Apoptosis Quotes

When cells are no longer needed, they die with what can only be called great dignity. They take down all the struts and buttresses that hold them together and quietly devour their component parts. The process is known as apoptosis or programmed cell death. Every day billions of your cells die for your benefit and billions of others clean up the mess. Cells can also die violently- for instance, when infected- but mostly they die because they are told to. Indeed, if not told to live- if not given some kind of active instruction from another cell- cells automatically kill themselves. Cells need a lot of reassurance. When, as occasionally happens, a cell fails to expire in the prescribed manner, but rather begins to divide and proliferate wildly, we call the result cancer. Cancer cells are really just confused cells. Cells make this mistake fairly regularly, but the body has elaborate mechanisms for dealing with it. It is only very rarely that the process spirals out of control. On average, humans suffer one fatal malignancy for each 100 million billion cell divisions. Cancer is bad luck in every possible sense of the term.

Apoptosis is natural death, brought about by the tiredness and exhaustion of matter. In Greek this word means “the dropping of petals.” The world has dropped its petals.

I grew up in a beautiful era, now sadly in the past. In it there was great readiness for change, and a talent for creating revolutionary visions. Nowadays no one still has the courage to think up anything new. All they ever talk about, round the clock, is how things already are, they just keep rolling out the same old ideas. Reality has grown old and gone senile; after all, it is definitely subject to the same laws as every living organism — it ages. Just like the cells of the body, its tiniest components — the senses, succumb to apoptosis. Apoptosis is natural death, brought about by the tiredness and exhaustion of matter. In Greek this word means ‘the dropping of petals.’ The world has dropped its petals.

Every day in the human body, some 10 billion cells die and are replaced by new cells. The cells that die do not meet a violent unpremeditated end, but are removed silently and unnoticed by apoptosis, all evidence of their demise eaten by neighbouring cells. This means that apoptosis balances cell division

are biased toward studying individual organisms. It is often difficult for scientists to grasp the idea that individual brains do not exist in nature. As much as one may adhere to the notion of the isolated self, humans have evolved as social creatures and are constantly regulating one another’s biology. Without mutually stimulating interactions, people (and neurons for that matter) wither and die. In neurons this process is called apoptosis (programmed cell death); in humans it is called failure to thrive, depression, or dying of a broken heart.

Your cells are preprogrammed to die naturally to make way for fresh cells through a process known as apoptosis (from the Greek ptosis, falling, and apo, away from). In a sense, your body is rebuilding itself every few months16 with the building materials you provide it through your diet. Some cells, however, overstay their welcome—namely, cancer cells. By somehow disabling their own suicide mechanism, they don’t die when they’re supposed to. Because they continue to thrive and divide, cancer cells can eventually form tumors and potentially spread throughout the body.

In quel caso, l'ossessione sarebbe un'altra cosa che ci accomuna.

Eighty billion human cells died every day from apoptosis. Another eighty billion were birthed. Biologically, he wasn’t the same person he was yesterday, and he’d be a different person the day after as well. Personality changed over time, too. People could become inflexible and rigid—hardening and crimping like a sponge left too long in the sun

For years I’ve been waiting for nature to react to our environmental bullshit, tell us to stop overpopulating and depleting resources, to shut up and stop messing around and just die. Species-level apoptosis. I think this could be the final warning—a real species killer.

The basis for the potential of all virolytic therapeutics resides in the exquisite selectivity they exhibit for infecting and killing cancer cells. The very nature of cancer cells makes them extremely susceptible to virus infection: they divide in an uncontrolled fashion and are metabolically hyperactive, thus they exhibit greatly diminished capacity for apoptosis and innate immune defense against virus infection. While normal cells reduce metabolic activity, activate apoptotic signaling pathways, and block cell cycle progression in response to virus infection, cancer cells remain oblivious. These are perfect conditions for the growth of viruses, particularly those that are attenuated for growth in normal cells. Consequently, oncolytic viruses are specific reagents that target cancer cells and spread from cell to cell within tumors. It has become apparent that the direct lytic effects of viruses on cancer cells is just one element of their therapeutic effects, the cytolisis of infected cells releases viral and cellular antigens that can provoke anti-tumor immune responses, and some cancer therapeutic viruses are engineered to deliver additional genes such as immune activators to augment these effects.

So how does a cell go about ending its own existence? The actual mechanism of ‘cell suicide’ depends upon mitochondria, termed the ‘angels of death’ by Nick Lane in his book, Power, Sex and Suicide: Mitochondria and the Meaning of Life . The first change occurs in the mitochondrial inner membrane, which becomes damaged by aberrant biochemical activity, leading to the formation of pores in the mitochondrial membrane (Figure 12b, d). At this point, the mitochondrion becomes committed to trigger apoptosis, and releases cytochrome c (a protein crucial to its normal function of energy production) which exits through the newly formed pores. This information came to light as a result of some neat experiments in which apoptotic mitochondria were introduced into perfectly healthy cells, resulting in apoptosis. The released cytochrome c binds to several other proteins in the cytoplasm to form a complex called the apoptosome which, in turn, activates a cascade of ‘executioner enzymes’ which not only kill the cell but cause fragmentation of the nucleus and cytoplasm into bite-size pieces ready to be phagocytosed by neighbouring cells.

