a disease characterized by premature aging, is associated with mutations in the human lamin A/C gene. These papers not only open the door to a better, molecular understanding of what goes wrong in these exceedingly rare disorders, but also point to the importance of the cytoskeleton, particularly the nuclear meshwork of intermediate filaments, in the aging process. They also suggest a new angle that could be investigated in neurodegenerative diseases.. Progeria is Greek for prematurely old. The disease derives its name from the two people who first described the syndrome: Jonathan Hutchinson in 1886 and Hastings Gilford in 1904. HGPS occurs in one in every eight million live births. Affected children share characteristic features, including a small face and jaw relative to head size and many early signs of aging, such as baldness, generalized atherosclerosis, ...
My laboratory is interested in why and how we age. Specifically, we focus on studying molecular mechanisms of Hutchinson-Gilford progeria syndrome (HGPS), a premature aging disease, and exploring the potential connections between HGPS and normal aging. Children with HGPS die at their early teens due to heart attack or stoke. Approximately 90% of the HGPS cases are causedby a de novo mutation at 1824 position of the lamin A gene (C1824T, G608G). This mutation does not affect the coded amino acid, but partially activates a cryptic splice donor site in the exon 11, leading to the production of a mutant lamin A mRNA that contains an internal deletion of 150 base pairs. This is then translated into a lamin A mutant protein missing 50 amino acids near the C-terminus, termed "progerin". ...
1219 Disorazole C1 is a potent, cytotoxic natural product, with IC50 values of , 20 nM in a variety of cancer cell lines. The addition of disorazole C1 disrupted microtubules in cells as early as 24 h after treatment, causing multinucleation and disorganized microtubules at interphase and misaligned chromosomes at the metaphase plate during mitosis. A549 cells that survived a 7 day treatment of disorazole C1 displayed an enlarged, flattened morphology similar to senescent cells treated with doxorubicin. These surviving cells displayed the characteristic β-galactosidase staining at pH 6.0 seen in senescent cells and changes in cell cycle markers indicative of premature or hypermitogenic senescence. A549 cells treated with the IC50 concentration of disorazole C1 (2 nM) for 7 days had increased protein levels of cyclin D, p53 and cyclin-dependent kinase inhibitor p21 as detected by Western blot. This resulted in decreased phosphorylation of Rb (Ser780) and a decrease in total Rb protein levels. A ...
A new case with the typical features of progeria (Hutchinson-Gilford) occurred in India. Histopathology of the skin showed atrophic epidermis and diffuse fibrosis of dermis with loss of appendages. Roentgenographic findings were characteristic of pro
We previously reported that the dried peel powder of Citrus kawachiensis, one of the citrus products of Ehime, Japan, exerted anti-inflammatory effects in the brain of a lipopolysaccharide-injected systemic inflammation animal model. Inflammation is one of the main mechanisms underlying aging in the brain; therefore, we herein evaluated the anti-inflammatory and other effects of the dried peel powder of C. kawachiensis in the senescence-accelerated mouse-prone 8 (SAMP8) model. The C. kawachiensis treatment inhibited microglial activation in the hippocampus, the hyper-phosphorylation of tau at 231 of threonine in hippocampal neurons, and ameliorated the suppression of neurogenesis in the dentate gyrus of the hippocampus ...
Progeria is a type of genetic disorder where aging is rapid and premature. There are different genetic disorders with this condition. All of them reflect rapid premature aging in victims. Collectively, they are called progeroid syndromes. But they...
Scientists at the University of Cambridge have identified a key chemical that can repair the damage to cells which causes a rare but devastating disease involving accelerated ageing. As well as offering a promising new way of treating the condition, known as Hutchinson-Gilford Progeria Syndrome (HGPS), the discovery could help in the development of drugs against cancer and other genetic diseases and might also suggest ways to alleviate diseases that we associate with normal ageing.. ...
Scientists at the University of Cambridge have identified a key chemical that can repair the damage to cells which causes a rare but devastating disease involving accelerated ageing. As well as offering a promising new way of treating the condition, known as Hutchinson-Gilford Progeria Syndrome (HGPS), the discovery could help in the development of drugs against cancer and other genetic diseases and might also suggest ways to alleviate diseases that we associate with normal ageing.. ...
A mutant protein responsible for Hutchinson-Gilford Progeria syndrome (HGPS) bars large proteins from entering the nucleus, according to a study in The Journal of Cell Biology.
2005). These secreted molecules affect nearby cells to provoke inflammatory responses, eventually producing aging-related chronic inflammation called inflammaging, one type of sterile persistent inflammation. Thus, long-term stimulation by SASP molecules induces various metabolic changes including cardiovascular changes (Franceschi and Campisi, 2014). Sometimes they lead to late-stage cancer (Campisi, 2013). Thus, blocking SASP production may be effective for achieving healthy aging. Many laboratories have been searching for agents to prevent the aging process itself. However, in our opinion, stopping cellular senescence may have other harmful effects on the body. Blocking cells to go into senescence cells means that they still have proliferating capacity, although they are old. This may deleteriously lead to cancer formation. In this respect, inhibition of SASP formation without affecting aging capacity (inhibition of inflammaging) seems to be a safe new target for healthy aging. To prove the ...
Progerias striking features resemble the aging process put on fast-forward and afflicted people rarely live beyond 13 years. Almost all of the patients die from complications of arteriosclerosis-the clogging or hardening of arteries or blood vessels caused by plaques-which leads to heart attack and stroke. Scientists are particularly interested in progeria in the hopes that it might reveal clues to the normal human aging process. However, the disease is exceedingly rare and only 64 children living with progeria are known making access to patients very difficult. Hutchinson-Gilford progeria is caused by a single point mutation in the gene encoding lamin A, which forms a protein scaffold on the inner edge of the nucleus that helps maintain chromatin structure and organize nuclear processes such as RNA and DNA synthesis. The mutation creates an alternative splice site that leads to the production of a truncated version of the protein known as progerin. Unlike the full-length protein, progerin does ...
College Park, MD (PRWEB) December 10, 2015 -- Progeria is a rare genetic disease that mimics the normal aging process at an accelerated rate. Symptoms
The same mechanism that causes children with a rare genetic disease called progeria to age at seven times the normal rate may play a role in normal aging as well.
BFE-fak tilbyr en rekke doktorgradsemner som er åpne for ph.d.-studenter fra UiT og andre universiteter. Hvilke emner som er aktuelle i din opplæringsdel, må du diskutere i samråd med veilederen din. Kanskje er det mer aktuelle kurs ved andre fakulteter eller ved andre utdanningsinstitusjoner? Under finner du informasjon om hvordan du søker opptak på doktorgradsemner ved BFE-fak, hvem som kan søke, frister for oppmelding, hvordan du bestiller karakterutskrift og en oversikt over BFE-fak sitt tilbud av doktorgradsemner.
