Studies of caloric restriction, resveratrol and SIRT1 gene regulation of intermediary metabolism and mitochondrial biogenesis prove a necessary condition? Continuum? Metabotype rejuvenation ‘of cellular aging, cancer, regardless of tumor cell growth or glycolysis Immortalizers.AbstractaDans suppressor top half of the twentieth century, Otto Warburg suggested that cancer cells could be characterized by dramatic high glycolysis and mitochondrial respiratory failure stuck in a report called? Aerobics. The affirmation of the respiratory deficiency was proven false and the biochemistry of cancer cells shifted his studies of oncogenes, growth factors and waterfalls cellular systems tumor suppressor of cell growth, apoptosis, immortalization telomeres, the recognition of cells and mechanisms for membership, etc. Any event focused global inefficiency or mitochondrial dysfunction associated with monitoring requirements anabolic and catabolic function of cancer cells, such as those proposed by G. Bambeck refused funding or publication, in fact, were quietly escorted outside the halls of science. Now, about 30 and 50 years later, the pariah of May proved to be visionary. Retrafficking glycolytic blockade and agents as dichloroacetate etc. can kill or â? Renormalization cancer cells. Caloric restriction, the only known mechanism for extending life far beyond its normal length, in everything from nematodes of primates, it is now known to rejuvenate aging of cells and regulate the initiation and growth of cancer cells by activating a series of 745 or more than one gene of a glycolysis renormalization and initiate phagocytosis inefficient mitochondrial biogenesis concomitant with efficient procedures, new mitochondria. Resveratrol is running on the same exact sequence (s) of genes, and by all measures, has the same impact cytology. Continuum? Metabotype cell “for children, the aging of cells, cancer cells have a more in an evolutionary context. ÂForwardÂIl is a comprehensive document review is presented as a narrative. There is no provision for peer review, in part for reasons given in the summary and main text. This does not mean that the job is important. In fact, it could be very important because it connects these lines of research converge on the medical consequences of great magnitude. It is written by a Ph.D. scientist, with over thirty years of fruitful scientific research under his belt, hopes it can have time to write an article more formal. This information should be out there in an informal and quick, rather than being out tout.Il No bibliography or references to this work, but at the end of this text, a short list of words the search engines and suggested readings are provided, so that most of the bibliography is a sufficient condition to see? The Big Picture ‘hypothesis presented by contained below. This article is limited to fundamental changes in anabolic and catabolic intermediary metabolism and how they relate to children, adults and tumor cells, as this field of cancer research has been left aside. Other areas of research very important, as the cell above, growth factors, etc., are tens of thousands of articles in May to référer.Cet section is devoted to a field of research that has been relegated to the arm, particularly with regard to intermediate products of metabolism of tumor cells. If it were not for anti-aging and results of research to prolong life, stumbling through a metabolic pathway? “back door” so to say, thirty years after a case of modified Warburg, are associated with some inhibitors of the metabolism of cancer, important links have not been done. Throughout history, Serendipity and / or convergences have come together to form systems with more holistic emerging as significant effects. We hope that this one of those fois.Enfin this article written to the science of the United States, meaning that hopefully is intended to be understood by the educated layman, but does not change the serious lack scientific c ‘too. The professional jargon will be held to a minimum. My hope is that further examination will not be necessary for the emergence of enough interest. It would certainly be much better if the parties take the debate or even open lines of inquiry that could link the edges of layers of semi-integrated into a more complete fabric reinforced, or completely new understanding. So, we more or less? In the short term. ” APlus Early Times                                                                                                                        ÂEnviron 96% of the organic biomass of a cell consists of carbohydrates, lipids, nucleotides and proteins. All four of these components can be used as fuel for fuel cells or as building material to replace defective parts in a cell rest or build a new cell, as in the case of a cell divides. In a normal, healthy cells quiescent, there is a balance between energy production and rates of compensation, so that the cell is said in homeostasis, or balance. In a normal life, cell division, growth factors, has created a cascade directions so that the mobile is to increase its energy production and importation of raw materials and the construction of these raw materials into components a new cell. In brief, nucleotides in DNA and RNA, proteins, amino acids, sugars, complex carbohydrates and fatty acids become become fat in a process called anabolism, while these four materials can alternatively be burned as fuel to produce energy in a process called catabolism. The products can still be obtained from intermediate anabolic anabolism in molecular compounds, such as ribosomes, enzyme complexes, etc., and also in organelles such as mitochondria, lysosomes, a cell nucleus, etc. Finally, a new cell is formed. Cancer cells do, but, as we shall see, are not the same way that metabolic cells divide normally. Instead, they are more like an extended version of Cell Metabolism old.                                                                                                                                                                                                                 ABIEN that what has been presented so far is a gross simplification, it is sufficient to say that by the mid-twentieth century, a sophisticated line of hundreds of channels interaction molecular traffic anabolic and catabolic molecular biological transitions have been mapped. Posters in classrooms evidence of these processes operate in a similar way to watch the traffic highway traffic from an aerial view of a large city. Many discoveries were made by observing the movement disorder, such as road accidents because of hooves on ramps, on ramps and thru-way of the motorway system.                                                                                                                                                                                         