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If cells in our body keep on dividing into new cells how do they ever grow old?
The only cells to grow old would be defunct cells or those who won't divide into new cells like nerve cells.
What am I missing here?
Human chromosomes contain certain DNA regions called telomeres. These regions are shortened on each cell division and once they are gone, the cell cannot divide. Therefore an average cell in our body can divide only about 50 times.
There are indications that longer telomeres may increase lifespan, however this remains controversial. Telomeres are believed to be a method of higher organisms to prevent uncontrolled cell division and cancer, therefore artificially increasing telomere length may not lengthen but shorten lifespan because of increased cancer risks.
Also, ageing is not (only) caused by individual cells growing old. Often it is the organization between the cells that breaks down. Scarring is a good example for this. The wound is closed but the tissue inside the wound was not able to organize into functional skin tissue again but rather "patched up" the wound with comparatively unorganized tissue.
The brain is another extreme example of ageing by disorganization. It has been shown that even adult brains contain neuron progenitor cells (albeit fewer than other tissues) so even adults can regrow neurons in the brain. However, while the cell body of the neuron can be replaced, all its (sometimes thousands) of connections to other neurons are lost. Therefore, brain tissue can be regenerated in principle, but the information it contained cannot.
New cause of cell aging discovered
New research from the USC Viterbi School of Engineering could be key to our understanding of how the aging process works. The findings potentially pave the way for better cancer treatments and revolutionary new drugs that could vastly improve human health in the twilight years.
The work, from Assistant Professor of Chemical Engineering and Materials Science Nick Graham and his team in collaboration with Scott Fraser, Provost Professor of Biological Sciences and Biomedical Engineering, and Pin Wang, Zohrab A. Kaprielian Fellow in Engineering, was recently published in the Journal of Biological Chemistry.
"To drink from the fountain of youth, you have to figure out where the fountain of youth is, and understand what the fountain of youth is doing," Graham said. "We're doing the opposite we're trying to study the reasons cells age, so that we might be able to design treatments for better aging."
What causes cells to age?
To achieve this, lead author Alireza Delfarah, a graduate student in the Graham lab, focused on senescence, a natural process in which cells permanently stop creating new cells. This process is one of the key causes of age-related decline, manifesting in diseases such as arthritis, osteoporosis and heart disease.
"Senescent cells are effectively the opposite of stem cells, which have an unlimited potential for self-renewal or division," Delfarah said. "Senescent cells can never divide again. It's an irreversible state of cell cycle arrest."
The research team discovered that the aging, senescent cells stopped producing a class of chemicals called nucleotides, which are the building blocks of DNA. When they took young cells and forced them to stop producing nucleotides, they became senescent, or aged.
"This means that the production of nucleotides is essential to keep cells young," Delfarah said. "It also means that if we could prevent cells from losing nucleotide synthesis, the cells might age more slowly."
Graham's team examined young cells that were proliferating robustly and fed them molecules labeled with stable isotopes of carbon, in order to trace how the nutrients consumed by a cell were processed into different biochemical pathways.
Scott Fraser and his lab worked with the research team to develop 3D imagery of the results. The images unexpectedly revealed that senescent cells often have two nuclei, and that they do not synthesize DNA.
Before now, senescence has primarily been studied in cells known as fibroblasts, the most common cells that comprised the connective tissue in animals. Graham's team is instead focusing on how senescence occurs in epithelial cells, the cells that line the surfaces of the organs and structures in the body and the type of cells in which most cancers arise.
Graham said that senescence is most widely known as the body's protective barrier against cancer: When cells sustain damage that could be at risk of developing into cancer, they enter into senescence and stop proliferating so that the cancer does not develop and spread.
"Sometimes people talk about senescence as a double-edged sword, that it protects against cancer, and that's a good thing," Graham said. "But then it also promotes aging and diseases like diabetes, cardiac dysfunction or atherosclerosis and general tissue dysfunction," he said.
Graham said the goal was not to completely prevent senescence, because that might unleash cancer cells.
"But then on the other hand, we would like to find a way to remove senescent cells to promote healthy aging and better function," he said.
Graham said that the team's research has applications in the emerging field of senolytics, the development of drugs that may be able to eliminate aging cells. He said that human clinical trials are still in early stages, but studies with mice have shown that by eliminating senescent cells, mice age better, with a more productive life span.
"They can take a mouse that's aging and diminishing in function, treat it with senolytic drugs to eliminate the senescent cells, and the mouse is rejuvenated. If anything, it's these senolytic drugs that are the fountain of youth," Graham said.
He added that in order for successful senolytic drugs to be designed, it was important to identify what is unique about senescent cells, so that drugs won't affect the normal, non-senescent cells.
"That's where we're coming in -- studying senescent cell metabolism and trying to figure out how the senescent cells are unique, so that you could design targeted therapeutics around these metabolic pathways," Graham said.
Ageing versus disease
Unless you are exceptionally thoughtful, unusually well informed or a bio-gerontologist (a specialist in the biology of ageing), everything you think you know about the relationship between the ageing process and diseases such as cancer or atherosclerosis is probably wrong.
We have always known that those around us will grow old, get sick and die. But few of us have stopped to think about how this actually happens. What is the relationship between “natural changes” like wrinkles and “diseases” that can actually kill us?
Greek doctor and philosopher Aelius Galen (c. 121-169 AD) set the conceptual framework for our understanding of ageing. He defined disease as an abnormal function. Since ageing is universal it cannot, he reasoned, be a disease by definition. Although there were later variations on this argument, they lead to the same conclusion. If ageing takes place in everyone and disease occurs in only a part of the population then disease and ageing are not synonymous. The former should be cured and the latter endured, or perhaps celebrated, went the conventional wisdom.
Upper image shows cells of a mouse before the accumulation of senescent cells. Lower image is after. Y tambe/wikimedia , CC BY-SA
But the people making these arguments had no meaningful idea of the mechanisms that cause either ageing or disease. It wasn’t until the 1980s that researchers started to really understand the biology of ageing. One hypothesis that emerged is that the accumulation of “senescent” cells may be a driving force of ageing.
Senescent cells are formed within the cell populations that divide during life. However, this division is limited as an anti-cancer mechanism and so after a variable degree of replication, cells stop dividing and enter the senescent state.
Once senescent these cells produce a range of inflammatory molecules and undergo other changes which damage tissue. These changes alert the immune system to their presence allowing it to remove them. Unfortunately as the immune system itself ages this capacity declines and the number of senescent cells in tissue increases, leading to ageing.