The Cologne Cluster of Excellence in Cellular Stress Responses in Aging-associated Diseases provides an extremely dynamic environment for research into the aging process and its diseases.
The Cologne Cluster of Excellence in Cellular Stress Responses in Aging-associated Diseases provides an extremely dynamic environment for research into the aging process and its diseases.
Project Title: Genetic modeling of the BANF1 A12T allele in mice and in iPSCs as tools to analyze the craniofacial skeletal defects seen in Nestor-Guillermo Progeria Syndrome. ...
Available online at www.ijpsdr.com International Journal of Pharmaceutical Sciences and Drug Research 2014; 6(4): 253-262 Review Article ISSN: 0975-248X CODEN (USA): IJPSPP Hutchinson-Gilford Progeria Syndrome: A Prematurely Aging Disorder Ahsas Goyal*, Neetu Agrawal, Bhupesh C. Semwal, Yogesh Murti Institute of Pharmaceutical Research, GLA University, Mathura-281406, Uttar Pradesh, India ABSTRACT Hutchinson-Gilford Progeria Syndrome (HGPS) is an extremely rare genetic disorder characterized by premature aging, involving aberrant splicing of the LMNA gene, resulting in the production of a disease-causing mutant lamin A protein called progerin. Clinical manifestations are evident by the first or second year of life and include the physical characteristics usually associated with the elderly. Because neither parent carries or expresses the mutation, each case is believed to represent a sporadic, new mutation that happens most notably in a single sperm or egg immediately prior to conception. ...
The Michaelis Laboratorys research goal is to dissect fundamental cellular processes relevant to human health and disease, using yeast and mammalian cell biology, biochemistry and high-throughput genomic approaches. Our team studies the cell biology of lamin A and its role in the premature aging disease Hutchinson-Gilford progeria syndrome (HGPS). Other research focuses on the core cellular machinery involved in recognition of misfolded proteins. Understanding cellular protein quality control machinery will ultimately help researchers devise treatments for protein misfolding diseases in which degradation is too efficient or not enough.. Research Areas: biochemistry, cell biology, protein folding, lamin A, aging, genomics, Hutchinson-Gilford progeria syndrome, yeast ...
Aging-associated alterations of cellular functions have been implicated in various disorders including cancers. Due to difficulties in identifying aging cells in living tissues, most studies have focused on aging-associated changes in whole tissues or certain cell pools. Thus, it remains unclear what kinds of alterations accumulate in each cell during aging. While analyzing several mouse lines expressing fluorescent proteins (FPs), we found that expression of FPs is gradually silenced in the intestinal epithelium during aging in units of single crypt composed of clonal stem cell progeny. The cells with low FP expression retained the wild-type Apc allele and the tissues composed of them did not exhibit any histological abnormality. Notably, the silencing of FPs was also observed in intestinal adenomas and the surrounding normal mucosae of Apc-mutant mice, and mediated by DNA methylation of the upstream promoter. Our genome-wide analysis then showed that the silencing of FPs reflects specific gene
A specific mutation in the LMNA gene has been found in most patients with Hutchinson-Gilford progeria syndrome, which is a condition that causes the dramatic, rapid appearance of aging beginning in childhood. This mutation changes a single DNA building block (nucleotide) in the gene. Specifically, the mutation replaces the nucleotide cytosine with the nucleotide thymine at position 1824 (written as C1824T). This mutation is also sometimes noted as Gly608Gly or G608G, which refers to the position in the lamin A protein affected by the mutation. Although the C1824T mutation is not predicted to change an amino acid, it alters the way the genes instructions are used to make a protein. The C1824T mutation leads to an abnormal version of the lamin A protein called progerin, which is missing 50 amino acids near one end. The location of this mutation does not affect the production of lamin C. Other mutations in the LMNA gene have been identified in a small number of people with the features of ...
Hutchinson-Gilford progeria syndrome (HGPS) is caused by a point mutation in the LMNA gene that activates a cryptic donor splice site and yields a truncated form of prelamin A called progerin. Small amounts of progerin are also produced during normal aging. Studies with mouse models of HGPS have allowed the recent development of the first therapeutic approaches for this disease. However, none of these earlier works have addressed the aberrant and pathogenic LMNA splicing observed in HGPS patients because of the lack of an appropriate mouse model. Here, we report a genetically modified mouse strain that carries the HGPS mutation. These mice accumulate progerin, present histological and transcriptional alterations characteristic of progeroid models, and phenocopy the main clinical manifestations of human HGPS, including shortened life span and bone and cardiovascular aberrations. Using this animal model, we have developed an antisense morpholino-based therapy that prevents the pathogenic Lmna ...
Hutchinson-Gilford Progeria Syndrome is caused by a single point mutation in the gene encoding lamin A, which forms a protein scaffold on the inner edge of the nucleus that helps maintain chromatin structure and organize nuclear processes such as RNA and DNA synthesis. The mutation creates an alternative splice site that leads to the production of a truncated version of the protein known as progerin. Unlike the full-length protein, progerin does not properly integrate into the nuclear lamina, which disrupts the nuclear scaffold and causes a host of problems ...
Scientists have discovered a drug they believe can reverse the effects of premature aging and could extend human life by over a decade. Rapamycin was created from a chemical found in the soil on Easter Island, which is one of the most remote places on Earth and 2,000 miles off the coast of Chile. The drug, which has been nicknamed the "forever young" drug, was used in experiments on children suffering from Hutchinson-Gilford Progeria Syndrome (HGPS). HGPS is a rare condition in which aging is hyper-accelerate and sufferers die of "old age" at around 12 years. HGPS causes a protein called progerin to build up in every cell of the body, causing them to age prematurely. Rapamycin cleaned the cells of progerin, which swept away the defects and left healthy cells. Researchers are expected to start looking at whether the drug could be used more widely, after similarities between HGPS and the normal aging process were uncovered. The drug is already used to suppress the immune system in organ ...
Looking for online definition of progeria in the Medical Dictionary? progeria explanation free. What is progeria? Meaning of progeria medical term. What does progeria mean?
Hayley Okines is just like any girl her age. She loves going to school and spending time with her friends. She goes on sleepovers and loves playing computer games. However, Hayley Okines is not like any other girl her age because Hayley Okines is a 12-year old girl with a 96-year old body (Bates, 2010). She is among the very few who suffer from a rare genetic condition called Hutchinson-Gilford Progeria Syndrome, more commonly known as the "rapid aging" disease…. Read >>. ...