Another magnificent healing mechanism that fasting triggers is the process of autophagy. Auto in Greek means “self,” and phagy means “to eat,” so autophagy refers to your body digesting its own damaged cells. It is a vital cleanout process—the equivalent of taking out the trash—that detoxifies your cells and recycles the parts of the organelles within them that are no longer needed, so that your cells behave more youthfully. Autophagy also destroys foreign invaders such as viruses, bacteria, and other pathogens. A similar process, apoptosis, is when the entire cell is recycled. When apoptosis is impaired, your risk for cancer increases dramatically because your ability to remove damaged cells is impaired. That is why fasting is so useful as an adjunctive strategy to not only prevent cancer, but also help treat it.

In several studies using mice, it has been demonstrated that AAV2 kills 100 per cent of breast cancer cells in the laboratory by activating proteins called caspases, which are essential for the cell’s natural death. Cancer cells infected with AAV2 also produced more Ki-67, a protein that activates the immune system, and c-Myc, a protein that helps to increase cell growth as well as induce apoptosis.

chromosomes. Normal aging happens because the chromosomes don’t regenerate all the way to their ends during the DNA replication cycle. Telomeres protect the information in those chromosomes; telomerase is the enzyme that activates the telomeres to replicate and replace themselves as they fall off. You have extra-long telomeres protecting your chromosomes, which might have already been genetic, or it might have come with the porphyria mutation when you were infected. We think that infection locked onto your DNA and has super-promoted your telomerase. So even if your telomeres were inclined to fall off as they normally would – a process that would allow the chromosomes to alter and change – your rocket-fuel telomerase makes new telomeres so fast there’s no time for apoptosis.

Horvitz and his colleagues discovered several genes that coded for the effectors of cell death in nematodes—the death genes. Their findings were fascinating in their own right, but by far the most unexpected and important discovery was that there were exact equivalents of the death genes in flies, mammals, and even plants. Cancer researchers had already identified some of these genes at the time, but why or how they were involved in cancer was still unknown. The link with nematodes made their function clear, while giving another demonstration of the fundamental unity of life. Not only were the human genes unambiguously related to the nematode genes, but also they could even be genetically engineered to replace the nematode genes in the worms themselves, where they worked equally well! Mutations that disabled any of the death genes prevented the nematodes from losing their 131 cells by apoptosis as usual. The implications for cancer were plain: if the same mutations had a similar effect in people, then incipient cancer cells would likewise fail to commit suicide, and would instead continue to proliferate to form a tumour.

Activation of the androgen receptor (AR) is crucial for tumor cell progression and survival of prostate cancer, and androgen deprivation therapy remains the main clinical approach in men with locally advanced tumors ■ Current therapies incompletely suppress the androgen–AR axis, but a multiple therapeutic approach, targeting androgens and their receptor, has potential to improve clinical outcomes ■ Treatment of prostate cancer cells with 5α-reductase inhibitors (5ARIs) inhibits cellular pathways regulating metabolism, cell growth and proliferation, triggering apoptosis and decreasing prostate size ■ Although 5ARI treatment reduces the risk of developing prostate cancer, patients treated with these drugs have tumors with higher Gleason scores than those who receive placebo ■ Use of 5ARIs to prevent and treat prostate cancer remains controversial, and further investigation is necessary to understand the presence of more-aggressive tumors in patients receiving these drugs

Le verità non sono altro che menzogne ben collaudate.

Avrò il diritto di spassarmela ogni tanto, no?

E non puoi farlo come le persone normali invece di crackare il sistema del locale.

Se cerchi un'informazione preziosa, io voglio essere lì con te quando la troverai, anzi voglio aiutarti a trovarla. È la nostra natura.

Finally, the degenerative phase completes the downward cycle by signaling for large-scale tendon cell apoptosis (death) with permanent damage, characterized by intratendinous calcification (calcium deposits within the tendon).

One study conducted on rats showed that Roundup might lead to excessive extracellular glutamate levels and glutamate excitotoxicity and oxidative stress.[1] In other words, Roundup can cause excessive levels of the neurotransmitter glutamate, which, in turn, can cause damage to the neurons. Another study showed that glyphosate could cause toxicity to the cells, oxidative effects, and apoptosis on human cells.[2] Yet another study showed that inhalation of glyphosate may cause DNA damage.

Cells and subcellular parts must be culled in the processes known as apoptosis and autophagy, respectively.

High levels of insulin/IGF-1, as seen in obesity and type 2 diabetes, not only encourage cell growth but also block the natural running of the apoptosis program, powerfully increasing growth signaling.

Reality has grown old and gone senile; after all, it is definitely subject to the same laws as every living organism—it ages. Just like the cells of the body, its tiniest components, the senses, succumb to apoptosis. Apoptosis is natural death, brought about by the tiredness and exhaustion of matter. In Greek this word means “the dropping of petals.” The world has dropped its petals.