These cancers tend to have some of the mutations described above and often have changes in the TP53 tumor suppressor gene.
People who have medullary thyroid cancer (MTC) have mutations in different parts of the RET gene than people with papillary carcinoma. Nearly all patients with the inherited form of MTC and about 1 of every 10 with the sporadic (non-inherited) form of MTC have a mutation in the RET gene. Most patients with sporadic MTC have gene mutations only in their cancer cells. People with familial MTC and MEN 2 inherit the RET mutation from a parent. These mutations are in every cell in the body and can be detected by DNA tests.
The Hallmarks of Cancer: 4 – Limitless Replicative Potential
The Hallmarks of Cancer are ten underlying principles shared by all cancers. The previous Hallmark of Cancer articles can be found here. The Fourth Hallmark of Cancer is defined as “Limitless Replicative Potential”.
The Hallmarks of Cancer are ten underlying principles shared by all cancers. The previous Hallmark of Cancer articles can be found here. The Fourth Hallmark of Cancer is defined as "Limitless Replicative Potential".
The first three Hallmarks of Cancer explain how independence from growth signals, insensitivity to antigrowth signals and resistance to apoptosis lead to the uncoupling of a cell's growth program from the signals in its environment. However, cancer is not just a result of disrupted signaling. Our cells carry an in-built, autonomous program that limits their multiplication, even in the face of disrupted signals from their environment. For a single cancer cell to develop into a visible tumor, this program must also be disrupted.
The Cellular Timekeeper
Normal cells are hard wired with a timer that keeps track of their age the number of times they divide and grow. Most cells in our body can only undergo a limited number of successive cell growth-and-division cycles. This limit is named the Hayflick Limit after its discoverer, Leonard Hayflick. After undergoing between 40 and 60 divisions, cell growth slows down and eventually stops altogether. This state is known as senescence, and it is irreversible although the cell does not grow or divide, it remains alive. When normal human cells are cultured in the lab in a petri dish, we can observe this phenomenon, where cells grow and divide a fixed number of times and then enter senescence. Some cells are able to make it past the senescence barrier and continue dividing however these cells then undergo a second phenomenon known as crisis, during which the ends of their chromosomes fuse with each other, and the cells all die on a massive scale via apoptosis.
How does a cell count its divisions? How does it 'know' when to stop? The answer is telomeres. Telomeres are regions of repetitive DNA, capping and protecting the ends of the chromosome from degrading or from fusing with another chromosome. Without telomeres, each time a cell divides our genomes would progressively lose information because the chromosomes would get shorter and shorter. A telomere is like the heat-shield of a spacecraft it protects the actual spacecraft and absorbs the damage instead. With every replication of a cell, about 50-100 nucleotides of telomeric DNA is lost. This progressive loss eventually causes the telomeres to lose their ability to protect the ends of chromosomal DNA. Left unprotected, these exposed ends become damaged. The DNA damage response is activated, leading to growth arrest senescence. When chromosome ends fuse with each other, this irreversible damage results in the activation of apoptosis the cell enters crisis, and dies.
The End Replication Problem
Why do the ends of chromosomes shorten? To understand this, first we need to go over the basic mechanisms of DNA replication. A cell must replicate its DNA before it divides. DNA is a double-stranded molecule, and each strand of the original DNA molecule serves as a template for the production of a complementary strand. The two strands have a directionality the two ends of a single strand are known as the 3' end and the 5' end. The numbers refer to the position of the carbon atom in the deoxyribose molecule at the end of the strand to which the next phosphate molecule in the DNA chain attaches. For a quick introduction into the structure of DNA, check out this YouTube video:
This directionality matters because DNA replication takes place under the direction of an enzyme known as DNA polymerase. This enzyme faithfully copies our genetic code letter by letter. However, DNA polymerase can only work in one direction the 5' to 3' direction. Therefore, although DNA replication is straightforward for one of the DNA strands (the 5' to 3' strand), the other strand (the 3' to 5' strand) is more complicated. This strand is replicated in short fragments instead of one continuous strand of DNA. Replication begins with an enzyme known as primase, which reads the template DNA and initiates the synthesis of very short complementary RNA fragments. DNA polymerase is now able to use these RNA fragments as a starting point to synthesize complementary fragments of DNA in between the RNA fragments. The RNA fragments are then removed and replaced with DNA, and the fragments of DNA are joined together by another enzyme, DNA ligase. This solves the directionality problem of DNA polymerase, but now we run into another problem, known as the end replication problem. This is because although the 5' to 3' strand can be replicated to the very end, the 3' to 5' strand cannot DNA polymerase enzyme requires RNA fragments to begin replication, and there is nothing for such a fragment to attach to at the very end of the DNA strand. Therefore, with every round of replication, a small fragment of the DNA would be lost from the end of the chromosome, since it cannot be replicated. The cell solves this problem by having telomeres at the ends of chromosomes, where they prevent the loss of valuable genetic information by acting as a disposable buffer. Over time, with each successive round of DNA replication, the telomeric DNA shortens until finally there is no more disposable buffer, at which point the cell stops dividing and enters senescence. For a visualization of the end replication problem check out this YouTube video:
When cells are grown in petri dishes in the lab, repeated cycles of cell division lead first to senescence and then, for those cells that make it past this barrier, to crisis phase. Fascinatingly, in very rare instances (about 1 in 10X7) a cell can emerge from this ordeal exhibiting unlimited replicative potential. This cell is now said to be immortalized, and it is a trait that most cancer cells growing in labs exhibit, including the famous HeLa cells.
Cancer cells have therefore not only uncoupled their growth program from the signals in their environment, they have also breached the in-built replication limit hard wired into the cell. How do they achieve this? All cancer cells maintain their telomeres. 90% of them do so by increasing the production of an enzyme known as telomerase. As its name implies, telomerase functions by adding telomeric DNA to the ends of chromosomes. Most normal cells do not divide frequently, and therefore are not in any danger of shortened telomeres these cells can get away with having low telomerase activity. Indeed, most cells apart from fetal cells and stem cells show low telomerase activity levels. Many cancer causing proteins (oncoproteins) are able to activate the production of telomerase, while many cancer preventing proteins (tumor suppressors) such as P53 (see previous Hallmark) produce factors that inhibit the production of telomerase. The other 10% of cancers rely upon the activation of a pathway known as the Alternative Lengthening of Telomeres (ALT), which swaps around telomeres to lengthen them.