ÂOtto Warburg head of a large body of research and well-respected researcher molecular in his time as at the beginning of the century to the mid-twentieth century, thought he saw a disturbance in the intermediary metabolism of the two unique and specific to all the cancer cells. In particular, it was thought that this disruption has been severely limited in the catabolic metabolism, or burning fuel, but also initiated a change in anabolic accordingly. More precisely, it has targeted the anomaly in the combustion of a single fuel, glucose, with the exclusion of other fuels.                                                                                                                                                                                          aLe Glucose is the main one, but in any case, only the fuel that is burned by the cells of the body, and is burned in two complex systems, glycolysis and the Krebs cycle. Glycolysis to obtain energy from glucose and other sugars by an anaerobic (without oxygen using) mechanism for the production of ATP, a molecule that carries energy. The Krebs cycle, contained in an organelle called the mitochondrion, burn the end product of glycolysis, pyruvate, consumers use (oxygen aerobic) mechanism to produce ATP. The combustion of oxygen with the process of gradually strips the hydrogen end product of glycolysis, the conversion of NAD NAD NADH2 and then couples the hydrogen with oxygen to form water, while the release of carbon sugar to form carbon dioxide . The formation of water is a gradual process in which the energy of hydrogen atoms and their electrons are trapped in a gradual process, called the electron transport and the energy of the process is captured by the conversion of ‘ADP to ATP, while H and O forms of water in a process called oxidative phosphorylation. Anabolism is the opposite process in which hydrogen and energy ATP NAD is used to obtain the cellular components. Thus, the two molecules Swing in the process are ATP and NAD how to switch from one form of energy and high and low forms of oxidation and reduction, respectively.                                                                                                                                     AIn a healthy cell homeostasis, many are the fuels used, and about 5% ATP is produced by glycolysis, whereas about 95% of ATP is produced by mitochondria. Anabolism and catabolism are in a state of balance, the balance of the mitochondrial production of this energy from ATP to about 99% efficiency. In a healthy cell division, the entire system of energy production to energy upregulation of ATP and NADH reducing power for anabolic needs to make a new cell. Otto Warburg see a uniqueness in the catabolism of tumor cells, since glycolysis was significantly higher than the respiration is depressed and that the mitochondria of cancer cells appear small, poorly trained and disorganized. Furthermore, he suggested that, unlike other fetal or normally dividing cells, the tumor cell was irreversibly â? Prisoner “of this metabolic phenotype. Although part of the glycolysis of his hypothesis has never been refuted, the notion respiratory failure was shot in a heated debate in 1955-1956. Mitochondrial Respiratory failure, even though in many tumor types is in all types of cancer, and was not considered necessary as a precondition of the state of tumor cells.                                                                                                                                                                            acommes above, Warburg is was a big name in his time. He has made and broken in many scientific careers, and was known to have a short temper. Well, most are, the more they fall. Many critics of Warburg became the magazine editors, reviewers and editors of laboratory. Woe to those who are facing all forms of mitochondrial abnormalities / cancer hypothesis, even after twenty five years.                                                                                                                                                                             Aapro rejection of the Warburg , cancer research has moved away from metabolic studies in oncovirus, oncogenes, growth factors and cellular cascades, systems suppressor of cell growth, the mechanisms of apoptosis, immortalization telomeres, cell adhesion recognition systems, etc. These studies have had an impact tremendous impact on our understanding of the normal process of transformation of cancer cells. It became clear that evolution has provided numerous obstacles in his attempts to carcinogenesis lethal control cell division. There is no doubt that these new areas of research would open regardless of the outcome of hypothetical Warburg. However, it is also true that the investigation of mitochondrial interaction in the game of intermediary metabolism in cancer cells, not all but dry, as it surely does not.                                                                                                                                                                                        ain in 1975, twenty years after the hype Warburg, very politically naive graduate student there named G. Bambeck was fascinated by mitochondria in a laboratory in Kent State University, happened to have a mouse model for lymphoblastic lymphoma. The mitochondria isolated from tissues of mice and observed that many had lymphoma mitochondria only low ADP: O ratios indicates that mitochondria are abnormally low production quantities energy from ATP consumed oxygen. This could mean either that ATP was decoupled from the consumption of ‘oxygen through the respiratory chain, which reduced NAD, or decoupled from oxygen or exported from the mitochondria of the abnormally high rate through a kind of chemiosmotic shuttle for anabolic steroids or a combination of these, by an unknown mechanism (s).                                                                                                                                                                                                                