Hmmmm, perhaps if I told you that I am a geneticist and that I know a lot about the genetics of aging, you might realize what an idiotic statement that is.
Then again, maybe not....
keeping a live brain in a jar for reals??
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Hmmmm, perhaps if I told you that I am a geneticist and that I know a lot about the genetics of aging, you might realize what an idiotic statement that is.
Then again, maybe not....
Hmmmm, perhaps if I told you that I am a geneticist and that I know a lot about the genetics of aging, you might realize what an idiotic statement that is.
Then again, maybe not....
Then again I could link you to sites that will prove my statements and make you look as if you aren't who you say you are at all.
Oh, Ill do it anyway."Genetic studies in simpler organisms demonstrate that specific genes have potent influences on life span. These findings provide a framework for understanding the factors by which life span is determined in lower organisms. More importantly, organism models provide interesting phenotypic characteristics and candidate pathways to be studied in relation to longevity, such as parameters of metabolic control, stress resistance and genetic instability. However, investigation of human homologues of these genes would naturally be more complicated because aging and susceptibility to diseases associated with aging in human is influenced by multiple genes as well as environment factors. "
http://www.scq.ubc.ca/genetic-studies-of-aging-and-longevity-in-model-organisms/
SALT LAKE CITY -- Researchers at the University of Utah have discovered that when a gene called smedwi-2 is silenced in the adult stem cells of planarians, the quarter-inch long worm is unable to carry out a biological process that has mystified scientists for centuries: regeneration.
The study published in the Nov. 25 issue of Science was led by Alejandro Sánchez Alvarado, Ph.D., Howard Hughes Medical Institute investigator and professor of neurobiology and anatomy at the U of U School of Medicine, and carried out by members of his laboratory, in particular Helen Hay Whitney Foundation post-doctoral fellow Peter W. Reddien who is now an Associate Member at the Whitehead Institute for Biomedical Research.
Elimination of smedwi-2 not only leads to an inability to mount a regenerative response after amputation, but also to the eventual demise of unamputated animals along a reproducible series of events, that is, regression of the head tip, curling of the body and tissue disintegration. These defects are very similar to what is observed after the planarian stem cells are destroyed by lethal doses of irradiation. The key difference, however, is that the irradiation-like defects observed in animals devoid of smedwi-2 occur even though the stem cells are still present in the organism.
This finding suggests something surprising: the instructions that a daughter stem cell needs to differentiate for regeneration or for maintaining tissue structure begin to be defined at the time of division of its parent cell. "Once the smedwi-2 molecule is eliminated, the animal is destined to die since the functions of the daughter cells are severely compromised" said Sánchez Alvarado.
http://www.worldhealth.net/p/silenced-gene-in-worm-shows-role-in-regeneration-2005-12-02.html
A genetic experiment to unlock the secrets of the ageing process has created organisms that live six times their usual lifespan, raising hopes that it might be possible to slow ageing in humans.
The geneticists behind the study say the increase in lifespan is so striking, they may have tapped into one of the most fundamental mechanisms that controls the rate at which living creatures age.
The tests were carried out in single-celled organisms, forcing them into what the researchers refer to as an "extreme survival mode". Instead of growing quickly and showing signs of ageing, the organisms became resilient to damage and were better able to repair the genetic defects that build up with age, often leading to cancer in later life.
http://www.worldhealth.net/p/geneti...immortality-will-have-to-wait-2005-12-01.html
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"Donovan's Brain" is a closer match. It was a book _and_ two b-movies.
http://en.wikipedia.org/wiki/Donovan's_Brain
Then again I could link you to sites that will prove my statements and make you look as if you aren't who you say you are at all.
You’re a fool.
All you’ve done is link to generalist and broad descriptions of studies into the genetics of aging, studies that you clearly don’t understand in the first place. This has done nothing to substantiate your incorrect assertion that
Yes, we have identified many of the genes that are implicated in the aging process. I never said otherwise. Yes, we can modify the aging phenotype in single celled organisms and simple vertebrate model organisms. I never said otherwise.
But, yeast and invertebrate organisms like Drosophila and C.elegans are not humans. The human aging process is considerably more complex and difficult to understand. We understand some of the genetics of the aging process in humans but what I said still stands. We are not even close to being able to stop the aging process in humans (as you've stupidly claimed) and nothing you’ve said or linked to prove otherwise. Hell, even your own links refute your own nonsense…
But they are finding genes that do seem to slow the aging process down. That would mean, to me, a layperson, that in the future scientists could find those same types of genes in humans as well.
Yes, you are quite correct that a number of important genes that control the aging process have been discovered in invertebrate model organisms, such as the fruit fly Drosophila melanogaster and nematode worm Caenorhabditis elegans. These are very well-studied organisms in which genetic manipulation techniques are well-established. By introducing genetic alterations to the genes implicated in the aging process, scientists have been able to significantly increase the lifespan of these organisms.