Intriguingly, telomere length is also affected by oxidative stress. Oxidative stress, in the form of free radicals, damages DNA. This damage is usually repaired by DNA repair mechanisms, but these mechanisms are less effective on telomeric DNA than elsewhere on the chromosome. Telomeres are therefore highly susceptible to oxidative stress. It also explains the rate of telomere shortening observed estimated loss per cell division because of the end replication problem has been estimated at 20 base pairs of DNA, yet the observed loss is much larger, between 50-100 base pairs of DNA. This difference shows that oxidative stress has a far greater impact on telomere length than the nuances of DNA replication. It is possible that cell senescence induced by telomere loss is therefore a stress response, evolved to block the growth and replication of cells that have been exposed to a high risk of DNA damage.
The defining feature of a cancer cell is its ability to divide endlessly, without exhaustion, generation after generation. They achieve this by destroying the cellular timekeeper, the telomere. Immortality comes at a price the accumulation of damaging mutations only increases with time, which is why cancer is primarily a disease of an aging population. The immortalization of cancer cells by telomere maintenance therefore represents an essential step in tumor progression.
The views expressed are those of the author(s) and are not necessarily those of Scientific American.
Biology of Aging
By Steven N. Austad, Ph.D.
Scientific Director – American Federation for Aging Research Director – Nathan Shock Center of Excellence in the Basic Biology of Aging, the University of Alabama at Birmingham Principal Investigator - the Nathan Shock Centers Coordinating Center.
What is aging? In the broadest sense, aging reflects all the changes that occur over the course of life. Over centuries, theories about aging have emerged and faded, but the true nature of the aging process is still uncertain. The fact is, aging is a part of everyone’s life. But the facts of aging—what is happening on a biochemical, genetic, and physiological level—remain rich for exploration. This article introduces some key areas of research into the biology of aging. Each area is a part of a larger field of scientific inquiry. You can look at each topic individually, or you can step back to see how they fit together in a lattice-work, interwoven to help us better understand aging processes. Research on aging is dynamic, constantly evolving based on new discoveries.
In our bodies, aging is a series of interconnected processes.
As the field of biomedical research on aging has grown over the past three decades, “hallmarks of aging,” have emerged.
On a cellular level, these processes or “hallmarks” are considered the core underlying machinery of how our bodies age.
image credit: Cell 2013 153, 1194-1217DOI: (10.1016/j.cell.2013.05.039) Copyright © 2013 Elsevier Inc
Epigenetic Alterations. Your genome is more than a long sequence of DNA letters. DNA strands are wound around spools of protein called histones, and both DNA and histones can have various chemical handles, cranks, and levers attached to them to help turn genes on or off. These handles, cranks, and levers comprise your epigenome. Your epigenome changes as you age--levers are lost, added inappropriately, or shifted around. As a result, precise coordination of gene activity can be compromised. One particularly well-studied group of molecules than influence the epigenome is the sirtuins, molecules that remove one type of epigenetic handle. Interestingly, your epigenome can be modified by diet, other lifestyle factors, and pharmaceuticals. Evidence that the epigenome affects aging comes mostly from the study of yeast, worms, and flies. However, dietary restriction in mice slows epigenetic changes, and when mice are made deficient in one of the seven mouse sirtuins, they show signs of accelerated aging. Moreover, when that same sirtuin is superabundant, male mice live longer.
Loss of Proteostasis. The main job of genes is to make proteins, which are the heart and soul of cells’ biology. Proteins regulate virtually all chemical reactions and provide cell structure. Protein homeostasis, or proteostasis, is the maintenance of all proteins in their original form and abundance. In order to perform their duties, proteins must be folded in precise, complex shapes like origami. However, with age proteins are damaged by normal cellular process and when damaged begin to misfold. Misfolded proteins not only fail to perform their normal job, they can clump together, and become toxic. Alzheimer’s disease is an example of an age-related disease caused by protein misfolding. The importance of maintaining proteostasis can be seen in the elaborate cellular systems for maintaining it: there are specialized molecular devices to repair and refold damaged proteins as well as to degrade irretrievably damaged proteins and replace them. Several pieces of evidence highlight the role of proteostasis in aging: misfolded proteins increase with ageprotein misfolding occurs in the brain and muscle of Alzheimer’s patients both genetic and drug-induced enhancement of protein quality control will extend life in mice.
Deregulated Nutrient Sensing. When nutrients are abundant, animals including humans grow and reproduce--the evolutionary imperative. When nutrients are scarce, evolutiona has designed animals to focus on maintenance and repair. Studies have been designed to inhibit the signaling of nutrient abundance in three ways: 1)by actually reducing food, 2)by fooling the body into thinking fewer nutrients are available, with drugs such as rapamycin, and 3)by inhibiting the signaling of insulin or its close relative, the insulin-like growth factor. All of these strategies enhance health and longevity in mice and other species.
Mitochondrial Dysfunction. Mitochondria--often called the “powerhouses of the cell”--are places where most of your cells’ energy is produced. Unfortunately mitochondria also produce most of the free radicals, or as scientists more commonly refer to them, Reactive Oxygen Species or ROS in your cells. As ROS damage nearly any molecule they touch, for many years it was thought that ROS were the major culprit behind aging and that minimizing them would lead to longer health and life. However, in the past decade, it was discovered that sometimes lowering ROS had no impact on health. Moreover, sometimes actually increasing ROS, by inhibiting mitochondrial function, seemed beneficial. The newer thinking is that ROS are important in signaling cellular stress. Cells, organs, and tissues that sense stress increase their maintenance and repair processes in response to the stress. Current thinking suggests that ROS production should be in a Goldilocks zone, not too much, not too little, just the right amount.
Cellular Senescence. Cells that once replicated vigorously but have now entered a permanent nondividing state are called senescent cells. We accumulate senescent cells with age. Alas, these cells do not die. They persist and secrete damaging molecules into the surrounding area. Telomere attrition is one cause of cellular senescence, although other types of damage can also trigger this state. For years, it was debated whether senescent cells contributed to aging or were simply a protective mechanism against the development of cancer. Recent work, in which mice were genetically engineered so that researchers could eliminate many of their senescent cells, has clearly shown many health benefits, including longer life. Work is now underway to identify drugs that target senescent cells for destruction.
