Discover The Secret Of Immortality

Discover The Secret Of Immotality

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Author: Chris George
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Highly Recommended

I've really worked on the chapters in this ebook and can only say that if you put in the time you will never revert back to your old methods.

My opinion on this e-book is, if you do not have this e-book in your collection, your collection is incomplete. I have no regrets for purchasing this.

Cancer Cells Are Immortal

The difference between cancer cells and normal cells is profound, not only because of the way they look and the way they behave, but because of the radical difference in their lifespans. Placed in tissue culture, cancer cells can live forever. Normal cells, on the other hand, die after about 50 generations. The best proof of cancer cell immortality comes from HeLa cells, a cultured cancer cell line that was established in 1951 from a cervical tumor that was isolated from a woman named Henrietta Lacks. The HeLa cell line has been growing well ever since, and cultures of these cells are maintained for research purposes by laboratories around to world. Henrietta Lacks, a native of Baltimore, Maryland, was 31 years old when the tumor was discovered. She died of cervical cancer eight months later. It may seem odd to think that the achievement of immortality is a bad thing. There is a tendency to believe that if a cell becomes immortal, it might immortalize the entire organism. But an...

Combining Cloning and Stem Cells for Immortality

The possibility of biological immortality rests on two premises (1) Anyone able to perpetually regenerate, reinvigorate, and replace aged or diseased parts of their body could live in the same body from birth to eternity with their persona intact. (2) A clone of one's own cells could serve as a source of embryonic stem cells able to support cellular renewal. The novel idea introduced here is that grafting a clone to an embryo would create a permanent generator of embryonic stem cells and immortalize the host organism (see Chapter 5 for details). A certain amount of difficulty or hesitance may greet this idea, since little in the history of biology prepares biologists to think synthetically about changing human life. Indeed, biologists can hardly be expected to think about creating new organs and tissues, since the evolution of tissues and organs in organisms is not even explained in standard works of evolutionary theory. Furthermore, standard works of developmental biology sometimes...

Why We Are Not Immortal Or What Is Life Anyway

A synthetic branch of biology never quite germinated from its root and stem. Instead, biologists became mired in a theory of life consisting of three down and dirty parts 1) flux, 2) discontinuity, and 3) waste. Flux moves the sameness of life from cell to cell and organism to organism, and everything else living things share with each other discontinuity creates individuals and allows them to gamble and compete or trade off differences with each other waste is life's great resource, supporting everything within life's capability. Taken together, the three parts of this theory of biological life circumscribe and prescribe mortality. This version of life also encapsulates the obstacles to both thinking about and achieving immortality.

Achieving Immortality Through Biotechnology

What then is needed to make human life immortal Life's flux must be limited to individuals genetic advantages must benefit individuals waste and selfishness must be played out within individuals. All this is within reach Human beings can be made immortal through the simple device of replacing germ cells with stem cells. Immortal human beings will be sterile, and their bodies will remain permanently in a prepubescent state, but stem cells will keep them perfectly balanced between development and aging, between growth and decay. The device for achieving immortality proposed here, namely, replacing germ-line cells with somatic-line stem cells, utilizes a cloned blastocyst grafted to an embryo for the purpose of replacing its rudimentary gonads and providing a durable generator of embryonic stem cells in perpetuity. The absence of sex cells should stop the process of aging at prepubescence, at a point before any of the genes for aging and degeneracy have acted or, at least, before they...

Immortal Sequences Homologies among Molecules

One might have thought that the last place one would look for immortality was in fragile molecules, but today the idea of homology has been extended from organisms to sequences of nitrogenous bases in DNA and amino acids in protein. Homologous, or conserved sequences, are simply similar sequences whose similarity is attributed, usually without independent evidence, to the sequences not having changed much from their originary form. The homologues may represent duplicates in the same species (paralogues), or they may represent related genes in different species (orthologues) sometimes in species that are only distantly related, to say the least. For example, homologues of ras (rat sarcoma sequence) occur in all eukaryotes examined so far, from yeast to C. elegans, Drosophila to mammals, (although in human beings the homologue is a pseudogene, incapable of transcription). Even the prokary-ote E. coli, has a ras homologue in the gene encoding the EF-Tu elongation factor.

Afterword Immortality Triumphant

Now, imagine longevity as a trait capable of evolving into immortality. Substitute the idea of performance advantage for anything resembling purpose or progress, and scale longevity for measurement and appropriate comparisons.127 One might also propose a phylogenetic scenario from comparative data and tease apart an order of events, since a trait may originate with or before a performance advantage (an aptation). Altruism might not however, seem quite as attractive to immortals. Would an immortal, let us say a 200-year old (the equivalent of a great, great, great, great, great, grandmother or grandfather), be happy as a baby-sitter for the umpteenth time, and would such a baby-sitter be a better baby-sitter than a mortal grandmother or grandfather, to say nothing of a trained child-care worker in a cr che Would a 200-year old worker even want to work after the fifth or sixth run-through at a career Could the immortal store more information than, say, a computer with a mega-giga hard...