ÂAinsi, began a search of the literature and, among other things, he faces the collapse of Warburg. But being socially unsophisticated, who has continued and has continued because he found something very interesting, very interesting, in fact, has virtually abandoned its wet lab (hands on) the search for a mental form of research. In basic research, we reviewed the work of other researchers in the hopes of a group? a unique combination of thought, or, in other words, a Neglected Big picture? ‘, which in this case could also be suitable for the Ph.D. Search AA.                                                                                                                                                                                                                                                               well initially, G. Bambeck found that there were numerous mitochondria of tumor cells with normal mitochondria papers there, some of them showing what Warburg respiratory failure was not there, as well as some cases . What is not found in all cases where data were taken as mitochondrial ATP production by mitochondria on a net basis and / or, more importantly, from the base of cells was significantly reduced compared to normal cells divide . It also noted that the net loss in mitochondrial ATP synthesis might be due to low number of mitochondria per cell, transport Electrona ineffective, increasing the NAD / export Nahda bus reduces the power, coupled with inefficient training ATP hydrogen chemiosmotic potential, displacement of the ATP synthase-ATPase a dynamic balance of metabolism or modify a few miles of track linking the chemical end of glycolysis Krebs cycle. All that may be blocking the connection between the NAD / NADH redox attack the formation of ATP, could tilt the balance of the flow of carbon anabolism. More importantly, these deficits in mitochondrial ATP production could change glycolytically manufactured product ratio of mitochondrial ATP production over 1000%. He suggests that this rate differential fuel forced dependence of glucose, while at the same time forcing other metabolites, reducing power and the flow of energy to ATP anabolism. In the light of modern discoveries, which will be discussed below, one could say that such a system of pre -cell metabolism in a suitable format as uncontrolled growth, when not necessarily indicated by a growth factor: a pre-cancerous or non-dividing state of hyperplastic growth, as could be. If carcinogenesis is a multistage process, because have a metabolic process, up to a metabolic state predicates administration process when changes are necessary, and the stimuli associated with it?                                                                                                                                                                                                                                                           AG. Bambeck optimism has presented its findings to the scientific results expected rejection. Although his argument was a po ‘heretical, received his doctorate, because the logic was basically sound. But with a place to publish and nowhere to work on its conclusions, which evaporates from obscurity to none in the annals of cancer research. Instead has pursued his profession in medical diagnostics and research tools of technology. The means of 1975-1980 are not available to respond to the logic of the collapse of the efficiency of mitochondria in cells. On the one hand, seems to be too many ways for that to happen . genetic switch of the gene and switching systems are just beginning their initial explanation. There were just too many unknowns, and alternatives. Bambeck G. took a shot at the problem, and notioned that reactive oxygen species ( ROS) called free radicals at the time, perhaps peppering of mitochondrial and nuclear genome, resulting in sequential randomization of mitochondria and shows a gradual decline in the effectiveness of fuel combustion. Paraphrasing, he said, â? by any means, the cell of mitochondrial ATP production deficit is there. “We now know that this is true, not only in tumor cells, but in cells of aging well. His most serious seems to occur in the tumor cell. The ratio of aerobic to anaerobic ATP production seems to increase over age and become transformed cells. Production of batteries to the heat and the adaptation to hypoxic conditions are characteristic of cells glycolytically adapted to the formation of poorly coupled ATP, as evidenced by the limited success with the export of hyperthermia acid, lactic acid, and block hypobaric treatments for cancer. Bambeck G. suggested that more specific systems of blocking agents of glycolysis and mitochondria, may have greater efficiency, whether to impose the death or differential renormalization of tumor cells. The facts now known as glycolysis blocker agents may kill or pyruvate kinase can block tumor cells of the fetus renormalization to a non-anabolic and non-state growth and the conditions and agents that create effective aerobic catabolism via mitochondrial biogenesis to reduce the incidence of cancer and increase cell regeneration, show a greater mechanical support for the concept. However, most of these data come from research areas initially perceived as only marginally related or not at all related to cancer.                                                                                                                                                              backhand Times PrésentsDepuis years 1980 to today, there was a lot of work with Ros and mutagenic effects of aging on the cells. Basically, ROS are highly reactive oxygen species that contains an electron shared ROS can react with almost all the available organic molecules, including DNA, RNA, proteins, etc. Of course, ROS are mutagenic and carcinogenic, therefore akin to ionizing radiation, causing the genome of the very specific and very organized and their protein products become more hazardous, or nonsense. Because they are immersed in an atmosphere of oxygen, either directly through the delivery of blood, the body’s cells to produce ROS and use of anti-free radical absorb these different nemesis. Anti-oxidants such as vitamin C, vitamin E, bioflavonoids, etc. are such anti – free radicals, and experiments with high doses of antioxidants and their effects on the induction of cancer and the rate of aging are common. In general, the results are positive, helping organizations better achieve their natural potential, the life expectancy of well-fed, but not beyond this potential.                                                                                                                                                                                     a ROS         aThe mitochondria produced more than any other part of the cell because it is the seat of the oxidative combustion of fuels, where the cascade of electrons from the respiratory chain is used for the pair energy of the Krebs cycle via electrons from hydrogen to the formation of ATP and, ultimately, oxygen to produce water. To protect its products internally ROS using anti oxidants and mitochondria endemic of a particular enzyme called SOD absorbing ROS.                                                                                                                                                                                                                                     ÂChaque mitochondrion has multiple copies of its DNA, and when asked to do so, the mitochondria may proliferate, similar cells. But, unlike the cells, the mitochondria can do something extraordinary. Through a process essentially unresolved, the mitochondrial biogenesis (to distinguish