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While it is always fun to see your materials and blogs tweeted and translated in to other languages. Truly, the reason I created and published the resource has little to do with international social media fame. It was ultimately a labor of love designed to demystify the model (as admittedly… it was even a little difficult for me to process and apply at first) and provide real world ideas for integration that anyone could digest.. But I feel like I can take this one step further… Truly the height of the SAMR model is about creating authentic learning experiences that draw from collaboration, online publishing, and even formative assessment. During the TCEA workshop, many thoughtful conversations were had amongst the attendees. In hindsight, I wish I had designated a scribe to document the insights, questions, and critical conversations to archive and share with others that were not able to attend.. The S.A.S.S.Y. SAMR workshop delivered at TCEA is officially over, BUT truly we never stop ...
Origin and meaning of progeria: 1902, Modern Latin, from Greek progeros prematurely old; from pro before, sooner (see pro-) + geras old man (see geriatric) + abstract noun ending -ia.
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... is the progressive and extremely rare genetic disorder which causes a child to age rapidly, beginning in the first 2 years of life. This is the forum for discussing anything related to this health condition
Advanced age is associated with chronic low-grade inflammation, which is usually referred to as inflammaging. Elderly are also known to have an altered gut microbiota composition. However, whether inflammaging is a cause or consequence of an altered gut microbiota composition is not clear. In this study gut microbiota from young or old conventional mice was transferred to young germ-free mice. Four weeks after gut microbiota transfer immune cell populations in spleen, Peyers patches, and mesenteric lymph nodes from conventionalized germ-free mice were analyzed by flow cytometry. In addition, whole-genome gene expression in the ileum was analyzed by microarray. Gut microbiota composition of donor and recipient mice was analyzed with 16S rDNA sequencing. Here we show by transferring aged microbiota to young germ-free mice that certain bacterial species within the aged microbiota promote inflammaging. This effect was associated with lower levels of Akkermansia and higher levels of TM7 bacteria and
Researchers at the Centro Nacional de Investigaciones Cardiovasculares (CNIC) and the Universidad de Oviedo have discovered a new molecular mechanism involved in the premature development of atherosclerosis in mice with Hutchinson-Gilford progeria syndrome (HGPS). Moreover, the results, published in EMBO Molecular Medicine, identify a potential therapeutic target for this severe genetic disease, which is characterized by the premature onset of cardiovascular disease and early death, usually from a heart attack or stroke, between the ages of 6 and 20 years.. Progeria is very rare genetic disease caused by a mutation in the LMNA gene. The disease affects an estimated 400 people worldwide. HGPS patients show accelerated aging linked to a high risk of cardiovascular disease. In the words of study leader Vicente Andrés, studying this disease "brings us closer to a possible treatment for disease victims and can provide important information about normal physiological aging and the factors that ...
The mission of The Progeria Research Foundation is to discover treatments and the cure for Hutchinson-Gilford Progeria Syndrome and its aging-related disorders, including heart disease. ...
INVESTIGATION OF LAMIN A PROCESSING AND REGULATION Wu, Di Lamin A is a major component of the lamina, which creates a dynamic network underneath the nuclear envelope. Mutations in the lamin A gene (LMNA) cause severe genetic disorders. One of the most striking cases is Hutchinson-Gilford progeria syndrome (HGPS). It is caused by a lamin A mutant protein named progerin. Due to the abnormal retaining of a permanent C-terminal farnesyl tail, progerin gradually accumulates on the nuclear membrane, resulting in abnormal nuclear morphology during interphase and perturbing a diversity of signaling and transcriptional events. To better understand lamin A genes function and regulation, I studied lamin A from three aspects in my dissertation, including its post-translational processing, post-transcriptional degradation, and transcriptional regulation. For post-translational processing, I examined the potential effects of cytoplasmic progerin based on a previous observation that membrane-associated ...
In an era of big data, many biological problems can be resolved through computational analysis and bioinformatics. These disciplines analyze large biological datasets using computer science, statistics and mathematical modeling to understand biological systems and relationships. Research in my laboratory is focused on adapting computational analysis and bioinformatics to biological problems while also relying on traditional experiments to validate bioinformatics-based predictions. We are employing big data analytics, genomics and cell biology to understand the comprehensive biological mechanisms underlying gene regulation in human aging, and how dysregulation of gene expression is associated with reduced lifespan and age-related disease. In particular, my laboratory is focused on the study of progeria, or Hutchinson-Gilford progeria syndrome, a rare, fatal genetic condition characterized by accelerated aging in children. The name, which is derived from the Greek, means "prematurely old." The aim ...
Structure-activity relationships (SARs) in the disorazole family have been revealed through the biological testing of natural disorazoles and their synthetic analogues, but little is known about the contribution of the oxazole to the anti-tubulin activity of disorazole C1 I. The development of a novel Evans-Tishchenko/alkyne metathesis (ET-AM) route towards the synthesis of disorazole C1 will provide straightforward access to disorazole C1 and its heterocyclic analogues, thus allowing the contribution of the oxazole to the natural product
Published in EMBO Molecular Medicine, the study consists of inducing cells to express telomerase, the enzyme which -- metaphorically -- slows down the biological clock. The research provides a
Duke researchers have discovered a new way to model progeria syndrome-a rare genetic disease that accelerates aging in children-which could help pave the way for future treatments.
POLK RIVER RANCH 6/20/98-POKIDS- Sarah Rodler,4,of Austria takes her turn soaking bystanders as her friend Megan Durel,5, of France looks on Saturday. The girls frolicked in the afternoon sun during a picnic that kicked off the Sunshine Foundations week long gathering for children diagnosed with the rare disease progeria.(staff/scott iskowitz)
Researchers have found the first drug to treat progeria, an extremely rare genetic disease that causes children to age so rapidly that many die in their
The aging process can be accelerated by numerous cellular and molecular variables. Progeroid syndromes are one such example. The phenotypes of Hutchinson-Gilford Progeria Syndrome (HGPS) and Restrictive Dermopathy (RD) are both caused by an irregular pathway of the processing of prelamin A to mature lamin A, an integral component of the nuclear lamina. In wild-type cells, prelamin A undergoes farnesylation followed by cleavage that is carried out by the enzyme Zmpste24. A 50 amino acid deletion in the LMNA gene found in HGPS patients eliminates the cleavage site in prelamin A, causing an accumulation of farnesylated prelamin A. The buildup of this protein, known as progerin/LA∆50, occurs at the nuclear rim. In RD, nonfarnesylated and farnesylated prelamin A build up due to a deficiency in the Zmpste24 cleaving enzyme. In both syndromes, however, the accumulation of the different forms of prelamin A causes nuclear shape abnormalities and leads to phenotypes resembling premature aging. Currently, there