Adjustments Required By Immortalization

No mortal can presently have any idea what life will be like for the immortals, the kind of social life the immortals will establish or the society mortals and immortals will create. One can be sure, however, that initially the immortals' problems will seem endless. Some problems can be anticipated and should be met with adequate prophylaxis. The genome of immortals would initially encompass a small part of the human genetic pool, a fraction of the biodiversity represented by human beings. Such a pool should be expanded as quickly as possible to offset the possibility of new diseases spreading rapidly among immortals. In the absence of adequate counter measures, new diseases might wipe out the first immortals in a single pandemic. Other problems are unforeseeable. Will the immortals bond together, identify with each other as a group, seek their own protection and mutual advantage in clans Would the immortals perform the same sorts of antisocial behavior performed by mortals Would the...

Contemplating Immortal Life

Chances are, the immortals' problems will not be that different from ours. For example, pressure on traditional families and kinship structures will certainly continue following immortalization. Technology, however, will be as much the parent of immortals as mortal parents. But we too have been replacing the family with some more nebulous institution ever since in vitro fertilization and surrogacy were invented. As Lori Andrews, the dean of lawyers specializing in the birth industry, points out, In the Clone Age, it would be possible for a child to have five parents a sperm donor, egg donor, surrogate mother, and the couple who intended to raise the child.16 In the case of surrogacy, parental assignment is usually awarded to those who pay for the procedure.17 If the same policy applies to immortalized people, parenthood may be decided by the highest bidder. The State, which will inevitably pick up a share of the tab, might also demand a role in parenting...

The World of Immortals

I should say something about what I think the world may look like to immortals. I approach this task with trepidation, not only because I appreciate how utterly speculative my opinion must be, but because I feel uncomfortable in the immortal's world as I see it. I imagine that the most glaring difference in the world of immortals in contrast to my world will be the experience of time in the sense of past, present, and future. Everything about life as I know it, having lived my life in a modern, developed, and still developing, Western culture, is predicated on this sense of time, and it is precisely this sense that will be radically different for people who live forever. Instead of living by the clock, time will be immaterial for the immortals. It will be infinitely accessible, neither running down nor running out. The difference will not be how an infinity of time affects the immortal's values whether the immortals will be lazy by today's standards (I imagine they will acquire a work...

Why Become Immortal

My guess is that the inspiration to become immortal is an extension of the awe experienced merely contemplating human life. Aesthetics and vanity aside, there is a more practical, and compelling, reason for becoming immortal to effect prolonged space travel when Earth becomes uninhabitable and we have to abandon our solar system. Human beings will ultimately have to escape from Earth for any of a number of reasons, including those that have caused the mass extinctions of living forms in the past, namely death from the sky or death from the mantle.4 In our case, a still more likely scenario would seem to be death from ourselves.5 I might also mention that the Sun will prove the ultimate and irresistible foe to life on Earth. If all goes according to schedule, the Sun will expand and No matter where the disaster comes from, if we are to preserve human life, we will have to send representatives of humanity to solar systems capable of sustaining human life. That such a solar system exists...

Immortality as Goal

Immortality research has its own narratives, including cloning, and continuous stem-cell therapy, which have mobilized individuals from various constituencies. These narratives may not offer anything different from those already discredited in human history, or they may pose new ways of achieving human potential in the future. The question, What must be sacrificed to achieve these goals is seldom asked and never answered. What is crucial for understanding narratives is the relationship of their components to each other, both temporally and spatially. If the consequences flowing from a component are entirely a function of known causal relationships, one might be able to make a case for predictability and the containment of consequences. The scenarios presently available for achieving immortality are still shy of meeting the criteria for containment and predictability, but never mind driven by our selfish genes, we will, no doubt, take care of the remaining problems

Making Immortals

Immortalization requires three major adjustments in human beings (1) They must be permanently juvenilized in order to remain in a developmental mode and prevent net-negative changes from gaining an edge (2) they must be equipped with exotic stem (es) cells (3) they must be provided with an indwelling generator, a new organ, introduced into embryos and capable of generating es stem cells in perpetuity. Miraculously, these requirements may work synergistically. Juvenilizing alone promotes longevity. For example, killing the germ line causes a 60 percent increase in longevity in C. elegans and extends the lifetime of short-lived Drosophila.94 But this effect of juvenilization is not the primary reason for germ-line elimination. The objective is to replace GS cells with es cells and supersede gonads with a permanent generator of es cells. Immortality would then result from the interplay of signals regarding requirements for es cells arising in the human organism and the generator's...

Hypothesis Construction and Data Mining essentials for Genetics

An exhaustive description of biological data and databases on the internet would be beyond the scope of this book. Confucius might not have been thinking of internet searching when he said 'give a man a fish and he will live for a day, teach a man to fish and he will live forever', but the principle still applies. So, instead of reviewing the data

Telomeric Dysfunction

The telomeric structure also can be lost when there are changes in the expression, regulation, or structure of certain telomere-associated proteins. Mammalian telomeres are now known to end in a large loop, termed the telomeric t loop, the precise structure of which is not yet known (48). Telomeric t loop formation is critically dependent on the telomere binding protein TRF2 (48) and is likely facilitated by other telomere-associated proteins, such as TRF1 and TIN2 (48,49). Disruption of TRF2 function (by expressing a dominant negative TRF2 mutant) causes immortal human tumor cells to die and normal human cells to undergo senescence (50). Interestingly, normal human cells can proliferate with subsenescent telomere lengths, providing telomerase is ectopically expressed (51). Many telomerase-positive tumor cells also proliferate indefinitely with very short telomeres. These findings suggest that telomerase may act preferentially on the shortest telomeres. The mechanisms by...