Stem Cell Exhaustion. The ability of our tissues and organs to regenerate and repair damage is critical to maintaining health. Our bodies’ ability to regenerate tissues and organs depends on healthy stem cells--the ultimate source of new cells--in virtually every tissue. Healthy stem cells must replicate when required, but not otherwise. The replication ability of stem cells--and their ability to replicate only when needed--declines with age. Several labs have now shown that stem cell function can be resuscitated by external factors such as the as-yet-unidentified rejuvenating factor(s) found in the blood of young mice or humans, opening the door for possible pharmacological prolongation of stem cell health.
Altered Intercellular Communication. Although a number of other hallmarks of aging focus on processes that lead to deterioriation of our cells, appropriate communication among cells and tissues is also important to maintaining health. Hormones, for instance, are one way cells communicate. Hormones produced in the brain alter the way cells behave in the rest of the body and vice versa. Your liver might chemically tell your brain to reduce hormone production or nerve cells that signal pain in your toe can chemically alert your immune system in the rest of your body. In relation to aging, perhaps the most important loss of appropriate communication in our bodies is the low-level, chronic inflammation that occurs as we grow older. In youth, inflammation is mainly a response to injury that is turned off once the injury heals. In later life, low-level inflammation is not injury-related, but constant. Moreover, this inflammation is damaging to surrounding tissue. Although the cause of age-related inflammation is unclear, considerable evidence points to senescent cells as the culprit. Restoring proper intercellular communication could extend health by reducing chronic age-related inflammation. Additionally, investigators are studying how intercellular communication influences the rejuvenating properties of young blood studies lend evidence that the blood of young animals contains molecules that can actually rejuvenate damaged heart, brain, and muscle in older adult animals.
Genomic Instability. Each cell in your body--except your red blood cells--contains the string of 3 billion DNA letters that defines your individual genome. Proper functioning of your genome is largely responsible for the smooth running of your body. However, your genome is under constant attack from both external sources such as radiation or pollution and internal sources such as oxygen free radicals. By one estimate the DNA in each of your cells is damaged up to 1 million times per day. Fortunately, DNA also encodes a number of processes that detect and repair virtually all of this damage. Still, repair is not perfect and as we age damage to our genome accumulates. Cancer is one result of unrepaired DNA damage. In both humans and mice, individuals with compromised DNA repair processes show multiple signs of accelerated aging and that therapies such as dietary restriction reduce the rate of DNA damage accumulation: this gives evidence that genomic accumulation is fundamental to aging.
Telomere Attrition. One specific type of genomic instability is telomere attrition. As it has received considerable individual attention, it will be mentioned separately. Telomeres are repetitive sequences of DNA that protect the ends of chromosomes and prevent them from being mistaken for broken DNA strands. Telomere attrition, or shortening, is a specific type of DNA damage to the ends of chromosomes. Normal cell division shortens telomeres as do other processes that damage DNA. When telomeres reach a critically short length, cells sense it and permanently turn off their replication machinery. An enzyme called telomerase, which is turned off in most adult cells, can prevent telomere shortening and even restore telomere length. Evidence linking telomere attrition to aging is that telomeres shorten with age in both people and mice. Mice genetically engineered to lack telomerase have shown some symptoms of premature aging, and mice engineered to express higher levels of telomerase than normal have been reported to live longer.
As biomedical research on healthy aging continues to evolve, these hallmarks provide a foundation for our knowledge of the basic biology of aging.
A 2013 article in Cell, “The Hallmarks of Aging,” first framed these hallmarks. Download the article here.
A 2014 article in Cell, “Geroscience: Linking Aging to Chronic Disease,” complemented this research by explaining the relationship between the processes of aging and major age-related diseases—a paradigm known as geroscience. Download the article here.
Excerpt: 'The Immortal Life of Henrietta Lacks'
The Immortal Life of Henrietta LacksBy Rebecca SklootPaperback, 400 pagesBroadwayList price: $16
The Woman in the Photograph
There's a photo on my wall of a woman I've never met, its left corner torn and patched together with tape. She looks straight into the camera and smiles, hands on hips, dress suit neatly pressed, lips painted deep red. It's the late 1940s and she hasn't yet reached the age of thirty. Her light brown skin is smooth, her eyes still young and playful, oblivious to the tumor growing inside her — a tumor that would leave her five children motherless and change the future of medicine. Beneath the photo, a caption says her name is "Henrietta Lacks, Helen Lane or Helen Larson."
No one knows who took that picture, but it's appeared hundreds of times in magazines and science textbooks, on blogs and laboratory walls. She's usually identified as Helen Lane, but often she has no name at all. She's simply called HeLa, the code name given to the world's first immortal human cells — her cells, cut from her cervix just months before she died.
Her real name is Henrietta Lacks.
I've spent years staring at that photo, wondering what kind of life she led, what happened to her children, and what she'd think about cells from her cervix living on forever --bought, sold, packaged, and shipped by the trillions to laboratories around the world. I've tried to imagine how she'd feel knowing that her cells went up in the first space missions to see what would happen to human cells in zero gravity, or that they helped with some of the most important advances in medicine: the polio vaccine, chemotherapy, cloning, gene mapping, in vitro fertilization. I'm pretty sure that she — like most of us — would be shocked to hear that there are trillions more of her cells growing in laboratories now than there ever were in her body.
There's no way of knowing exactly how many of Henrietta's cells are alive today. One scientist estimates that if you could pile all HeLa cells ever grown onto a scale, they'd weigh more than 50 million metric tons — an inconceivable number, given that an individual cell weighs almost nothing. Another scientist calculated that if you could lay all HeLa cells ever grown end-to-end, they'd wrap around the Earth at least three times, spanning more than 350 million feet. In her prime, Henrietta herself stood only a bit over five feet tall.
I first learned about HeLa cells and the woman behind them in 1988, thirty-seven years after her death, when I was sixteen and sitting in a community college biology class. My instructor, Donald Defler, a gnomish balding man, paced at the front of the lecture hall and flipped on an overhead projector. He pointed to two diagrams that appeared on the wall behind him. They were schematics of the cell reproduction cycle, but to me they just looked like a neon-colored mess of arrows, squares, and circles with words I didn't understand, like "MPF Triggering a Chain Reaction of Protein Activations."
I was a kid who'd failed freshman year at the regular public high school because she never showed up. I'd transferred to an alternative school that offered dream studies instead of biology, so I was taking Defler's class for high-school credit, which meant that I was sitting in a college lecture hall at sixteen with words like mitosis and kinase inhibitors flying around. I was completely lost.
"Do we have to memorize everything on those diagrams?" one student yelled.