Hutchinson-Gilford progeria syndrome is an extremely rare developmental autosomal dominant condition, characterized by premature and accelerated aging (~7 times the normal rate)[65] beginning at childhood. It affects 1 in ~4 million newborns; over 130 cases have been reported in the literature since the first described case in 1886.[66] The mean age of diagnosis is ~3 years and the mean age of death is ~13 years. The cause of death is usually myocardial infarction, caused by the severe hardening of the arteries (arteriosclerosis).[67] There is currently no treatment available.[68]. Individuals with HGPS typically appear normal at birth, but their growth is severely retarded, resulting in short stature, a very low body weight and delayed tooth eruption. Their facial/cranial proportions and facial features are abnormal, characterized by larger-than-normal eyes, a thin, beaked nose, thin lips, small chin and jaw (micrognathia), protruding ears, scalp hair, eyebrows, and lashes, hair loss, large ...
In a study, researchers found that decreased levels of HDL cholesterol may contribute to premature heart disease in children with Hutchinson-Gilford Progeria Syndrome, or Progeria.
The progeria story is a beautiful cascade of discovery.. The work of the PRF led to finding mutations in the lamin A gene that cause progeria, and that revealed the mechanism, which in turn led to realization that a shelved pediatric cancer drug, lonafarnib, targeted the same pathway. Would it work against progeria? My second post, "From Rapid Aging to Common Heart Disease," chronicled that story.. The short version: A class of drugs called farnesyl transferase inhibitors would remove a small organic molecule, farnesyl, from one end of lamin A protein. The problem behind progeria is that farnesyl groups arent removed, as they should be, due to mutation affecting a splice site that would otherwise enable the group to be jettisoned. The result is a version of the protein called progerin.. Normally lamin A forms part of the scaffolding that hugs the inner face of the nuclear membrane, contacting the threads of DNA and their associated proteins (chromatin) in the nucleus. With the farnesyl groups ...
What could be a better reason than a child in need to buy or make a purse? Following is explains through the short story about her Grandson, Cameron and how we can all help. Lets help by clearing her shop stock or making a purse. The Purses for Progeria. What could be a better reason than a child in need to buy or make a purse? The following explains as a Grandmother tells about her Grandson, Cameron and how we can all help. Lets help by clearing her ETSY shop stock (FREE SHIP) or making a purse. What is Progeria?. Carolyn: My grandson, Cameron, was diagnosed with this rare disease a short time after birth. Progeria is a disease of premature aging with the life expectancy of afflicted children barely reaching. 13 years. Within a few years after birth, Progeria children experience stiff joints, hip dislocation, atherosclerosis, and ultimately succumb to heart disease. I have created, knitted and felted purses for many years, giving them as gifts until, in 2007, my Grandson, Cameron, was ...
in Journal of Cell Science (1991), 100((Pt 3)), 649-55. The Hutchinson-Gilford syndrome (progeria) is a rare disorder in childhood characterized by premature and accelerated aging. This study reports the effect of a potent growth factor, EGF, on the ... [more ▼]. The Hutchinson-Gilford syndrome (progeria) is a rare disorder in childhood characterized by premature and accelerated aging. This study reports the effect of a potent growth factor, EGF, on the proliferative capacities and extracellular matrix macromolecules and collagenase expression of two strains of progeria skin-derived cells. At low population doubling levels (PDL less than 10), confluent cultures of progeria fibroblasts made quiescent by lowering the concentration of serum in the medium did not respond to EGF while the mitotic activity of normal PDL-matched fibroblasts was almost maximally restored upon addition of EGF. No obvious difference between normal and low PDL progeria fibroblasts was observed in the number and in the ...
Progeria is a type of genetic disorder where aging is rapid and premature. There are different genetic disorders with this condition. All of them reflect rapid premature aging in victims. Collectively, they are called progeroid syndromes. But they...
Yu, S.L.f, Lin, S. B.f, Yu, Y.L., Chien, M.H., Su, K.J., Lin, C.J., Way, T.D., Yiang, G.T., Lin, C.C., Chan, D.C., Harn, H.J., Chen YL* (共同第一作者), "Isochaihulactone protects PC12 cell against hydrogen peroxide induced oxidative stress and attenuates the aging effect in D-galactose aging mouse model. Acta Pharmacologica Sinica 10: 1532-1540. (SCI, IF=1.783, 49/140, in Chemistry, Multidisciplinary)" , Acta Pharmacologica Sinica 10: 1532-1540., 2010年01月 ...
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My laboratory would like to further examine the causative relationship between progerin production and the aging process, to study the regulation of progerin production in normal cells, and to determine the contribution of progerin in normal human aging. ...
Post-traumatic brain injury may be linked with a heightened risk for accelerated aging or premature senescence according to a new study.
Recent research from the research group of Professor Mark Distefano. In collaboration with Professor Brian Shoichet at UCSF, the Distefano lab has investigated the off-target inhibition of protein farnesyltransferase (PFTase) by commercial drugs. The results of their work have been submitted to the Journal of Medicinal Chemistry. The inhibition of protein prenylation has been a target for disease intervention for the past two decades. Drugs that block PFTase have been evaluated as chemotherapeutics for some forms of cancer, anti-parasitic agents to treat malaria and chagas disease, and tools to ameliorate the symptoms of Hutchinson-Gilford progeria syndrome. The Shoichet lab created the Similarity Ensemble Approach (SEA) to relate proteins based on the set-wise chemical similarity among their ligands. SEA has previously revealed cross talk between drugs acting primarily on G-protein coupled receptors (GPCRs). In this work, SEA was used to look for potential off-target inhibition of the PFTase by ...
El desorden de deficiencia de reparación del ADN es una condición médica que se da debido a la reducción de la funcionalidad de la reparación del ADN. Los defectos de reparación del ADN pueden causar tanto la enfermedad de envejecimiento acelerado como un incremento en el riesgo de contraer cáncer. Los defectos de reparación de ADN pueden ser observados en casi todas las enfermedades conocidas como enfermedades de envejecimiento acelerado, en donde varios tejidos, órganos o sistemas del cuerpo humano envejecen prematuramente. Debido a que las enfermedades de envejecimiento acelerado muestran diferentes aspectos de envejecimiento, pero nunca todos los aspectos, a menudo son llamadas por los biogerontólogos como progerias segmentarias. Algunos de los ejemplos incluyen: Ataxia telangiectasia[1]​ Síndrome de Bloom Síndrome de Cockayne Anemia de Fanconi Progeria (síndrome de Hutchinson-Gilford Progeria)[2]​[3]​ Síndrome de Rothmund-Thomson[4]​[5]​ Tricotiodistrofia[6]​ ...