Oncogenes Mitogenic Signals

In recent years, it has become apparent that strong mitogenic stimuli also can induce normal mammalian cells to express a senescentlike phenotype. This phenomenon was first described for overexpression of the oncogenic (mutated) form of RAS-HA in rodent or human cells (22,88). Oncogenic RAS was known to transform immortal human and rodent cells and facilitate their conversion to tu-morigenicity. However, in normal cells, overexpression of the RAS oncoprotein induced a senescence growth arrest. This senescence response was not induced if mutations or the expression of viral oncogenes inactivated the p53 and pRb tumor suppressor pathways. Consistent with this result, activated forms of two downstream effectors of RAS function the RAF and MEK signaling protein kinases also induce a senescence response when overexpressed in normal mammalian cells (23,25,89). In addition, overexpression of E2F1, a transcription factor important for regulating cell cycle progression into the S phase,...

Hello Dolly And Salutations To Stem Cells

And then came Dolly, cloning, and stem-cell research, providing, in combination, a cure for mortality This miracle cure does not merely cater to our long-time anxieties over longevity it closes the gap between body and soul, offering for the first time, genuine corporeal immortality Together, cloning and stem cells can work miracles. Separately, they are just pieces of the puzzle, neither alone capable of making immortal organisms. Cloning only promises to replicate organisms (their parts or stem cells), and stem cells are merely self-renewing, pluripotential cells (having the ability to differentiate into other kinds of cells37).

Telomere Shortening

The understanding of the molecular mechanisms underlying replicative aging was significantly advanced by demonstrations that telomeric shortening occurred both in vivo and in culture as a function of population doublings (12-15). Although a few earlier reports had speculated about possible roles of telomeric shortening (e.g., see Refs. 16 and 17), a series of reports in the 1990s directly addressed the issue and established that telomeres shortened in tissues as a function of donor age (e.g., see Refs. 12, 13, and 18-21) and in culture as a function of the number of cell divisions (e.g., see Refs. 14, 19, 22, and 23). The hypothesis that telomeric shortening limited the proliferative capacity of normal cells (14,24,25) was strengthened by the contrast of normal versus cancer cells. Replicative aging has been thought to be a brake against the formation of cancer since at least the early 1970s. Cancer cells need to accumulate many mutations to become malignant, and it probably requires...

Telomeres And Direct Proof Of Their

Telomeric shortening was incorporated as the mechanism driving the two-stage model by postulating that shortening would be the mitotic clock that counts cell divisions. The Ml mechanism would be induced not when perhaps one or a few telomeres became too short, but when there were still some telomeric repeats remaining. Later in the chapter, several models for this induction will be considered. If the Ml mechanism were blocked by agents such as T antigen, then the cells could continue dividing. Telomerase is not induced by T antigen, and telomeres continue to shorten during the period of extended life span prior to crisis (27,91). The M2 mechanism would represent terminal telomeric shortening when there were so few repeats remaining that the direct consequences of the lack of repeats (e.g., end-to-end chromosome fusions, potential detachment of the telomeres from the nuclear matrix) would cause cells to stop dividing and eventually die. Escape from M2 would represent the inactivation...

Mechanisms Of Interaction Of Aging And Carcinogenesis

Potential immortality of cancer cells due to avoiding apoptosis ability to invade surrounding tissues due to reduced sensitivity to signals from neighboring cells aimed to offset proliferation cell de-differentiation with re-appearance of some embryonal proteins (e.g. a-fetoprotein) in cytoplasm

The Road To Oncogenesis

Their bacterial ancestors are immortal creatures that have existed for millions of years. But in order to produce multicellular organisms, protozoans had to come to some kind of mutual understanding, which limited the reproductive ability of some of the cells, forcing them to become postmitotic, while allowing others to divide for the life of the organism. For the postmitotic crowd, the arrangement may have seemed impossible, as they were being asked to do something that went against their very nature. Genes that regulated their reproduction, which had undergone millions of years of adaptive evolution to ensure the cells could divide rapidly, were now being asked to shut down and remain silent. For the mitotic crowd, the agreement meant that each cell division had to be tightly controlled no variation in the daughter cells would be allowed as it might have been with their free-living ancestors. When a human cell becomes cancerous it is simply reawakening its ancestral urge for...

Cancer and the Cell Cycle

The T cells of our immune system can detect abnormal, potentially dangerous cells, and when they do they order those cells to commit suicide. The gross changes in a cancer cell's genetic structure, however, often knock out its ability to respond to those signals. When this happens, the cancer cell has gained immunity to apoptosis and is well on its way to fulfilling its quest for immortality and assuming the lifestyle enjoyed by its protozoan ancestors.