Yes, Defler said, we had to memorize the diagrams, and yes, they'd be on the test, but that didn't matter right then. What he wanted us to understand was that cells are amazing things: There are about one hundred trillion of them in our bodies, each so small that several thousand could fit on the period at the end of this sentence. They make up all our tissues — muscle, bone, blood — which in turn make up our organs.
Under the microscope, a cell looks a lot like a fried egg: It has a white (the cytoplasm) that's full of water and proteins to keep it fed, and a yolk (the nucleus) that holds all the genetic information that makes you you. The cytoplasm buzzes like a New York City street. It's crammed full of molecules and vessels endlessly shuttling enzymes and sugars from one part of the cell to another, pumping water, nutrients, and oxygen in and out of the cell. All the while, little cytoplasmic factories work 24/7, cranking out sugars, fats, proteins, and energy to keep the whole thing running and feed the nucleus. The nucleus is the brains of the operation inside every nucleus within each cell in your body, there's an identical copy of your entire genome. That genome tells cells when to grow and divide and makes sure they do their jobs, whether that's controlling your heartbeat or helping your brain understand the words on this page.
Defler paced the front of the classroom telling us how mitosis — the process of cell division — makes it possible for embryos to grow into babies, and for our bodies to create new cells for healing wounds or replenishing blood we've lost. It was beautiful, he said, like a perfectly choreographed dance.
All it takes is one small mistake anywhere in the division process for cells to start growing out of control, he told us. Just one enzyme misfiring, just one wrong protein activation, and you could have cancer. Mitosis goes haywire, which is how it spreads.
"We learned that by studying cancer cells in culture," Defler said. He grinned and spun to face the board, where he wrote two words in enormous print: HENRIETTA LACKS.
Henrietta died in 1951 from a vicious case of cervical cancer, he told us. But before she died, a surgeon took samples of her tumor and put them in a petri dish. Scientists had been trying to keep human cells alive in culture for decades, but they all eventually died. Henrietta's were different: they reproduced an entire generation every twenty-four hours, and they never stopped. They became the first immortal human cells ever grown in a laboratory.
"Henrietta's cells have now been living outside her body far longer than they ever lived inside it," Defler said. If we went to almost any cell culture lab in the world and opened its freezers, he told us, we'd probably find millions — if not billions — of Henrietta's cells in small vials on ice.
Her cells were part of research into the genes that cause cancer and those that suppress it they helped develop drugs for treating herpes, leukemia, influenza, hemophilia, and Parkinson's disease and they've been used to study lactose digestion, sexually transmitted diseases, appendicitis, human longevity, mosquito mating, and the negative cellular effects of working in sewers. Their chromosomes and proteins have been studied with such detail and precision that scientists know their every quirk. Like guinea pigs and mice, Henrietta's cells have become the standard laboratory workhorse.
"HeLa cells were one of the most important things that happened to medicine in the last hundred years," Defler said.
Then, matter-of-factly, almost as an afterthought, he said, "She was a black woman." He erased her name in one fast swipe and blew the chalk from his hands. Class was over.
As the other students filed out of the room, I sat thinking, That's it? That's all we get? There has to be more to the story.
I followed Defler to his office.
"Where was she from?" I asked. "Did she know how important her cells were? Did she have any children?"
"I wish I could tell you," he said, "but no one knows anything about her."
After class, I ran home and threw myself onto my bed with my biology textbook. I looked up "cell culture" in the index, and there she was, a small parenthetical:
In culture, cancer cells can go on dividing indefinitely, if they have a continual supply of nutrients, and thus are said to be "immortal." A striking example is a cell line that has been reproducing in culture since 1951. (Cells of this line are called HeLa cells because their original source was a tumor removed from a woman named Henrietta Lacks.)
That was it. I looked up HeLa in my parents' encyclopedia, then my dictionary: No Henrietta.
As I graduated from high school and worked my way through college toward a biology degree, HeLa cells were omnipresent. I heard about them in histology, neurology, pathology I used them in experiments on how neighboring cells communicate. But after Mr. Defler, no one mentioned Henrietta.
When I got my first computer in the mid-nineties and started using the Internet, I searched for information about her, but found only confused snippets: most sites said her name was Helen Lane some said she died in the thirties others said the forties, fifties, or even sixties. Some said ovarian cancer killed her, others said breast or cervical cancer.
Eventually I tracked down a few magazine articles about her from the seventies. Ebony quoted Henrietta's husband saying, "All I remember is that she had this disease, and right after she died they called me in the office wanting to get my permission to take a sample of some kind. I decided not to let them." Jet said the family was angry — angry that Henrietta's cells were being sold for twenty-five dollars a vial, and angry that articles had been published about the cells without their knowledge. It said, "Pounding in the back of their heads was a gnawing feeling that science and the press had taken advantage of them."
The articles all ran photos of Henrietta's family: her oldest son sitting at his dining room table in Baltimore, looking at a genetics textbook. Her middle son in military uniform, smiling and holding a baby. But one picture stood out more than any other: in it, Henrietta's daughter, Deborah Lacks, is surrounded by family, everyone smiling, arms around each other, eyes bright and excited. Except Deborah. She stands in the foreground looking alone, almost as if someone pasted her into the photo after the fact. She's twenty-six years old and beautiful, with short brown hair and catlike eyes. But those eyes glare at the camera, hard and serious. The caption said the family had found out just a few months earlier that Henrietta's cells were still alive, yet at that point she'd been dead for twenty-five years.
All of the stories mentioned that scientists had begun doing research on Henrietta's children, but the Lackses didn't seem to know what that research was for. They said they were being tested to see if they had the cancer that killed Henrietta, but according to the reporters, scientists were studying the Lacks family to learn more about Henrietta's cells. The stories quoted her son Lawrence, who wanted to know if the immortality of his mother's cells meant that he might live forever too. But one member of the family remained voiceless: Henrietta's daughter, Deborah.
As I worked my way through graduate school studying writing, I became fixated on the idea of someday telling Henrietta's story. At one point I even called directory assistance in Baltimore looking for Henrietta's husband, David Lacks, but he wasn't listed. I had the idea that I'd write a book that was a biography of both the cells and the woman they came from — someone's daughter, wife, and mother.