In 2008, European clinical trials began on twelve children suffering from Progeria. The treatment is based on a combination of two existing molecules: statins (prescribed in the treatment and prevention of atherosclerosis and cardiovascular risks) and aminobisphosphonates (prescribed in to treat osteoporosis and to prevent complications in some forms of cancer). The use of both these molecules aims to chemically alter progerin to reduce its toxicity. However, although this treatment aimed to slow down the development of the disease, it did not reduce the quantities of progerin. To study this aspect, researchers needed to obtain a relevant animal model. An "authentic" Progeria model… To generate a model of this kind, Spanish and French researchers decided to introduce a gene mutation (G609G), equivalent to that identified in humans (G608G), in mice to reproduce the exact pathological mechanism found in the children, with a view to then blocking it. The mice models were created under the ...
A premature aging disease that begins in adolescence or early in adulthood and results in apparent old age by 30 40 years of age. The characteristic features of Werner syndrome include short stature, premature graying and balding, wizened face,…
Bern was diagnosed at 22 months with the condition that accelerates aging. . His parents established a foundation to find a cure.
0028]FIG. 14 shows Cisd2 which is primarily localized in the outer mitochondrial membrane and Cisd2 deficiency leads to mitochondrial dysfunction. (14A) EGFP-tagged Cisd2 protein is directed to the mitochondria by an N-terminal signal sequence. The EGFP-Cisd2 proteins were expressed in NIH3T3 cells. EGFP-tagged full-length Cisd2 protein was colocalized with MitoTracker Red, whereas deletion of the N-terminal 58 amino acids completely abolished mitochondria localization. When the N-terminal 58 of 36 amino acid sequence was fused to EGFP, this construct was able to redirect EGFP from a nuclear and cytoplasmic localization to the mitochondria. (14B) Subcellular localization of the Cisd2 and Cisd1 proteins analyzed by Western blotting using protein extracts of the mitochondrial (Mito) and cytosolic (Cyto) fractions prepared from skeletal muscles of 12-week old mice. Polyclonal antibody (Ab) against Cisd2 protein (15 kDa) was generated; this antibody cross-reacts with Cisd1 protein (12 kDa). ...
PRFs phenomenal 2018 Night of Wonder, signature gala & auction, was a huge success! We truly did Rock the Cure! TOGETHER we raised just over $580,000, breaking all gala records! This tremendous effort would not have been possible without the passion and commitment of our donors, sponsors and attendees. All funds raised will go directly to our research, where the ideas that will lead us to a cure are born . . .. Please enjoy these photos from this very special evening….. ...
The general goal of this project is to increase our understanding of how genomic stability relates to aging and development. This proposal focuses mainly on the...
A single gene mutation is responsible for progeria. The gene, known as lamin A (LMNA), makes a protein necessary for holding the center (nucleus) of a cell together. When this gene has a defect (mutation), an abnormal form of the lamin A protein called progerin is produced and makes cells unstable. This appears to lead to progerias aging process.. Unlike many genetic mutations, progeria is rarely passed down in families. The gene mutation is a rare, chance occurrence in the majority of cases.. ...
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For patients and families who may be considering attending this international conference, RECQ2018 will have greater emphasis than RECQ2016 on the mechanisms of aging observed in the progeroid syndromes (which traditionally include Blooms syndrome), with less general attention on Blooms syndrome. To some measure, RECQ2018 is intended to bring balance to the investigation of the RecQ and progeroid syndromes not covered in depth at RECQ2016 (i.e., Werner syndrome, Hutchinson-Gilford progeria, xeroderma pigmentosum, and Cockayne syndrome). While patients and families are ultimately welcome to attend this meeting, the substance will be technical and no funding for P&F travel assistance is anticipated. However… more patient- and family-centered educational opportunities for the Blooms syndrome community are coming, including a Blooms syndrome conference in New York (w/name, date, and exact location TBD) and RECQ2019 (reprising the integrated format of RECQ2016, w/date and mid-continental USA ...
Protein Kinase-A Inhibition Is Sufficient to Support Human Neural Stem Cells Self-Renewal.. Stem Cells. 2015 Dec;33(12):3666-72. doi: 10.1002/stem.2194. Epub 2015 Sep 16.. Georges P, Boissart C, Poulet A, Peschanski M, Benchoua A.. Pluripotent stem cells to model Hutchinson-Gilford progeria syndrome (HGPS): Current trends and future perspectives for drug discovery.. Ageing Res Rev. 2015 Nov;24(Pt B):343-8. doi: 10.1016/j.arr.2015.10.002. Epub 2015 Oct 22. Review.. Lo Cicero A, Nissan X.. Dp412e: a novel human embryonic dystrophin isoform induced by BMP4 in early differentiated cells.. Skelet Muscle. 2015 Nov 14;5:40. doi: 10.1186/s13395-015-0062-6. eCollection 2015.. Massouridès E, Polentes J, Mangeot PE, Mournetas V, Nectoux J, Deburgrave N, Nusbaum P, Leturcq F, Popplewell L, Dickson G, Wein N, Flanigan KM, Peschanski M, Chelly J, Pinset C.. In Vitro and In Vivo Modulation of Alternative Splicing by the Biguanide Metformin.. Mol Ther Nucleic Acids. 2015 Nov 3;4:e262. doi: ...
Could a component of red wine be helpful? Two studies published recently point to a possible role of resveratrol in progeria. While the biochemistry is complex, basically researchers found that resveratrol improves the binding of A-type lamins with a factor called SIRT1 (sirtuin1), and that resveratrol also can slow down loss of body weight, improve bone mineral density and structure, and significantly extend the lives of mice. The drug rapamycin (also known as sirolimus), an immunosuppressant typically given to organ transplant patients to prevent organ rejection, has demonstrated an ability to reduce levels of progerin in an in vitro study conducted by experts at the National Human Genome Research Institute. Experts observed that rapamycin enhanced the destruction of progerin in progeria cells as well as reduced the formation of certain progerin aggregates, among other benefits. These findings led the authors to note that "rapamycin treatment could provide clinical benefit for children with ...
The Progeria Research Foundation is rated 4 out of 4 stars by Charity Navigator. The Progeria Research Foundation receives 92.09 out of 100 for their Charity Navigator rating. The Progeria Research Foundation is a Diseases, Disorders, and Disciplines charity located in Peabody, MA. The organization is run by Meryl Fink and has an annual revenue of $2,147,287.
Lamins are structural protein components of the nuclear lamina, a protein network underlying the inner nuclear membrane that determines nuclear shape and size. There are three types of lamins, A,B and C. The lamin A/C (LMNA) gene contains 12 exons. Alternative splicing within exon 10 gives rise to two different mRNAs that code for pre-lamin A and lamin C. Lamin A/C mapped to 1q21.2-q21.3 and mutations in this gene cause a variety of human diseases including Emery-Dreifuss muscular dystrophy, dilated cardiomyopathy, and Hutchinson-Gilford progeria syndrome. Lamin A/C deficiency is thus associated with both defective nuclear mechanics and impaired mechanically activated gene transcription. ...