Personal Belief Knowledge Behavior

There are beliefs and behaviors of the adolescent that would impact on their access to oncology care. Adolescents have a strong sense of immortality and invincibility. Out of denial or embarrassment, they may delay seeing a physician for symptoms. Like providers, they rarely suspect cancer. Because no cancers in this age range are targets of screening or self-detection, adolescents are not being programmed to watch for any specific signs or symptoms of cancer. A Canadian study of the time from symptom onset to first healthcare contact showed older adolescents averaged

Problems and Solutions

May yet change us sufficiently to permit our immortality. Evolution and development suffer from a lack of sideways movement, of devices for reshuffling and mixing as opposed to an overweening insistence on progress and accumulation. Evolution and development are supposed to add up. Once the pieces are in place, they should fall into an upward trajectory. the sort of linear equations describing close-to-equilibrium chemistry. Rather, life begins far-from-equilibrium, in the domain of the nonlinear and the brink of chaos. The elements of contingency, random events, unforeseen opportunity, death, and extinction dominate biological scenarios at all levels of integration, and none of these elements is consistent with the premise of perfection. As long as life is not linear, biological planning based on linear models of biological progress is not suitable. Hence, cloning and continuous stem-cell therapy would seem to fly in the face of human life rather than with it. But the apparent might...

Chromatin Versus Other Determinants Of Aging

A longstanding issue in aging research concerns the immortality of germ line and primitive stem cell lineages. Immortality implies that such cells escape cumulative chromosomal instability in obvious contrast to most somatic cells. A variety of explanations have been offered to account for this difference. Most often, it is argued that germ cells are far better protected from the cumulative oxidative and other metabolic insults than are somatic cells. This is in keeping with the theory of antagonistic pleiotropy and is thought to reflect allocation of limited metabolic resources. A second approach to the problem is taken by those interested in mitochondrial chromosomes. Here it is suggested that the germ line has a mechanism to sense and select for mitochondrial genome integrity. If so, the age-related accumulation of mi-tochondrial DNA defects in somatic cells does not apply to germ line cells. The same hypotheses apply, at least in principle, to the protection of higher order...

The Cause Of Replicative Senescence Telomere Shortening

Shorter telomeres undergo end-to-end fusions and initiate chromosomal breakage-fusion cycles that cause the cells to undergo apoptosis. There is massive loss of cells from the culture, whereas in replicative senescence (M1) cells do not die, and are in fact more resistant to apoptosis11 . About 1 in 107 cells undergoes an unknown change that permits escape from crisis M2 12. Such a cell line is said to be immortal in the jargon of cell culture, a term that should not be interpreted as implying the reversal of a cellular aging process. In most of these immortalized cell lines the TERT gene has become reactivated 13, but some activate a recombination-based process call ALT (alternative lengthening of telomeres) 14. Although human fibroblasts can form immortal cell lines in this way by escaping from crisis, they never spontaneously immortalize by escaping from replicative senescence M1. Most cancer cells that can be grown in culture are also immortal and express TERT. The mechanisms by...

Yoram Schiffmann Cambridge

Expecting to relax during a routine flight home, I casually glanced through the contents of the airline's magazine and practically suffered a heart attack. The first feature article was entitled, How to Live Forever 1 Believing for a moment that Becoming Immortal had been scooped, I tore through the magazine only to find that the article concerned achieving enduring fame not eternal life. Relieved but not soothed, I imagined that others, glancing at the title of my book, might think that I was writing out of narcissism or wishful thinking. I was not. Becoming Immortal was conceived as the last of three books intended to critique current concepts of change in the biological sciences. The first two books, Death of Life2 and Evolution of Sameness and Difference,3 examined the legacy of molecular biology and provided a perspective on the human genome project. Becoming Immortal was supposed to anticipate further directions in research on biological change, but my plan was overtaken by...

The Working Draft of the Human Genome

Those hoping to find genes for immortality or even for prolonging longevity must be disappointed with the working draft of the human genome released on February 15, 2001.80 The most up-beat analysis was that of Aravinda Chakravarti who emphasized that For the first time, nearly every human gene and genomic region is marked by a sequence variation.81 Just as soon as a few problems are solved and variation can be studied more efficiently, studies on sequence variations might make it possible to identify the underlying differences in susceptibility to or protection from all kinds of diseases, the age of onset, severity of illness, and responses to treatment. David Baltimore urges caution in evaluating the working draft, since o nly 1.1 to 1.4 is sequence that actually encodes protein that is just 5 of the 28 of the sequence that is transcribed into RNA.82 In other words, the greatest amount of DNA found in the nucleus of human cells still represents a vast secret. WHAT IS AN EVOLUTIONARY...

Defects in G1S Checkpoint and Cancer

Mutations in the p53 gene are responsible for the large majority of sporadic human cancers, and thus p53 is a key target for cancer therapy (67,108,110,135). p53 gene mutations can also be inherited in a subset of families with the Li-Fraumeni syndrome (LFS), which is characterized by a predisposition to sarcomas, brain and breast tumors, and childhood adrenocortical carcinoma (258). The inactivation of the INK4a ARF (or CDKN2a) locus, which engages the pRB and p53 tumor suppressor pathways through its capacity to encode the two distinct gene products p16INK4a and p14ARF, is also a common genetic event in the development of human melanoma (259). Human cells harboring pRB and p53 mutations also cause telomere dysfunction that results in the chromosomal end-end joining and fusion-bridge-breakage cycles that trigger the aneuploidy observed in most cancer cells (67). Both p53- and ARF-deficient mice spontaneously develop tumors and die of cancers early in life, and the primary MEFs...