Yes, you are quite correct that all organisms are genetically related and that there are human homologues of these same Drosophila and C.elegans genes. The human versions of these genes are performing the same cellular functions as the invertebrate genes do in those organisms. Furthermore, aging has also been studied in great detail in mammalian organisms (viz. mice).
But!......
Firstly, all those instances of increased lifespan in those invertebrate organisms were due to genetic engineering, but we cannot genetically engineer humans like we can with those invertebrate organisms. There is only one way (that I am aware of) to increase lifespan without genetic engineering – calorie restriction. It has been well-established using mice that calorie restriction increases lifespan, although it’s only around 10-15% rather than the 6-fold increase that can be achieved in invertebrate organisms like Drosophila and C.elegans. Calorie restriction would likely lessen the generation of reactive oxygen species (ROS), the production of which is theorized to be one of the major underlying causes of aging in mammals. And it prompts the question: would you want to extend your lifespan if you’re constantly hungry?
Secondly, the aging process is significantly more complex in mammals than in invertebrate organisms. Aging is intimately associated with immune system functioning, endocrine functioning, inflammation, muscle maintenance, energy production and much more. To stop aging in mammals we will have to combat all these aspects. In organisms like Drosophila and C.elegans scientists can alter lifespan with the alteration of single genes. Not surprisingly, this is not the case in mammals. It has been shown many times that the same single gene alterations that reduce the aging process in worms and flies do not do so in mice (the only mammal that can be routinely genetically engineered).
Thirdly, it is a common mistake for internet science forum denizens to assume that simply identifying the underlying gene(s) responsible for a given physiological trait will automatically and immediately lead to a “cure” for that trait. This is not necessarily the case. For instance, if I told you that FoxO and SIRT genes have recently been identified as longevity factors in mammals., what then? What would you do now that you that?
Fourthly, the human aging syndrome is a combination of environmental and genetic factors (see below for a brief description). If we were to somehow prevent aging we would have to somehow overcome our cells innate genetically pre-programmed senescence as well as somehow reverse/prevent the cellular damage that occurs simply from living and being exposed to the environment. It’s an all but impossible task.
So......
We have come a long way in understanding the mechanisms of aging and lifespan and are continuing to learn more every day. Whilst it is probably somewhat correct to say that scientists might be able to significantly prevent aging, we are talking of future advances that will not occur any time soon. It is simply not correct to say that…
This is what I pointed out. If you still wish to impugn my genetics knowledge or capability, then we can take this up a notch and start talking specifics rather than these generalities.
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One of my previous posts on aging:
The causes of aging are not fully understood, so if you’re looking for precise explanations then you are bound to be disappointed. It is a very complex biological phenomenon. The general senescent phenotype is characteristic of each species. One major theory sees our metabolism as the cause of our aging. According to this theory, aging is a by-product of normal metabolism; no mutations are required. Some of the oxygen atoms taken up by the mitochondria are reduced insufficiently to reactive oxygen species (ROS). ROS can oxidize and damage cell membranes, proteins, and nucleic acids.
General wear-and-tear and genetic instability is another theory of aging and are among the oldest hypotheses proposed to account for the general senescent phenotype. As one gets older, small traumas to the body build up. Point mutations increase in number, and the efficiencies of the enzymes encoded by our genes decrease. Moreover, if a mutation occurred in a part of the protein synthetic apparatus, the cell would make a large percentage of faulty proteins. If mutations arose in the DNA-synthesizing enzymes, the rate of mutations would be expected to increase markedly.
The mutation rate in mitochondria is many times faster than the nuclear DNA mutation rate. It is thought that mutations in mitochondria could (1) lead to defects in energy production, (2) lead to the production of ROS by faulty electron transport, and/or (3) induce apoptosis. Age-dependent declines in mitochondrial function are seen in many animals, including humans.
In addition to environmental factors, there is also a genetic aging program -- several genes have been shown to affect aging. So as human life expectancy increases due to our increased ability to prevent and cure disease, we are still left with a general aging syndrome that is characteristic of our species. This is worth remembering because unless attention is paid to the genetic mechanisms controlling our aging syndrome, we risk ending up like Tithonios - the miserable wretch of Greek mythology to whom the gods awarded eternal life, but not eternal youth.
I will stand corrected on what I said. I will thank you for your most valuable information as to showing me my error and enlightning me to what is going on.
the jar probbably wuldn't work, maby freezing or other presorvation. and as for why, it is to expermnt and maby someday be brought back to life(watchoung frankstein, might help)
who cares?
good point, ok, but if you were oce dead and now you aren't, why should you be picky?:bugeye:in fact, how can you even choose one, or how can you reserve a body?
you were a man, but then you got a woman's body. your mind is basicly concousness, so you would be peverted for yourself for a while