Save your skin from premature agingSave your skin from premature aging

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Endurance Exercise Prevents Premature AgingEndurance Exercise Prevents Premature Aging

... 22.02.2011. Endurance exercise may stop you looking and feeling old, it may even ... found that premature aging in nearly every organ in the body was completely prevented in mice that ran on a treadmill three ... CIHR »Canadian Light Source »DNA »brain aging »cellular powerhouses »endurance »exercise »health services »mitochondria » ... Further reports about: , CIHR , Canadian Light Source , DNA , brain aging , cellular powerhouses , endurance , exercise , ...
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Articles, tagged with premature agingArticles, tagged with "premature aging"

Of course the major reason of skin wrinkling is aging. Although aging cannot be prevented, we can control ... Read ,. Author: ... Skin Aging: How Your Lifestyle Affects Your Skin. 11th March 2010. For a few individuals, growing old could be a testament that ... And this is somewhat the rewarding half of aging- gaining a lot of experiences and growing wiser. However, there are also folks ... it cannot retain its perfect shape as we age. When we gain weight suddenly over a short p... Read ,. Author: jsocratous ...
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New Drug Reverses Affects Of Premature Aging - RedorbitNew Drug Reverses Affects Of Premature Aging - Redorbit

Scientists have discovered a drug they believe can reverse the effects of premature aging and could extend human life by over a ... HGPS is a rare condition in which aging is hyper-accelerate and sufferers die of "old age" at around 12 years. ... He added: "It should be emphasized that we are not recommending rapamycin as an anti-aging medicine at this point. Safer ... HGPS causes a protein called progerin to build up in every cell of the body, causing them to age prematurely. ...
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Premature Aging Addressed At Olds - tribunedigital-chicagotribunePremature Aging Addressed At Olds - tribunedigital-chicagotribune

Can GM take the ``old`` out of Oldsmobile?It`s going to try, as indicated by the appointment last week of Michael Losh to be general manager of Olds, GM`s upscale car division.Losh, 43, succeeds
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JCI -
New vascular insights into premature agingJCI - New vascular insights into premature aging

The pathogenesis of HGPS is studied intensively because the mechanisms of premature aging may lead to a better understanding of ... Hutchinson-Gilford progeria syndrome (HGPS) is a fatal disease characterized by premature aging in which young children fail to ... normal aging. In this issue of the JCI, Osmanagic-Myers and colleagues identify the cellular mechanisms that lead to vascular ...
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Two Vital Genes Balance Function for Premature AgingTwo Vital Genes Balance Function for Premature Aging

Spns1 gene was found to induce degradation and premature aging while atp6vca gene was found to suppress the effects of Spns1 ... in premature aging, these symptoms could occur at a much earlier age. An individual who shows signs of premature aging could be ... it is known as premature ageing. There are many factors that contribute to premature aging *Genes ... An understanding of the genes that play an important role in premature aging will aid in tailoring lifestyle and diet to suit ...
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Articles, tagged with premature aging - 2Articles, tagged with "premature aging" - 2

Premature aging is a problem for everyone. All of us will grow old but many wants to grow old healthy and still looking younger ... Articles, tagged with "premature aging", page 2. 10th September 2010. A product to make your eye contour appear brighter and ... Most people, deep down, would probably love to reduce the signs of premature aging but cannot continuously afford to keep ... than their real age. If you are tired of exercising and your anti-aging creams are not working, then better try this new produc ...
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premature aging | Natural Health 365premature aging | Natural Health 365

Powerful antioxidant helps us burn fat, lose weight and avoid premature aging. Lori Alton, staff writer December 5, 2018 ... NaturalHealth365) A stunning two out of three American adults are overweight or obese, putting them at risk for premature aging ... Lower the risk of premature death from cancer and heart disease by taking HIGHER levels of vitamin C. November 26, 2018 ... EXPOSED: Insurance company offers medical doctor payouts of $400 per child, if fully vaccinated by age 2. May 30, 2018 ...
more infohttps://www.naturalhealth365.com/tag/premature-aging/

12 Beauty Blunders That Cause Premature Aging | Lifescript.com12 Beauty Blunders That Cause Premature Aging | Lifescript.com

Skin solution: Apply anti-aging facial cream on your neck and on the backs of hands to prevent premature aging, and cover both ... Its causing fine lines around your mouth, a sign of premature aging. "Over the long-term, pursing your lips to sip out of a ... Yo-yo dieting also causes premature aging. Repeated weight gains and losses stretch your skin and make it loose. [Get the best ... Your makeup may contain some sunscreen - but probably not enough to ward off skin damage and premature aging. "Most makeup ...
more infohttp://www.lifescript.com/well-being/articles/0/12_beauty_blunders_that_cause_premature_aging.aspx

New Characteristics of Premature Aging Protein Discovered at Stevens - PR.comNew Characteristics of Premature Aging Protein Discovered at Stevens - PR.com

This adult-onset disease causes premature aging and increased susceptibility to other old-age diseases such as cancer, heart ... New Characteristics of Premature Aging Protein Discovered at Stevens. Dr. Joseph Glavy, Assistant Professor of Chemical Biology ... buzz.stevens.edu/index.php/glavy-lab-premature-aging-discovery. Reporters are encouraged to contact Stevens faculty directly.. ...
more infohttps://www.pr.com/press-release/277457

Hyper telomere recombination accelerates replicative senescence and may promote premature aging | PNASHyper telomere recombination accelerates replicative senescence and may promote premature aging | PNAS

Study of accelerated aging phenotypes affords insight into normal human aging processes, as well as the age-related increase in ... the premature aging associated with this case is not likely to be mediated by telomere hyper recombination. Instead, premature ... How might elevated T-SCE contribute to cancer risk and premature aging? An in vivo study of the tissues of baboons found the ... WS is a rare, autosomal recessive premature aging disease caused by truncation mutations of WRN, a member of the RecQ helicase ...
more infohttps://www.pnas.org/content/107/36/15768?ijkey=db8300461c0f7ca50842abd61c183dc4e212f6a1&keytype2=tf_ipsecsha

Uh Oh: Anxiety Linked to Premature Aging - HealthUh Oh: Anxiety Linked to Premature Aging - Health

So in other words they can't say with 100% certainty that mental stress actually caused the more rapid aging. But if you ... showing a connection between a common form of psychological stress-phobic anxiety-and a plausible mechanism for premature aging ... How did researchers discover this potentially anxiety-provoking info? They took blood samples from more than 5,000 women aged ... t love because of that awful impending-doom way it makes us feel-may also speed up aging. ...
more infohttps://www.health.com/anxiety/anxiety-premature-aging

FSU researchers solve puzzle posed by family of rare premature aging disordersFSU researchers solve puzzle posed by family of rare premature aging disorders

State University is beginning to piece together the stubborn puzzle posed by a family of rare and debilitating premature aging ... FSU researchers solve puzzle posed by family of rare premature aging disorders. *Download PDF Copy ... "We first need to identify the commonalities between these diseases and how they relate to natural and premature aging," Rivera- ... In popular culture, notions of premature aging syndromes are typically expressed in the stories of fanciful characters like ...
more infohttps://www.news-medical.net/news/20171128/FSU-researchers-solve-puzzle-posed-by-family-of-rare-premature-aging-disorders.aspx

Body Transformation: Lose Weight, Gain Energy & Reverse Premature Aging by Julie Chrystyn | LibraryThingBody Transformation: Lose Weight, Gain Energy & Reverse Premature Aging by Julie Chrystyn | LibraryThing

Reverse Premature Aging by Julie Chrystyn. LibraryThing is a cataloging and social networking site for booklovers ... Body Transformation: Lose Weight, Gain Energy & Reverse Premature Aging. by Julie Chrystyn. ...
more infohttp://www.librarything.com/work/2729326