I couldn't have imagined it then, but that phone call would mark the beginning of a decadelong adventure through scientific laboratories, hospitals, and mental institutions, with a cast of characters that would include Nobel laureates, grocery store clerks, convicted felons, and a professional con artist. While trying to make sense of the history of cell culture and the complicated ethical debate surrounding the use of human tissues in research, I'd be accused of conspiracy and slammed into a wall both physically and metaphorically, and I'd eventually find myself on the receiving end of something that looked a lot like an exorcism. I did eventually meet Deborah, who would turn out to be one of the strongest and most resilient women I'd ever known. We'd form a deep personal bond, and slowly, without realizing it, I'd become a character in her story, and she in mine.
Deborah and I came from very different cultures: I grew up white and agnostic in the Pacific Northwest, my roots half New York Jew and half Midwestern Protestant Deborah was a deeply religious black Christian from the South. I tended to leave the room when religion came up in conversation because it made me uncomfortable Deborah's family tended toward preaching, faith healings, and sometimes voodoo. She grew up in a black neighborhood that was one of the poorest and most dangerous in the country I grew up in a safe, quiet middle-class neighborhood in a predominantly white city and went to high school with a total of two black students. I was a science journalist who referred to all things supernatural as "woo-woo stuff" Deborah believed Henrietta's spirit lived on in her cells, controlling the life of anyone who crossed its paths. Including me.
"How else do you explain why your science teacher knew her real name when everyone else called her Helen Lane?" Deborah would say. "She was trying to get your attention." This thinking would apply to everything in my life: when I married while writing this book, it was because Henrietta wanted someone to take care of me while I worked. When I divorced, it was because she'd decided he was getting in the way of the book. When an editor who insisted I take the Lacks family out of the book was injured in a mysterious accident, Deborah said that's what happens when you piss Henrietta off.
The Lackses challenged everything I thought I knew about faith, science, journalism, and race. Ultimately, this book is the result. It's not only the story of HeLa cells and Henrietta Lacks, but of Henrietta's family — particularly Deborah — and their lifelong struggle to make peace with the existence of those cells, and the science that made them possible.
Excerpted from The Immortal Life of Henrietta Lacks by Rebecca Skloot Copyright 2010 by Rebecca Skloot. Excerpted by permission of Crown, a division of Random House Inc. All rights reserved.
Researchers do not agree as to the causes of aging. Some claim our genes are programmed to deteriorate, wither and die, while others believe accumulated damage is the root of our senescence. Muddying the waters further, many believe that a combination of several factors contributes to aging.
Around since 1882 when biologist August Weismann first introduced it, at its fundamental level, the cell damage theory holds that the body succumbs to “wear and tear“: “Like components of an aging car, parts of the body eventually wear out from repeated use, killing them and then the body.”
Building on this fundamental idea, a number of researchers today are exploring particular physiological aspects to reveal where and how this “wear and tear” occurs.
Somatic DNA Damage
Focusing on the deterioration of DNA over a lifetime, according to this theory:
DNA damages occur continuously in cells . . . . While most of these damages are repaired, some accumulate . . . . [and] genetic mutations occur and accumulate with increasing age, causing cells to deteriorate and malfunction. In particular, damage to mitochondrial DNA might lead to . . . dysfunction. . . [where] aging results from damage to the genetic integrity of the body’s cells.
Mitochondrial DNA (mtDNA) mutate faster than DNA in a cell nucleus, so mtDNA create more damaging “free radicals” that are believed to induce aging. Given that mitochondria (the power plants of cells) work harder the more fuel (a.k.a. “food”) is available, the less an organism eats, the fewer free radicals are produced. As a result, some scientists have opined that calorie restriction (CR) can act as a fountain of youth: “A diet severely restricted in calories (about 30 percent below normal, but above starvation levels) can increase lifespan, lower rates of cancer, and slow declines in memory and movement.”
Others are more cautious when it comes to recommending a CR diet: “Restricted-diet animals grow more slowly, reproduce less, and have dampened immune systems . . . [because the] dietary restriction seems to switch the body into a survival mode in which growth and energy consumption are suppressed.”
In addition, detractors note that just because: “Lifespan extensions [were] seen in mice [this] may not be observed in large mammals like humans . . . [because unlike small animals] large mammals can migrate in times of famine . . . .”
Nonetheless, at least one study has shown that people on a CR diet will “lower blood cholesterol and insulin and . . . reduce[ the] risk of atherosclerosis,” all conditions that contribute to aging and mortality.
Another branch of the cell damage theory focuses on “cross-linking,” a process whereby damaged and obsolete proteins, which would otherwise be broken down by enzymes (proteases), are protected from that action by making inappropriate attachments, allowing them to “stick around and . . . cause problems.” Over time: “An accumulation of cross-linked proteins damages cells and tissues, slowing down bodily processes . . . .”
This phenomenon has been identified in at least one sign of aging, and implicated in another:
Cross-linking of the skin protein collagen, for example, has proven at least partly responsible for wrinkling and other age-related dermal changes [and] . . . in the lens of the eye is also believed to play a role in age-related cataract formation. Researchers speculate that cross-linking of proteins in the walls of arteries or the filter systems of the kidney account for at least some of . . . atherosclerosis . . . .
Looking at the blueprints that drive organisms, each of these theories explores the idea that, at the cellular level, we are “programmed” for obsolescence.
Many researchers believe that: “Aging is the result of a sequential switching on and off of certain genes, with senescence [old age] being defined as the time when age-associated deficits are manifested . . . .”
To support this theory, scientists have studied aging with the help of Caenorhabditis elegans: “The classic laboratory nematode . . . [which are] tiny, transparent worms . . . [that are] easy to manipulate genetically, and with a life span of just two weeks . . . provide a quick time-lapse view of the aging process . . . .”
In 1993, one group of researchers discovered that: “C. elegans with a specific single-gene mutation lived twice as long as members of the species that lacked [it. This] . . . led to a shift in thinking . . . that [as opposed to many genes] a single gene could dramatically regulate how long an organism lived . . . .”
This gene, daf-2, is a protein remarkably similar to our receptor protein insulin, and, at least in C. elegans, was shown in later research to be a very bossy gene: “Daf-2 normally controls many other genes . . . . For example, in their studies of C. Elegans, researchers have found a large set of genes that are either “turned on” or “turned off” in worms that carry two copies of the daf-2 mutation . . . .”
The types of genes that are regulated by daf-2 include stress resistance, development and metabolism. This is significant because these: “Various genes encode for proteins that extend life by acting as antioxidants, regulating metabolism and exerting an antibacterial effect . . . .”
Other researchers ascribe to the theory that age-regulating genes carry: “Biological clocks [that] act through hormones to control the pace of aging [through] . . . the evolutionarily conserved insulin/IGF-1 signaling (IIS) pathway . . . .”
