Unraveled the secret of longevity? Passions around aging. Bugged. Exasperate many. Aging is to be extended?
Or active period of life to be extended? Or maybe just to make life healthier, period? Life, know supplies are examples where interference principle of nature leads to tragic consequences.
Can notice one thing - need a healthy philosophy, or else ...
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Roundworm Caenorhabditis elegans grow old and die within a few weeks, while people in some cases even survive centenary. This suggests that mutations accumulated in the course of evolution, which resulted in the appearance of human life expectancy increased at least 2000 times. For centuries, people have been trying to unravel the secret of longevity, but only recently, scientists have become a little closer to a solution.
For many years, molecular biologists specializing in the mechanisms of regulation of physiological and biochemical processes, ignored issues of aging, because, according to traditional notions associated with the aging of tissue deterioration is the result of a passive process of wear and tear. However, we now know that the aging process, as well as many other biological processes that govern the classical signaling mechanisms and transcription factors. Typically, these mechanisms are identified in the study of small organisms with short duration of life, such as yeast, worms and flies, fruit flies, but most of them are having similar effects on mammals.
The study of these mechanisms and the impact of physiological and environmental factors on their work offers the prospect of creating drugs that slow the aging process rights.
There is a view that attempts to slow down the aging process means certain death from age-related diseases, such as cancer or Alzheimer's disease. However, as the results of scientific research, anti-aging mutations tend to postpone and the beginning of the development of such diseases.
The mechanisms that regulate aging
Many mutations affecting life-prolonging genes encoding receptors of nutrients and proteins involved in the formation of stress responses. With an abundance of food and lack of stress, these genes contribute to the growth of the organism and its reproduction. In unfavorable conditions for the life of the activity of these genes varies: some of them are starting to work actively, while others are blocked.
As a result, the global physiological changes aimed at protecting cells and maintain their livelihoods. This shift not only allows the body to survive the unfavorable period, but also increases the life expectancy.
The most prominent of the factors that increase longevity is calorie diet, as shown in a wide range of organisms ranging from yeast and ending monkeys. This phenomenon was first discovered in experiments on rats conducted in the Great Depression amid fears that chronic malnutrition is fraught with decreasing life expectancy. Initially, experts explain the magic effect of starvation by reducing the rate of accumulation of cellular damage, which are the by-product of normal metabolism. However, well-designed experiments on flies, fruit flies (Mair et al., Demography of dietary restriction and death in Drosophila. Science 301, 1731-1733 (2003)) showed that a low-fat diet leads to a sharp decrease in the mortality rate (number of deaths per day) . This indicates that the effects are the result of acute starvation flowing process.
We now know that in the development of a low calorie diet effects of mechanisms involved recognition nutrients including mediated by proteins such as enzymes and AMP kinase, also related to the class of kinases target of rapamycin (target of rapamycin, TOR), and sirtuins (sirtuins) and hormones insulin and insulin-like growth factor-1 (IGF-1). A surprising finding was the fact that the main role of a mechanism to extend the life of the organism depends on the nature of fasting. For example, experiments in C.elegans showed that three options schemes limiting caloric intake (fasting for a lifetime, feeding through the day and the transition to a low-calorie diet in middle age) to launch a variety of mechanisms with the same end result - an increase in life expectancy.
Life expectancy may increase by many other factors, including chemo-and thermosensor signals (both increase and decrease in ambient temperature) heating, oxidative stress signals to the reproductive system, as well as the decrease in the rate of cellular respiration or translation. In most, and perhaps in all of these cases, the process of increasing life expectancy actively manage specific regulatory proteins.
Aging causes a global weakening of the functions of all body tissues, so at first glance, it looks like an impossible task slowdown. However, experiments on laboratory animals have shown that it does not have to deal separately with each of the manifestations of aging, such as atrophy of muscle tissue, wrinkles, and the accumulation of damaged mitochondria - just change the work of a single gene, and the rest of the body does the rest. In other words, living beings have the potential to live longer than is considered normal.
Insulin and insulin-like growth factor-1
First discovered by scientists from the controls the rate of aging is the signaling mechanism mediated by insulin and insulin-like growth factor-1. Mutation that reduces the activity of the genome C.elegans daf-2 gene encoding a hormone receptor, similar to the insulin receptor and IGF-1 in a mammal, more than twice prolongs the life of the worms. Mutations affecting the activity involved in the signaling mechanism of kinase enzymes: phosphatidylinositol 3-kinase (PI (3) K), AKT-pyruvate dehydrogenase kinase (PDK), also prolongs the life of the organisms.
The most impressive feature of these (and many others), long-lived mutants is their ability to save for a long time all the signs of a young body. Suppression signaling mechanism mediated by insulin and IGF-1 influences life by altering the expression of genes encoding a number of transcription factors (including DAF-16, FOXO, HSF-1 and SKN-1). These factors, in turn, stimulate or inhibit the expression of other genes including those involved in the development of stress reactions provide mechanisms autophagy (processing defective cell fragments for the synthesis of organelles) and encoding antimicrobial peptides chaperone proteins, apolipoproteins, lipase and ion channels.
Cumulative effect of changes taking place at the same time and is the increase in life expectancy. An interesting fact is that the number of genes normally expressed in embryonic cells abnormally expressed in somatic cells daf-2 mutants. Apparently, these genes (at least in part) cause an increase in life expectancy of the body, and a detailed study of their work can give scientists more than one surprise.
For example, the activity of some of these genes in the cells of daf-2 mutants increased twice. While one can only guess what will happen if their activity is increased tenfold.
The Secret of Bulgarian Longevity - HUSSE Pro.test /Riots in Sofia 2013/
We shot and edited this video for less than 24 hours during the anti-govt protests in Sofia in the summer of 2013. Please, share/comment if you like it! Thanks for watching
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