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19 Cards in this Set
- Front
- Back
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Throughout life we continuously generate new.... |
blood cells, lymphocytes, keratinocytes, and digestive tract epithelium from stem cells. |
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Metamorphosis |
the transition from a larval stage to an adult stage. A large portion of the animals structure changes. The larva and the abut are unrecognizable as being the same individual |
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Regeneration |
the creation of a new organ by an adult animal after the original one has been removed. |
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types of postembroyonic development |
metamorphosis and regeneration Some also say gerontology |
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aging in adult organisms |
aging involves the random decay of normative processes. |
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Gerontology |
the scientific study of aging. |
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aging process has 2 major facets |
how long an organism lives the physiology deterioration or senescence, that characterizes old age |
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aging and senescence |
are viewed as being interrelated both have genetic and environmental components the interplay among mutations, environmental factors, and random epigenetic change makes these phenomena both fascinating and frustrating to study. |
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maximum lifespan |
is the maximum number of years an individual of a given species has been known to survive and is characteristic of the species. (as of 2013 human max lifespan is 122.5 years) |
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Life expectancy |
the average length of time a given individual of a given species can expect to live. the age at which half the population still survives. |
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molmolecuar evidence indicates... |
certain genetic components of longevity are conserved between species-- flies, worms, mammals, etc. all appear to use the same set of genes to promote survival and longevity |
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4 sets of genes involved in aging and its preventiion |
DNA repair enzymes Protein of the insulin signaling pathway Proteins in the mTOR signaling pathway, a cascade that regulate translation Chromatin remodeling enzymes |
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DNA repair enzymes |
appear to be critically important in preventing senescence Premature aging syndromes (progerias) caused by mutations that prevent the functioning of DNA repair enzymes
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Hutchinson-Gilford preogeria |
Hair loss, fat distribution, and skin transparency are characteristic of the normal aging pattern as seen in elderly adults. The mutation causes an aberrant nuclear envelope protein that appears to prevent DNA repair
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2 major soured of mutation |
Radiation and reactive oxygen species (ROS) |
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ReacReactive oxygen species (ROS) |
produced by normal metabolism can oxidize and damage cell membranes, proteins, and nucleic acids. some 2-3% of the oxygen atoms taken up by our mitochondria are reduced insufficiently and form ROS: superoxide ions, hydroxyl radicals, and hydrogen peroxide |
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Transcription factor p53 |
is one of the most important regulators of cell division, can stop the cell cycle, cause cellular senescence in rapidly dividing cells, instruct genes to initiate cellular apoptosis, and activate DNA repair enzymes p53 is bound to a repressor protein that keeps p53 inactive. if repressed or damaged can lead to cancer. |
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Damage to telomeres |
will lead to p53 initiating apoptosis. this will reduce the number of cells produced and if it is skin cells it will create an aged phenotype. The relationship between shortened telomeres and stem cell depletion has been seen in degenerative diseases such as mouse muscular dystrophy |
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Telomerase |
is the enzyme complex that maintains telomere integrity. It acts as an anti-senescence complex. Over-expressing telomerase or reactivating it in senescent cells extend longevity in mice without increasing cancer. |