Molecular Basis Of Cancer Phenotypes

Properties that are characteristic of tumor cells and that are now known to be the basis for the behaviors exhibited by neoplastic cells. Some of the features that will be discussed in detail include immortality, decreased dependence on growth factors to support proliferation, loss of anchorage-dependent growth, loss of cell cycle control, reduced sensitivity to ap-optotic cell death, and increased genetic instability. Other morphological and biochemical characteristics used to identify the transformed phenotype are cytological changes, altered enzyme production, and the ability to produce tumors in experimental animals (28).

Games and Competition Longevity and the Individual

Genes are reputed to be immortal, and one can imagine our pursuing immortality by playing the game genes play. That game is replication, and genes are extraordinarily good replicators. Their evolutionary stable strategy (ESS) for winning and getting into new generations is unbeatable, but it has one characteristic that may put it out of contention from human immortality The immortality of some genes is only achieved at the expense of vast numbers of other genes. Sex is enormously wasteful of genes. The theory of sexual reproduction generally taught to biology students predicts that for every sex cell or gene getting into the next generation, three are wasted. In practice, the waste is vastly greater. Great numbers of sex cells (eggs as well as spermatozoa) are ordinarily produced and lost without contributing to reproduction. Sex pursues a saturation strategy for overcoming the difficulty sex cells have finding each other and developing into offspring following fertilization. Most sex...

Problems between Cells and Organisms

Speaking of a composite of cells as if it were an ideal organism is a distortion, especially exacerbated when statistical treatments are extended over time. Likewise, the characteristics of cells do not add up simply to the characteristics of organisms. For instance, cancer cells celebrated for their immortality are rather less than salubrious for organisms. Cancer cells and immortalized cell lines carry on indefinitely in vitro but kill organisms in vivo.

Polyclonal And Monoclonal Antibodies

An animal immunized with an antigen (Ag) increases its population of antibody (Ab)- producing lymphocytes. These cells are short lived and can exist in cell cultures only for a few days. Malignant plasma cells are separately cultured. These cells are essentially immortal, and can be cultured for years, but they are poor producers of Abs. Some malignant plasma cells are deficient in the enzyme hypox-anthine phosphoribosyltransferase (HPRT), and will die unless HPRT is supplied to the culture medium. These are the malignant cells that are used for the production of hybridomas. Hybridomas (or fused cell culture lines) are produced by fusing lymphocytes isolated from the spleen of an immunized animal with the HPRT deficient malignant plasma cells. The lymphocytes. The unfused cells die, since spleen cells survive only a few days, while the malignant plasma cells lack HPRT. Fused cells, however, are HPRT positive as well as immortal these hybridomas, or hybrid cells, retain the...

Oncogenes and Protooncogenes

Aggressive growth, but still not immortal or immune to apoptosis. P53 mutated. Proliferating, immortal cancer cell, immune to apoptosis. A dangerous mix of genes. The deadliness of a cancer cell depends on the mix of genes it can turn on or off. Activating two oncogenes while telomerase (tm) remains off and tumor suppressor genes (TSGs) remain normal leads to cell growth but not immortality or metastasis. Activating two oncogenes and telomerase and mutating P53 leads to the formation of an aggressive metastatic cancer.

Darwinism The Evolution of Mortality

The problem posed by mortality and immortality for evolutionary theory reminds me of the problem of potato confronting contestants at a spelling bee to e or not to e. Mortality and immortality do not follow the rules and easily fit into the spectrum of variety and difference found among living things as explained by Darwin's and Wallace's theory. For Darwin and Wallace, descent with modification was not an abstract principle derived by mathematical rumination but an explanation for empirical data, specifically, the many observations made during their travels on the variety of traits found among species and the great number of different species found on Earth. In contrast, the qualities of immortality and mortality are absolute and opposite. Neither has different forms, nor do they grade into one another. Furthermore, immortality defies empirical observation, since we have not been and will not be around long enough to observe it.90 Mortality and immortality must be reconfigured if...

The Bcrabl Signalosome

Ectopic expression of p210BCR-ABL results in growth factor independence and transformation of immortal hematopoietic cell lines (refer Refs. 1,3 and the references therein). Transplantation of BCR-ABL-transduced hematopoietic stem cells or transgenic expression of p210BCR-ABL induces leukemia and myeloproliferative disorders indicating a direct, causal role of BCR-ABL in CML (4) However, most in vitro studies have relied on the use of growth factor-dependent hematopoietic cell lines, whereas most in vivo studies have used BCR-ABL genes linked to strong promoters. Despite the ample literature on the mechanisms of BCR-ABL-induced transformation, the paucity of data in human hematopoietic progenitors from chronic and blastic phase CML and the limitations of the existing murine models leave many open questions regarding the relevant effects of BCR-ABL in blastic transformation of CML cells.