This signaling pathway is significant: “The IIS system is an ancient system that is highly conserved and coordinates growth, differentiation and metabolism in response to changing environmental conditions and nutrient availability . . .”
Thus, under this theory, individuals adapt at a cellular level, in response to environmental conditions, to foster the best outcome for continuation of the species: “In response to harsh environmental conditions . . . [cells adapt to produce] enhancement of cellular stress resistance and protection, suppression of low-grade inflammation and enhanced mitochondrial biogenesis [increased energy in the cell].”
Thus, in tough times the organism’s life is extended, at least long enough for it to fulfill its biological imperative to breed.
The third gene-coding proposal to explain aging provides that: “The immune system is programmed to decline over time, which leads to an increased vulnerability to infectious disease and thus aging and death.”
Proponents of this theory note that: “As one grows older, antibodies lose their effectiveness, and fewer new diseases can be combated effectively by the body, which causes cellular stress and eventual death.”
This last argument has been called into question by recent research that studied mortality and fertility across 46 different species (including humans), which produced remarkable results: “Although . . . most of the 46 species can be roughly classified along a continuum of senescence . . . [displaying] strong deterioration with age [other species demonstrated] negative deterioration, to negative senescence and improvement with age.”
This means that unlike people, some species: “Are the opposite of humans, becoming more likely to reproduce and less likely to die with each passing year.“
In fact, there is so much diversity of aging across species that, even among those that age like us, there are some, such as the alpine swift, that become more fertile (likely to reproduce) as they approach their demise.
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No, no and no. All wrong. We age because God hates us.
Well, He hates you. Me he’s just indifferent toward.
well actually, we age because of the way DNA replicates. Think if it this way- when you are born, you have a fresh code of DNA, and because it hasn’t replicated a lot yet, it is very “long.” Everytime DNA replicates, it gets smaller. Somatic and other cells will keep dividing until DNA is too short to divide correctly without problems. That point is ageing. Although we have enzymes that extend our DNA, such as trees have, this “fake” DNA only extends for replication, it is not viable coding for anything.
so if you can sequence a person’s DNA at a certain age, you can generate new stem cells with young DNA and prevent aging.
This is correct, I think that’s why this article talks about bad funtion of dna, iven they don’t say nothing about it here, but thats the reason of why in some point of a long life our organs don’t work right.
When we are young, we live the moment and we think that moment is our eternity and we will live forever (this helps!) when we get old, we miss those past moments and we think we have no more, we think that the current moment is the last one and that it is too short, and we will die soon.
We are a machine that reconstructs itself every moment using food energy as the rebuilding blocks. With this hard work everyday, some mechanisms of that machine eventually breaks and becomes unable to reconstruct itself. It ages. If it is an important mechanism in the whole system, a dominoe effect is triggered and the whole body is comprimised. Take the heart, for instance. If it does not feed itself with oxigenated blood in the first place, it degrades quickly and takes the whole body away with it.
I believe that thinking positively (as the young ones that think they will live forever) is a kind of fuel that helps to regenerate our bodies. Those who think negatively (like some elders) have a broken mechanism already (but they can fix it, if they wish).
The only way to stop aging is by placing the reconstructing system outside the body. One part of this system is, in some way, outside the body and, currently, it is the only one we have at our disposal to help us to live longer: our mind. Try it.
Over the lifespan of an individual, human body cells have the ability to regenerate the tissues. The regenerative power of tissues and organs declines as we age. Adult stem cells are important as it keeps human tissues healthy by replacing old and damaged cells accumulated over time.This is because of the DNA at the end of chromosomes called telomeres that get shorter with each division. When they run out, the cell dies. As you can see, aging is mostly due to the short span of cells regenerative.
The reasons of aging happens in our body?
The number of stem cells reduces due to environmental factors, among others, mental depression and malnutrition. Decreasing number of stem cells also results in a number of age-related diseases. With Mesenchymal stem cells therapy, the new and young cells will repair and regenerate your body, thereby creating better health benefits.
(Side Note: Mesenchymal stem cells (MSCs) are multipotent cells which have the unique ability of self-renewal. MSCs also divide and proliferate throughout the lifetime of an individual.)
Wharton Jelly of the umbilical cord has been found to be rich in MSCs and it tends to be the most primitive stromal population in the human body. These attributes could potentially be harnessed to increase our body’s defence mechanism. They are also beneficial in terms of enhancement of immune system, prevention of diseases, better organ health and even anti-ageing process.
These attributes also help divide and differentiate into a variety of mesenchymal tissues. The mesenchymal tissues include adipose tissues, tendons and ligaments, skeletal muscle tissues, bone and cartilage tissues and etc. Current stem cell research is generating strong evidences about how healthy stem cells, when under the right conditions or signals, could give rise to differentiated cells. It helps repair a host of ailments that occur because of tissue damage as people age.
Ageing is essential for organisms to continue to evolve over time in response to environmental change. If a species didn’t age then parents would normally out compete with their offspring because they would be better at finding food, shelter and avoiding predation. This would slow the small incremental changes that occur in populations over time due to evolution as a result of mutations. This is less of a disadvantage for populations living in a stable environment but if predators can evolve faster than some of their prey species then those slower evolving species may die out altogether.
This is in the same way that animals that are large in size that may only have one offspring every one or two years can’t respond as quickly to environmental change as those species that produce larger numbers of offspring and as a result have a greater chance of favourable mutations.
We are supposed to live forever but we are dying because of sin. We are spiritual beings and there is a creator. God created everything for his purpose and glory. God created us in his image and likeness. He loves us so much that he does not want us to perish eternally because of sin. For God so loved the world that he gave his one and only son Jesus, for whoever so believes in Him shall not perish but have eternal life. Jesus says .. “I am the way, the truth, and the life. No one comes to the father except thru me”…God loves you and me. If we repent of our sins and accept Jesus as our Lord , we will live forever. Physically we will die because of sin but if we repent and trust in Jesus we will not spend eternity in Hell but in Heaven. There will come a time when we will have new bodies made for eternity. Don’t miss out on this gift that God offers you. Your choice …Heaven or Hell? God loves you and He wants you to be in Heaven , a better place. He does not want you to be in Hell. Don’t miss out on this….repent from your sin and trust and follow Jesus..this is the only answerbto what your searching for. You can explain all life forms or dna but God made all these, so don’t miss out on Jesus…
How do cells age and die if they are dividing into new cells? - Biology
Replication is one of the hallmark features of living matter. The set of processes known as the cell cycle which are undertaken as one cell becomes two has been a dominant research theme in the molecular era with applications that extend far and wide including to the study of diseases such as cancer which is sometimes characterized as a disease of the cell cycle gone awry. Cell cycles are interesting both for the ways they are similar from one cell type to the next and for the ways they are different. To bring the subject in relief, we consider the cell cycles in a variety of different organisms including a model prokaryote, for mammalian cells in tissue culture and during embryonic development in the fruit fly. Specifically, we ask what are the individual steps that are undertaken for one cell to divide into two and how long do these steps take?