JCI -
Dysfunction of the MDM2/p53 axis is linked to premature agingJCI - Dysfunction of the MDM2/p53 axis is linked to premature aging

Several mouse models with aberrantly increased p53 activity display signs of premature aging. However, the relationship between ... Facial image of the index patient IV:7 at the age of 19 years. Note the patients short stature (151 cm on the scale), ... In addition to its well-established role in tumorigenesis, p53 has also been associated with aging in mice. ... dysfunction of the MDM2/p53 axis and human aging remains elusive. Here, we have identified an antiterminating homozygous ...
more infohttps://www.jci.org/articles/view/92171/figure/1

Premature aging in telomerase-deficient zebrafish | Disease Models & MechanismsPremature aging in telomerase-deficient zebrafish | Disease Models & Mechanisms

Premature aging in telomerase-deficient zebrafish Message Subject (Your Name) has sent you a message from Disease Models & ... Premature aging is a feature of the genetic disorder dyskeratosis congenita (DC). DC is caused by progressive shortening of ... Although mouse models have provided insight into the role of telomeres in premature aging, they do not recapitulate all human ... Here, María Cayuelas group show that telomerase-deficient zebrafish demonstrate the hallmark features of premature aging in ...
more infohttp://dmm.biologists.org/content/6/5/1051.5

Vitamin C Helps You Resist Premature Aging - Chempedia - LookChemVitamin C Helps You Resist Premature Aging - Chempedia - LookChem

Can you imagine that vitamin C can even help you resist premature aging? Now, the anti-aging effect of vitamin C will be ... Vitamin C is considered as a kind of important nutrient to affect the aging of skin. The adequate supplementation of vitamin C ... Vitamin C can also resist aging for senile people. As for the old, they can be seriously endangered by the deficiency of ... The deficiency of vitamins can seriously hurt the human body and accelerate the aging. The anti-oxidation of vitamin C can ...
more infohttp://www.lookchem.com/Chempedia/Health-and-Chemical/18447.html

New Premature Aging Research Spurs Potential Anti-aging TreatmentsNew Premature Aging Research Spurs Potential Anti-aging Treatments

New research done in Singapore and Germany shows genetic abnormalities to be responsibile for some premature aging and possibly ... New Premature Aging Research Spurs Potential Anti-aging Treatments. September 21, 2009 Contact Author Close. Thank you for your ... New research done in Singapore and Germany shows genetic abnormalities to be responsibile for some premature aging and possibly ... Age-defying and anti-wrinkling treatments for common disorders related to aging may also benefit from sustaining proline ...
more infohttp://www.skininc.com/skinscience/physiology/59989752.html?page=2

New Premature Aging Research Spurs Potential Anti-aging TreatmentsNew Premature Aging Research Spurs Potential Anti-aging Treatments

New research done in Singapore and Germany shows genetic abnormalities to be responsibile for some premature aging and possibly ... New research done in Singapore and Germany shows genetic abnormalities to be responsibile for some premature aging and possibly ... Age-defying and anti-wrinkling treatments for common disorders related to aging may also benefit from sustaining proline ... displayed signs of premature aging. They identified the PYCR1 gene on chromosome 17 of these patients to be defective and found ...
more infohttps://www.skininc.com/skinscience/physiology/59989752.html

Cdc42 GTPase-activating protein deficiency promotes genomic instability and premature aging-like phenotypes | PNASCdc42 GTPase-activating protein deficiency promotes genomic instability and premature aging-like phenotypes | PNAS

Cdc42GAP−/− mice display premature aging-like phenotypes in various tissues. (A) H&E sections of 8-month-old female homozygous ... Cdc42 GTPase-activating protein deficiency promotes genomic instability and premature aging-like phenotypes. Lei Wang, Linda ... We demonstrate that Cdc42GAP deficiency causes the early onset of senescence in cells and premature aging-like phenotypes in ... One well recognized contributing factor to mammalian premature aging and cell senescence is increased genomic instability (15 ...
more infohttps://www.pnas.org/content/104/4/1248?ijkey=c5b2466c106966e73fd66f633f1bbed124a32ca4&keytype2=tf_ipsecsha

Metabolic dysfunction consistent with premature aging results from deletion of Pim kinases.  - PubMed - NCBIMetabolic dysfunction consistent with premature aging results from deletion of Pim kinases. - PubMed - NCBI

Metabolic dysfunction consistent with premature aging results from deletion of Pim kinases.. Din S1, Konstandin MH1, Johnson B1 ... Pim kinases prevent premature cardiac aging and maintain a healthy pool of functional mitochondria leading to efficient ... To demonstrate that myocardial senescence is promoted by loss of Pim leading to premature aging and aberrant mitochondrial ... Metabolic Dysfunction Consistent with Premature Aging Results from Deletion of Pim Kinases ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/24916111

Experimental Drug Is First To Help Kids With Premature-Aging Disease | KUOW News and InformationExperimental Drug Is First To Help Kids With Premature-Aging Disease | KUOW News and Information

... an extremely rare genetic disease that causes children to age so rapidly that many die in their ... Experimental Drug Is First To Help Kids With Premature-Aging Disease By Jon Hamilton • Sep 24, 2012 ... Sam Berns, 15, who has the very rare premature-aging disease progeria, plays the drums in his high schools marching band. ... "Sam was acting like his age. And he had friends his own age," she says. "He was just much, much smaller than the rest of his ...
more infohttp://kuow.org/post/experimental-drug-first-help-kids-premature-aging-disease

Unlocking the Key to Premature Aging in Children - Healthcanal.com : Healthcanal.comUnlocking the Key to Premature Aging in Children - Healthcanal.com : Healthcanal.com

"Understanding the cellular and molecular basis for the premature aging disorder progeria may provide us with a better ... Geriatrics and Aging*Hematology*Immune System*Vaccines & Immunizations. *Kidneys and Urinary System*Male Reproductive*Low ... January 4, 2010 Tags: aging, cell biology, HGPS, Hutchinson-Gilford progeria syndrome, lamin A, Michaelis, progeria, proteins, ... Children born with progeria seem normal at birth, but by the time they reach their first birthday, they begin to age at a ...
more infohttps://www.healthcanal.com/medical-breakthroughs/4754-unlocking-the-key-to-premature-aging-in-children.html

Developing Sunscreens for the Preventive Treatment of Photodamage and Premature AgingDeveloping Sunscreens for the Preventive Treatment of Photodamage and Premature Aging