Uman Biochemistry

However, most normal somatic cells lack telomerase. Consequently, upon every cycle of cell division when the cell replicates its DNA, about 50-nucleotide portions are lost from the end of each telomere. Thus, over time, the telomeres of somatic cells in animals become shorter and shorter, eventually leading to chromosome instability and cell death. This phenomenon has led some scientists to espouse a telomere theory of aging that implicates telomere shortening as the principal factor in cell, tissue, and even organism aging. Interestingly, cancer cells appear immortal because they continue to reproduce indefinitely. A survey of 20 different tumor types by Geron Corporation of Menlo Park, California, revealed that all contained telomerase activity.

Embryogenesis The process of embryo initiation and development

Immortalization The attainment by a finite cell culture, whether by perturbation or intrinsically, of the attributes of a continuous cell line. An immortalized cell is not necessarily one that is neoplastically or malignantly transformed. Immortal cell culture See 'Continuous cell culture'.

Derivation And Characterization Of Human Embryonic Stem Cells

Human ES cells were derived from spare cleavage-stage embryos of in vitro fertilized eggs, grown to the blastocyst stage (5,6). Cells of the inner cells mass from these blastocysts were plated onto mitotically inactivated murine embryonic fibroblast feeder cells, and formed compact colonies of human ES cells. It was shown that these cells have a normal karyotype even when they are grown for an extended period of time in culture (5,6). Human ES cells were found to have high activity levels of telomerase (5), a protein responsible for maintaining the chromosome length and that is tightly correlated with immortality in human cell lines (7). Undifferentiated human ES cells are characterized by specific cell surface markers and enzymatic activities. For example, the stage-specific embryonic antigens 3 and 4 and the markers TRA-1-60 and TRA-1-81 are expressed in human ES cells and are downregulated during their differentiation (5). Pluripotency is defined as the ability of the cells to...

Forcing Blastocysts to Devolve into Generators

The generator ensconced in the immortal's body must devolve into a resident organ and not develop into a Siamese twin The problem of preserving normality in the generator's cells while turning it into a new organ might seem monumental, but the anecdotal records collected by sonographers performing routine ultrasonic diagnoses of human pregnancy suggest that the solution may be at hand. Twinning, it would seem, is much more common during early pregnancy than at late pregnancy and at birth. The disappearance of twins during the course of pregnancy, while usually attributed to resporption by the uterus, may also be explained by absorption into the surviving twin. Were this the case, a lot of human beings would be chimeras, having both their own original cells and those of an absorbed twin. Placing a twin under wraps, therefore, may not be as difficult as one might initially imagine, especially when the twin is a clone. Having overcome the problems of installing and containing a...

Not on the Agenda but

The realistic prospects for immortality are hard to judge simply because immortality research is not presently on the agenda of any national agency, nonprofit enterprise, or even biotech startup company. Rather, human-machine synthe sis is seen as the next stage of human evolution1 and the avant-garde of research devotes itself to work on cyborgified longevity. I expect that the cyborgification of human beings will continue, since it is profitable and efficacious in many circumstances. My guess is that cyborgian replacement therapy will become the mode for mortal human beings, and the human-machine synthesis will only be enhanced if mortals ever attempt to compete in longevity with truly immortal beings. The human-machine lobby will probably attempt to dampen enthusiasm for immortality, but the growth of an immortality lobby will ultimately overwhelm resistance. I imagine that such a lobby will emerge rapidly once the first immortal mammals are produced. These mammals, probably sheep...

The Difficult Matter of Choice

The immortality that I have described would not be available to anyone alive today. On the contrary, the gift of immortality would be a legacy bestowed on children by a conscious decision of their mortal parents, or governments, as the case may be. Those most affected by the decision would have no choice regarding their immortality (barring suicide, which is always an option). How should parents make such a choice What does a mortal parent say to an immortal child when asked, Why did you make me immortal Unless I am mistaken, generational conflict could enter a new, high-energy orbit unless suitable answers are available. I can just imagine the wrongful immortality suits (and wrongful mortality suits for that matter) brought by children against their parents, but I cannot imagine the judicial outcomes. Why, after all, would anyone want to make their children immortal One possibility is that parental choices are rather bleak to begin with, so why not. Alternatively, would-be parents...

Technology and Human Dignity

The flip side of technological progress is frequently the erosion of human dignity. Immortality is not likely to be any different, and debates over human dignity surrounding immortality are not likely to be resolved to everyone's satisfaction. Controversy over artificial means of controlling human life generally settles on two problems (which may be one and the same) objections to human experimentation and to treating human beings as means to ends (objectification).14 I can offer no solution to the problem posed by human experimentation without indulging in self-contradiction, since achieving immortality will inevitably require human experimentation. I would imagine that, contrary to the experience with other forms of cyborgian birthing, such as in vitro fertilization and embryo transfer, experiments with other animals will precede human experimentation.15 Current law would seem to preclude the possibility of using human beings in experimentation on immortality until research on other...

Prologue

If you want to produce an immortal human being, you must produce an immortal mind. Looking into my mind's rearview mirror, I see that research for Becoming Immortal actually began when, as a child, like many other children, I was prone to ask Why questions. The most burning of these questions was, Why do we have to grow up and die This question burns with an even hotter flame today but now in a more academic form Why did life evolve a dynamics in which living things are constantly exchanged Why didn't a stasis evolve in which living things remained more or less constant What I failed to appreciate as a child and throughout most of my adult life was that in order to achieve immortality, human life, as we know it, would have to change biologically in ways that were virtually excluded by evolution and development. The idea of biological change without natural selection and contrary to the central dogma was precisely the idea that had eluded me until I began to realize that what we know...