Sono cresciuta in un'epoca bellissima che purtroppo è passata. C'era una grande disposizione ai cambiamenti e la capacità di immaginare visioni rivoluzionarie. Oggi non c'è più nessuno che abbia il coraggio di inventare qualcosa di nuovo. Si parla sempre e soltanto di quello che c'è, e si sviluppano idee vecchie. La realtà è invecchiata, è rimbambita, perché soggiace chiaramente alle medesime leggi degli organismi viventi: invecchia. I suoi elementi più piccoli - i sensi - sono soggetti all'apoptosi così come le cellule del corpo. L'apoptosi è una morte naturale, provocata dalla stanchezza e dall' esaurimento della materia. In greco la parola significa "caduta dei petali". Al mondo sono caduti i petali.

Plasticity of neuroendocrine-thymus interactions during aging N.Fabris12E.Mocchegiani2M.Provinciali2 Abstract Thymic regrowth and reactivation of thymic endocrine activity may be achieved even in old animals by different endocrinological or nutritional manipulations such as, (a) intrathymic transplantation of pineal gland or treatment with melatonin, (b) implantation of a growth hormone (GH) secreting tumor cell line or treatment with exogenous GH, (c) castration or treatment with exogenous luteinizing hormone-releasing hormone (LH-RH), (d) treatment with exogenous thyroxine or triiodothyronine, and (e) nutritional interventions such as arginine or zinc supplementation. These data strongly suggest that thymic involution is a phenomenon secondary to age-related alterations in neuroendocrine-thymus interactions and that it is the disruption of such interactions in old age that is responsible for age-associated dysfunction. Melatonin or other pineal factors may act through specific receptors, but experimental evidence is still lacking. The role of zinc, whose turnover is usually reduced in old age, is diverse. The effects range from the reactivation of zinc-dependent enzymes, required for both cell proliferation and apoptosis, to the reactivation of thymulin, a zinc-dependent thymic hormone. The role of zinc may even be more crucial. According to recent preliminary data obtained both in animal and human studies, it appears that the above reported endocrinological manipulations capable of restoring thymic activity in old age, may act also by normalizing the altered zinc pool.

Apoptosis is natural death, brought about by the tiredness and exhaustion of matter. In Greek this word means ‘the dropping of petals’. The world has dropped its petals.

The survival of an older person is of no evolutionary consequence since that person can no longer reproduce—unless one wants to argue for the role of grandparents in prolonging the lives of their descendants. It might even, in a Darwinian sense, be better to remove the elderly before they can use up any more resources that might otherwise go to the young. In that case, you could say that there is something almost altruistic about the diseases of aging. Just as programmed cell death, apoptosis, cleanly eliminates damaged cells from the body, so do the diseases of aging clear up the clutter of biologically useless older people—only not quite so cleanly. And this perspective may be particularly attractive at a time, like now, when the dominant discourse on aging focuses on the deleterious economic effects of largely aging populations. If we didn’t have inflammatory diseases to get the job done, we might have to turn to euthanasia.

There appears to be significant research indicating a dramatic drop in inflammation, improvements in insulin signaling, and a near total “reset” of immune function with fasts of 3–5 days. Abnormal and or pre-cancerous cells appear to be pushed towards apoptosis, which essentially selects for healthy cell types. In total this describes a process which should (in theory) reverse many of the signs and symptoms of aging while reducing the processes that appear to be at play in autoimmunity and cancer.

TP53 initiates apoptosis whenever it detects cell damage in normal cells, releasing agents to do its bidding called Puma, Noxa, and Bax, among others.

From this perspective of cancer as a metabolic disease, insulin and IGF promote the cancer process through a series of steps. First, insulin resistance and elevated levels of insulin trigger an increased uptake of blood sugar (glucose) as fuel for precancerous cells. These cells then begin producing energy through a mechanism known as aerobic glycolysis that is similar to what bacteria do in oxygen-poor environments. (This phenomenon is known as the Warburg effect and was discovered in the 1920s by the German biochemist and later Nobel Laureate Otto Warburg, although its importance in the cancer process was not embraced until recently.) Once cancer cells make this conversion, they burn enormous amounts of glucose as fuel, providing them, apparently, with the necessary raw materials to proliferate. By metabolizing glucose at such a rapid rate, as Thompson suggests, these cancer cells generate relatively enormous amounts of compounds known technically as “reactive oxygen species” and less technically as “free radicals,” and these, in turn, have the ability to mutate the DNA in the cell nucleus. The more glucose a cell metabolizes and the faster it does so, the more free radicals are generated to damage DNA, explains Thompson. And the more DNA damage, the more mutations are generated, and the more likely it is that one of those mutations will bestow on the cells the ability to proliferate without being held in check by the cellular processes that work to prevent this pathological process in healthy cells. The result is a feed-forward acceleration of tumor growth. While this is happening, the insulin and IGF in the circulation both work to signal the cell to keep proliferating, and to inhibit the mechanism (technically known as apoptosis, or cell suicide) that would otherwise kick in to shut it down.