His days shall be an hundred and twenty years
Posted: Sun Aug 26, 2012 12:23 pm
Genesis 6:3 And the LORD said, My spirit shall not always strive with man, for that he also is flesh: yet his days shall be an hundred and twenty years.
In conjunction with the system of spatiotemporal control there are many other systems that have been asserted to exist within the living form and aging is one of those that keeps popping up. I think for a change of pace we can see what is happening on this front as well to see if maybe we can answer why life has to die;
Aging Theories
Everyone gets old and everyone dies. But why? The question is very fundamental and as difficult to answer as why we are alive.
Normal human cells die out after dividing a number of times, even when kept alive in ideal laboratory nutrient conditions. But some cancer cells and virus-infected cells can be "immortal" and divide indefinitely. What makes human cells inherently full of death?
An interesting question is whether people would die if they had a "perfect" environment. Is the human body capable of immortality given the right environment? If a human could get the ideal atmosphere, diet, light, and other external factors, would they live forever? Or is there a programmed age limit for cells no matter what environment humans live in?
If there is a preset limit for human lifespan, it is probably of the order of around 120 years.
In my opinion, death like growth is probably programmed. But if so, why so? Religious answers are numerous. Evolutionary theories state that the death of the old helps the gene pool diversify and so confers evoluationary advantages. All such theories are interesting, but inherently unprovable and of little value in detailed analysis.
http://www.rightdiagnosis.com/genetics/aging.htm
Origin and spatiotemporal dynamics of the peroxisomal endomembrane system
Recent studies have uncovered new roles for the peroxisomal endomembrane system in orchestrating important developmental decisions and in regulating cellular aging.
The Issue will critically evaluate the mechanisms underlying the spatiotemporal dynamics of the peroxisomal endomembrane system, linking it to various developmental programs, and enabling it to develop a pro- or anti-aging cellular pattern.
Determination of the Aging Gene
Over the last several decades, C. elegans has been the subject of many published studies, but perhaps the most famous of these appeared in 1993. In that paper, researcher Cynthia Kenyon and her associates showed that C. elegans with a specific single-gene mutation lived twice as long as members of the species that lacked this mutation (Kenyon et al., 1993). This finding was groundbreaking for a number of reasons. First, it challenged the prevailing concept that aging occurs as the body deteriorates over time. Second, it led to a shift in thinking, even among researchers who already believed that aging was subject to some sort of genetic control. Prior to this point, most such scientists figured that aging, age-related illnesses, and death were consequences of multiple cellular and physiological processes, and therefore under the regulation of a wide and diverse set of genes. Kenyon's paper, however, suggested that a single gene could dramatically regulate how long an organism lived, thus opening the door to new hypotheses about modifying life span through genetic manipulation.
Why Limit Life Span?
Why, then, do animals have a gene such as daf-2, whose apparent purpose (when not mutated) is to limit life span?
So, how does one gene control life span? Quite simply, it acts by controlling a lot of other genes that just happen to coordinate the survival system within worms.
http://www.nature.com/scitable/topicpag ... e-span-847
Aging May Be Controlled by Brake and Accelerator Genes
Can we tweak certain genes to stave off the aging process—or, conversely, to speed it up? New research indicates that it may one day be possible.
Scientists have discovered genetic switches in roundworms (Caenorhabditis elegans)—whose genetic makeup is remarkably similar to that of humans—that apparently cause the spineless critters to grow old when flicked on but, when off, may extend their lives.
"This is a new and potentially powerful circuit that has just been discovered," says Brown University biologist Marc Tatar,
Kim believes that it is possible to slow—or even reverse—senescence if scientists can figure out how to keep the master genes from changing course. "What we found was this developmental regulatory system [that keeps worms young] had become unbalanced in old age," Kim says.
http://www.scientificamerican.com/artic ... d-by-genes
Harvard scientists reverse the ageing process in mice – now for humans
Harvard scientists were surprised that they saw a dramatic reversal, not just a slowing down, of the ageing in mice. Now they believe they might be able to regenerate human organs
At Harvard, they bred genetically manipulated mice that lacked an enzyme called telomerase that stops telomeres getting shorter. Without the enzyme, the mice aged prematurely and suffered ailments, including a poor sense of smell, smaller brain size, infertility and damaged intestines and spleens. But when DePinho gave the mice injections to reactivate the enzyme, it repaired the damaged tissues and reversed the signs of ageing.