Photodamage and Skin Aging. Exposure to solar radiation causes sunburn, edema, premature aging expressed as wrinkles and fine ... Photodamage and Skin Aging. Exposure to solar radiation causes sunburn, edema, premature aging expressed as wrinkles and fine ... Developing Sunscreens for the Preventive Treatment of Photodamage and Premature Aging. May 7, 2013 , Contact Author , By: Linda ... DL Bissett, DP Hannon and TV Orr, An animal model of solar-aged skin: Histological, physical and visible changes in UV- ...
more infohttp://www.cosmeticsandtoiletries.com/formulating/category/suncare/206469671.html
  • The study, published today in the prestigious science journal Proceedings of the National Academy of Sciences (PNAS), found that premature aging in nearly every organ in the body was completely prevented in mice that ran on a treadmill three times a week for five months. (innovations-report.com)
  • Although mouse models have provided insight into the role of telomeres in premature aging, they do not recapitulate all human symptoms. (biologists.org)
  • Their findings not only suggest that increasing levels of the PYCR1 protein could reverse conditions that cause fast aging and wrinkly skin but also provide insight into how some unexpected genes help maintain youthful skin. (skininc.com)
  • Study of the pathological effects resulting from genetic deletion of all Pim kinase family members could provide important insight about cardiac mitochondrial biology and the aging phenotype. (nih.gov)
  • These mice were genetically engineered to age faster due to a defect in a gene for polymerase gamma (POLG1) that alters the repair system of their mitochondria - the cellular powerhouses responsible for generating energy for nearly every cell in the body. (innovations-report.com)
  • In addition to its well-established role in tumorigenesis, p53 has also been associated with aging in mice. (jci.org)
  • Here, María Cayuela's group show that telomerase-deficient zebrafish demonstrate the hallmark features of premature aging in the first generation, in contrast with mice, which have to be bred for several generations. (biologists.org)
  • We found that natural aging of WT mice is marked with increased Cdc42 activity in various tissues. (pnas.org)
  • Interestingly, an examination of Cdc42 activity in WT adult mice of various ages reveals that the relative Cdc42-GTP level of older animals is significantly higher than that of younger ones in diverse tissues, including heart, brain, lung, liver, bone marrow, spleen, and kidney ( Fig. 1 A and data not shown), raising the possibility that increased Cdc42 activity is involved in the normal aging process. (pnas.org)
  • Increased Cdc42 activity in the course of natural aging in mice and the effects of Cdc42GAP gene targeting on the growth, bone structure, life span, and fertility period of adult mice. (pnas.org)
  • A ) Normal aging in mice is associated with increased Cdc42 activity. (pnas.org)
  • HGPS is a rare condition in which aging is hyper-accelerate and sufferers die of "old age" at around 12 years. (redorbit.com)
  • Researchers are expected to start looking at whether the drug could be used more widely, after similarities between HGPS and the normal aging process were uncovered. (redorbit.com)
  • The pathogenesis of HGPS is studied intensively because the mechanisms of premature aging may lead to a better understanding of normal aging. (jci.org)
  • Many cleansers have anti-aging ingredients, but they're typically not in high enough concentrations or in contact with your skin long enough to provide significant results," says Dee Anna Glaser, M.D, professor of dermatology at St. Louis University School of Medicine. (lifescript.com)
  • New research from Florida State University is beginning to piece together the stubborn puzzle posed by a family of rare and debilitating premature aging disorders. (news-medical.net)
  • Age-defying and anti-wrinkling treatments for common disorders related to aging may also benefit from sustaining proline metabolism. (skininc.com)
  • Identifying new genes which could affect the aging process. (medindia.net)
  • While the process of aging is normal, when this process is advanced, resulting in symptoms that are normally identified in old age but now being identified at an early stage, it is known as premature ageing. (medindia.net)
  • Since skin and bone contain high levels of the PYCR1 protein under normal circumstances, developing therapies that could increase the activity of the PYCR1 protein could possibly reverse the process of aging in affected individuals or slow it down in normal people. (skininc.com)
  • However, you might have things in your life that are actually causing your body's aging process to speed up. (thehealthsuccesssite.com)
  • The natural aging process would continue to come as long as the earth is turning. (arganoilshop.com)
  • Others have tried to treat these animals with "exercise pill" drugs and have even tried to reduce their caloric intake, a strategy felt to be the most effective for slowing aging, and these were met with limited success," said Tarnopolsky. (innovations-report.com)
  • However, if you include a new plant extract into your anti-aging regime, you may just achieve the beautiful, ageless skin of your dreams. (sheknows.com)
  • To ensure your vitamin D (sunshine vitamin) intake, you supplement with low-cost cholecalciferol (vitamin D3) as well as ingest foods (e.g. salmon, mushrooms) rich in this critical hormone-vitamin rather than subjecting your skin to the sun's damaging age-accelerating rays. (sheknows.com)
  • Unless you never the leave the house without being slathered in high sun protection factor (SPF) sunscreen or make-up with a high SPF, ultraviolet radiation is aging your skin (not to mention increasing your risk of skin cancer). (sheknows.com)
  • Since about 80 percent of our lifetime accumulated sun exposure is incidental, Polypodium extract represents a breakthrough strategy in the form of a dietary supplement that can help guard your skin from accelerated aging. (sheknows.com)
  • Of course the major reason of skin wrinkling is aging. (articlealley.com)
  • At night, skin goes into a renewal state," says Jeannette Graf, M.D., an assistant professor of dermatology at Mount Sinai Medical Center in New York and author of Stop Aging, Start Living . (lifescript.com)
  • Not only does skin repair itself, but there's also a difference in its pH and circulation so anti-aging products penetrate better. (lifescript.com)
  • Vitamin C is considered as a kind of important nutrient to affect the aging of skin. (lookchem.com)
  • The adequate supplementation of vitamin C can not only whiten the skin, but also resist aging. (lookchem.com)
  • We are excited by these findings of Bruno and colleagues, which open up new possibilities in the field of aging and skin research,' added Birgit Lane, PhD, a skin biologist and executive director of IMB, one of the research institutes sponsored by Singapore's A*STAR, or Agency for Science, Technology and Research. (skininc.com)
  • These results suggest a role of Cdc42 activity in regulating mammalian genomic stability and aging-related physiology. (pnas.org)
  • Accelerated Brain Gray Matter Loss in Fibromyalgia Patients: Premature Aging of the Brain? (jneurosci.org)
  • We found that fibromyalgia patients had significantly less total gray matter volume and showed a 3.3 times greater age-associated decrease in gray matter than healthy controls. (jneurosci.org)
  • All children, we were told, die of heart attacks or strokes between the ages of maybe 7 and 20 years," she says. (kuow.org)
  • It has been thought that lifelong accumulation of mitochondrial DNA mutations lead to energy crisis that result in a progressive decline in tissue and organ function, ultimately resulting in aging. (innovations-report.com)
  • Scientists have discovered a drug they believe can reverse the effects of premature aging and could extend human life by over a decade. (redorbit.com)
  • A study performed on biological markers showed that there was more aging in people who suffered from certain conditions. (thehealthsuccesssite.com)
  • It's OK to use products with anti-aging agents, such as retinol, peptides and antioxidants, to improve the skin's appearance, but not in a cleanser. (lifescript.com)
  • Don't let these 12 beauty blunders age you. (lifescript.com)
  • This oil which comes from the southwestern parts of Morocco is exported to different parts of the world because of its magnificent effects to beauty and anti-aging. (arganoilshop.com)