Agglutination

Avoid ageing higher plants often seem capable of unlimited vegetative propagation. Regeneration-and renewal in many simple invertebrates seem to permit escape from senescence, germ li nbs of sexual metazoa are potentially immortal (see weismann). Expressed as disintegration of somatic tissue, ageing may be due to gradual accumulation of somatic mutations or to late expression of genes not subject to strong selection. Some evidence suggests loss of dna methyl ation maybe involved. In the population context, it maybe due to inbreeding or to some other factor reducing genetic variation.

Alveolus

Behaviour benefiting another individual at the expense -of the agent. Widespread and apparently at odds with Darwinian theory, which predicts that any genetic component of such behaviour should be selected against. Theories of altruism in biology tend to be concerned with cost-benefit analysis, as dictated by the logic of natural selection. One component of Darwinian fitness may be the care a parent bestows upon its offspring, although this is not usually considered altruism, Hamilton's rule indicates the scope for evolutionary spread of genetic determinants of altruistic character traits, compatibly with Darwinian theory, and explains the evolution of parental care, while showing that reciprocal altruism can evolve even in the absence of relatedness between participants (e.g. members of different species). mul t i cel l ul arity may afford opportunities for sacrifice of somatic cells (e.g. leucocytes) for a genetically related germ line harbouring the potentially immortal...

Chromosomes

Becoming immortal is only one of many things that must happen before a cell becomes cancerous. A cell that simply divides indefinitely can produce a tumor mass, but as long as it remains benign it can usually be removed surgically. The real danger occurs when some of the cancer cells break away from the original

Stem cells

Long before stem cells became prime subjects in immortality research, stem cells were studied for their role in normal tissue maintenance.63 The idea was that individuals were constantly refurbished by stem cells, thereby maintaining life. The constant turnover of cells in the outer layer of skin (epidermis), the inner layer of the digestive track (absorptive cells), and blood and lymphatic systems were known since World War II. At that time, the advent of radioactive elements and labeled materials (especially tritiated thymidine) had made it practical to track cellular turnover. Commons approved 366 to 174 new rules allowing scientists to derive and use stem cells from human embryos and perform experiments with nuclear transfer.68 In the United States, the National Bioethics Advisory Commission recommended easing the strictures on research utilizing human embryos and fetuses.69 President Clinton partially lifted the ban on cloning and President Bush has decided to allow research...

History

The development of hybridoma technology by Milstein and Koohlerin the mid-1970s revolutionized the generation of specific antibodies for use in research and clinical applications Hybridomas are made by fusing antibody-forming B-cells with an immortal, non-antibody-secreting plasma cell line resulting in a population of hybrid cells that are selected for secretion of an antibody specific for an antigen of interest. The secret to this technology is that the immortal plasma cell line does not secrete antibody and is deficient in a purine enzymatic salvage pathway, hypoxanthine phosphoribosyl transferase (HPRT). When these plasma cells are fused to B-cells and placed in medium containing hypoxanthine-aminopterin-thymidine (HAT), the aminop-terin poisons the de novo purine synthesis pathway. Unfused cells die, and only the hybridomas survive in HAT, while the B-cell component of the hybridoma provide the purine salvage pathway and the plasma cells con

Cotards Syndrome

Other psychiatric symptoms associated with nihilistic delusion are paranoia, guilt, fear of demonic possession, auditory hallucinations, delusion of omnipotence, and suicidal complex. Somatisation includes hyperkinesias, muscular rigidity, and alternating retention of urine and faeces and incontinence. Some patients with Cotard's syndrome reportedly refused to eat or drink, claiming that their muscles and nerves were not cooperating. These patients improved dramatically after electroshock therapy, which may be one of the best treatments for the depressive type of Cotard's syndrome.

Arginine Butyrate

Arginine butyrate and other histone deacetylase inhibitors induce the activity of certain genes. Exposure of EBV-positive tumor cells to butyrate results in robust induction of herpesvirus in immediate-early and early (lytic) genes, including thymidine kinase (TK), and a modest induction of lytic replication. There is now extensive experience in the administration of arginine butyrate over extended periods of time to adults and children with sickle cell anemia or P-thalassemia to therapeutically reactivate fetal globin expression. In vitro studies demonstrated that induction of EBV-TK activity was possible in EBV-immortal-ized B cells and that these previously ganciclovir-resis-tant cells were then rendered susceptible to antiviral nucleoside analogs. Faller et al. have used arginine butyrate to induce the latent viral TK gene expression and enzyme induction in tumor cells and then treated the patients with ganciclovir 5 of 10 previously refractory patients experienced a complete...

Longevity as a Trait

No claims are generally made for immortality among mammals, vertebrates (other than turtles and tortoises), or most other multicellular animals for that matter, but longevity varies considerably among these organisms and offers many opportunities for contemplating how physiology and evolution collude in the imposition of limits.96 This collusion is not simple or straightforward.