"These were severely aged animals, but after a month of treatment they showed a substantial restoration, including the growth of new neurons in their brains," said DePinho.
In conjunction with the system of spatiotemporal control there are many other systems that have been asserted to exist within the living form and aging is one of those that keeps popping up. I think for a change of pace we can see what is happening on this front as well to see if maybe we can answer why life has to die;
Aging Theories
Everyone gets old and everyone dies. But why? The question is very fundamental and as difficult to answer as why we are alive.
Normal human cells die out after dividing a number of times, even when kept alive in ideal laboratory nutrient conditions. But some cancer cells and virus-infected cells can be "immortal" and divide indefinitely. What makes human cells inherently full of death?
An interesting question is whether people would die if they had a "perfect" environment. Is the human body capable of immortality given the right environment? If a human could get the ideal atmosphere, diet, light, and other external factors, would they live forever? Or is there a programmed age limit for cells no matter what environment humans live in?
If there is a preset limit for human lifespan, it is probably of the order of around 120 years.
In my opinion, death like growth is probably programmed. But if so, why so? Religious answers are numerous. Evolutionary theories state that the death of the old helps the gene pool diversify and so confers evoluationary advantages. All such theories are interesting, but inherently unprovable and of little value in detailed analysis.
http://www.rightdiagnosis.com/genetics/aging.htm
Origin and spatiotemporal dynamics of the peroxisomal endomembrane system
Recent studies have uncovered new roles for the peroxisomal endomembrane system in orchestrating important developmental decisions and in regulating cellular aging.
The Issue will critically evaluate the mechanisms underlying the spatiotemporal dynamics of the peroxisomal endomembrane system, linking it to various developmental programs, and enabling it to develop a pro- or anti-aging cellular pattern.
Determination of the Aging Gene
Over the last several decades, C. elegans has been the subject of many published studies, but perhaps the most famous of these appeared in 1993. In that paper, researcher Cynthia Kenyon and her associates showed that C. elegans with a specific single-gene mutation lived twice as long as members of the species that lacked this mutation (Kenyon et al., 1993). This finding was groundbreaking for a number of reasons. First, it challenged the prevailing concept that aging occurs as the body deteriorates over time. Second, it led to a shift in thinking, even among researchers who already believed that aging was subject to some sort of genetic control. Prior to this point, most such scientists figured that aging, age-related illnesses, and death were consequences of multiple cellular and physiological processes, and therefore under the regulation of a wide and diverse set of genes. Kenyon's paper, however, suggested that a single gene could dramatically regulate how long an organism lived, thus opening the door to new hypotheses about modifying life span through genetic manipulation.
Why Limit Life Span?
Why, then, do animals have a gene such as daf-2, whose apparent purpose (when not mutated) is to limit life span?
So, how does one gene control life span? Quite simply, it acts by controlling a lot of other genes that just happen to coordinate the survival system within worms.
http://www.nature.com/scitable/topicpag ... e-span-847
Aging May Be Controlled by Brake and Accelerator Genes
Can we tweak certain genes to stave off the aging process—or, conversely, to speed it up? New research indicates that it may one day be possible.
Scientists have discovered genetic switches in roundworms (Caenorhabditis elegans)—whose genetic makeup is remarkably similar to that of humans—that apparently cause the spineless critters to grow old when flicked on but, when off, may extend their lives.
"This is a new and potentially powerful circuit that has just been discovered," says Brown University biologist Marc Tatar,
Kim believes that it is possible to slow—or even reverse—senescence if scientists can figure out how to keep the master genes from changing course. "What we found was this developmental regulatory system [that keeps worms young] had become unbalanced in old age," Kim says.
http://www.scientificamerican.com/artic ... d-by-genes
Harvard scientists reverse the ageing process in mice – now for humans
Harvard scientists were surprised that they saw a dramatic reversal, not just a slowing down, of the ageing in mice. Now they believe they might be able to regenerate human organs
At Harvard, they bred genetically manipulated mice that lacked an enzyme called telomerase that stops telomeres getting shorter. Without the enzyme, the mice aged prematurely and suffered ailments, including a poor sense of smell, smaller brain size, infertility and damaged intestines and spleens. But when DePinho gave the mice injections to reactivate the enzyme, it repaired the damaged tissues and reversed the signs of ageing.
"These were severely aged animals, but after a month of treatment they showed a substantial restoration, including the growth of new neurons in their brains," said DePinho.