Cloning

Cloning Dolly

Cloning did not, however, embody the essence of immortality, that is, personal continuity. The microneedle sometimes used in cloning to inject the nucleus of an adult's cell into the cytoplasm of an egg is hardly a fountain of youth, and cloning hardly reanimates the nuclear donor (e.g., the long dead ewe whose udder cell donated the nucleus used in the cloning of Dolly).58 Cloning is not about rejuvenating individuals. Cloning only replicates them, and then, only as far as their nuclear-genetically encoded traits. follow a trajectory to oblivion. After all, cloning had already been done in fiction and movies (e.g., Boys from Brazil), only to be repudiated as a means for preserving desirable individuals. Yet, before hurdling to a fiery death, cloning received a boost and became relevant to immortality again. The thrust came from another breakthrough technology in this struggle against perishability.

Background

Although yeast cultures are immortal, individual yeast cells display a finite life span (3,4). S. cerevisiae divides asymmetrically, giving rise to a larger mother cell and a smaller daughter cell with each cell division. A circular bud scar on the mother cell's surface is left at the site of division, serving as a physical marker of the number of cell divisions a yeast cell has undergone. The cell wall and many other constituents of daughter cells are synthesized de novo, and most daughters have the potential for a full life span. Thus, the yeast population is immortal. The number of cell divisions that the mother cell undergoes varies somewhat between yeast strains. By a laborintensive process, the number of divisions a mother cell undergoes can be determined by microscopic observation of individual large mother cells and manual separation by micromanipulation of the smaller daughter cells. Yeast aging has most often been defined as the number of times the yeast mother cell divides....

Discontinuity

The life death transition may be viewed as the foremost of life's discontinuities, possibly the most obvious, but actually only one among many. Life is, after all, dispersed in discontinuous, living things that also exhibit discontinuities within themselves within organisms (between cells, tissues, organs, and organ systems), between organisms (age, sex, individual), and between taxa (species, genera, families, orders, class, phyla). Life, if anything, abounds with discontinuities. Next to flux, discontinuity may well be life's main characteristic, and bringing discontinuity into conformity with immortality will be as challenging as turning flux into equilibrium. Immortal human beings could take a lesson from genes. Like immortal replicators, immortal human beings will not change, or, when they do, will remain constant in their new form. But, immortal human beings will all be different from each other and must preserve their individual differences for the sake of their humanity. In...

Development Always

The problems for immortality implied by developmental endpoints may be tucked under the proverbial rug by substituting the phenotype for sexual maturity. Ordinarily, the phenotype includes all the qualities of an organism starting with the fertilized egg and ending with the death of the organism. Susan Oyama remarks, and even severe damage to an organ may yet be reversible by appealing to quantitative genes supporting regeneration. In many organisms, both multicellular and unicellular, growth is allied to asexual reproduction, or to a period in which potential germ cells are amplified prior to the onset and differentiation of sex cells.28 Genes with a potential for supporting immortality may be operative during asexual reproduction, growth, or even germ-cell proliferation.

Conclusions

So why aren't we immortal A half billion years or so of developing mortal animals supplies an abundance of answers We are not immortal because our development is determined by genes, inherited through genes, and constrained by natural selection around the poles of fertilization and death because the components of our developing systems germ layers, cell lines, and stem cells rely in part on history to get their bearings and are generally eliminated or narrowed in scope with maturity because our internal organs cannot dump effete cells as easily as surface organs can dump cells into external sinks because internal organs have acquired controls over their growth that result in the accumulation of damaged DNA because adults have insufficient supplies of stem cells to sustain adult life because the stem cells they have are not sufficiently malleable to replace all the cells in an organism requiring replacement. Can all the reasons we do not develop immortality be turned on their head and...

Making Generators

The use of cloned blastocysts for generators may also solve most of the problems of synchronizing and reprogramming the host and generator. Clones raised to the point of blastocysts are natural generators of ES cells. Indeed, blastocysts do not even have to be coaxed to make ES cells, since this is precisely the task nature has assigned to them for making embryos, and it is a rare egg that has no embryo (a wind egg in birds, a barren germinal vesicle in mammals). The blastocyst cultured in vitro prior to implantation in the host also offers the option of supplementing the blastocyst's ES cells with designer es cells made by genetic modification to meet specific needs, such as correcting hereditary defects in the developing immortal.

Degeneration

The fact that aging is just a functional state should be very encouraging. We might not be in a position to bring on immortality through engineering negligible senescence, but a better understanding of the metabolism of the aged neuron could open important avenues for therapeutic intervention that will impede or delay the possible cognitive decline of the aged.

At What Cost

It has never been my intention to pretend that immortality could be achieved without sacrifice. Beyond all the problems of communication, the simple pleasures offered by birth, if not death, will be increasingly rare as more and more people enter the population as sterile immortals. Moreover, the preference some of us have for human diversity may not be rewarded as richly as it is today, since some human traits will, no doubt, not be represented among the immortals. How the immortal humans will look and behave is a matter of conjecture, but some consequences of the indwelling generator would seem inevitable, most conspicuously the morphological and physiological juvenilization of the immortals. Unquestionably, the immortals will be in unbelievably good physiological shape. They will be ballet dancers, gymnasts, karate experts with great stamina and grace. Immortals will not resemble the Eloi envisaged by H. G. Wells in The Time Machine, fragile, easily fatigued, of slight stature, a...

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