Figure 1: The 150 min cell cycle of Caulobacter is shown, highlighting some of the key morphological and metabolic events that take place during cell division. M phase is not indicated because in Caulobacter there is no true mitotic apparatus that gets assembled as in eukaryotes. Much of chromosome segregation in Caulobacter (and other bacteria) occurs concomitantly with DNA replication. The final steps of chromosome segregation and especially decatenation of the two circular chromosomes occurs during G2 phase. (Adapted from M. T. Laub et al., Science 290:2144, 2000.)
Arguably the best-characterized prokaryotic cell cycle is that of the model organism Caulobacter crescentus. One of the appealing features of this bacterium is that it has an asymmetric cell division that enables researchers to bind one of the two progeny to a microscope cover slip while the other daughter drifts away enabling further study without obstructions. This has given rise to careful depictions of the ≈150 minute cell cycle (BNID 104921) as shown in Figure 1. The main components of the cell cycle are G1 (first Growth phase, ≈30 min, BNID 104922), where at least some minimal amount of cell size increase needs to take place, S phase (Synthesis, ≈80 min, BNID 104923) where the DNA gets replicated and G2 (second Growth phase, ≈25 min, BNID 104924) where chromosome segregation unfolds leading to cell division (final phase lasting ≈15 min). Caulobacter crescentus provides an interesting example of the way in which certain organisms get promoted to “model organism’’ status because they have some particular feature that renders them particularly opportune for the question of interest. In this case, the cell-cycle progression goes hand in hand with the differentiation process giving readily visualized identifiable stages making them preferable to cell-cycle biologists over, say, the model bacterium E. coli.
The behavior of mammalian cells in tissue culture has served as the basis for much of what we know about the cell cycle in higher eukaryotes. The eukaryotic cell cycle can be broadly separated into two stages, interphase, that part of the cell cycle when the materials of the cell are being duplicated and mitosis, the set of physical processes that attend chromosome segregation and subsequent cell division. The rates of processes in the cell cycle, are mostly built up from many of the molecular events such as polymerization of DNA and cytoskeletal filaments whose rates we have already considered. For the characteristic cell cycle time of 20 hours in a HeLa cell, almost half is devoted to G1 (BNID 108483) and close to another half is S phase (BNID 108485) whereas G2 and M are much faster at about 2-3 hours and 1 hour, respectively (BNID 109225, 109226). The stage most variable in duration is G1. In less favorable growth conditions when the cell cycle duration increases this is the stage that is mostly affected, probably due to the time it takes until some regulatory size checkpoint is reached. Though different types of evidence point to the existence of such a checkpoint, it is currently very poorly understood. Historically, stages in the cell cycle have usually been inferred using fixed cells but recently, genetically-encoded biosensors that change localization at different stages of the cell cycle have made it possible to get live-cell temporal information on cell cycle progression and arrest.
Figure 2: Cell cycle times for different cell types. Each pie chart shows the fraction of the cell cycle devoted to each of the primary stages of the cell cycle. The area of each chart is proportional to the overall cell cycle duration. Cell cycle durations reflect minimal doubling times under ideal conditions. (Adapted from “The Cell Cycle – Principles of Control” by David Morgan.)
How does the length of the cell cycle compare to the time it takes a cell to synthesize its new genome? A decoupling between the genome length and the doubling time exists in eukaryotes due to the usage of multiple DNA replication start sites. For mammalian cells it has been observed that for many tissues with widely varying overall cell cycle times, the duration of the S phase where DNA replication occurs is remarkably constant. For mouse tissues such as those found in the colon or tongue, the S phase varied in a small range from 6.9 to 7.5 hours (BNID 111491). Even when comparing several epithelial tissues across human, rat, mouse and hamster, S phase was between 6 and 8 hours (BNID 107375). These measurements were carried out in the 1960s by performing a kind of pulse-chase experiment with the radioactively labeled nucleotide thymidine. During the short pulse, the radioactive compound was incorporated only into the genome of cells in S phase. By measuring the duration of appearance and then disappearance of labeled cells in M phase one can infer how long S phase lasted The fact that the duration of S phase is relatively constant in such cells is used to this day to estimate the duration of the cell cycle from a knowledge of only the fraction of cells at a given snapshot in time that are in S phase. For example, if a third of the cells are seen in S phase which lasts about 7 hours, the cell cycle time is inferred to be about 7 hours/(1/3) ≈20 hours. Today these kinds of measurements are mostly performed using BrdU as the marker for S phase. We are not aware of a satisfactory explanation for the origin of this relatively constant replication time and how it is related to the rate of DNA polymerase and the density of replication initiation sites along the genome.
The diversity of cell cycles is shown in Figure 2 and depicts several model organisms and the durations and positioning of the different stages of their cell cycles. An extreme example occurs in the mesmerizing process of embryonic development of the fruit fly Drosophila melanogaster. In this case, the situation is different from conventional cell divisions since rather than synthesizing new cytoplasmic materials, mass is essentially conserved except for the replication of the genetic material. This happens in a very synchronous manner for about 10 generations and a replication cycle of the thousands of cells in the embryo, say between cycle 10 and 11, happens in about 8 minutes as shown in Figure 2 (BNID 103004, 103005, 110370). This is faster than the replication times for any bacteria even though the genome is ≈120 million bp long (BNID 100199). A striking example of the ability of cells to adapt their temporal dynamics.
Are You a Candidate for Stem Cell Transplantation?
Stem cell transplantation has been used to cure thousands of people who have cancer, but there are serious risks to this treatment. Before undergoing stem cell transplantation, patients considering this treatment should discuss the risks and benefits with their doctors.
Not all patients are eligible for stem cell transplantation because not all patients can withstand the conditioning regimen and the side effects of treatment. Some patients also may not be eligible for standard transplantation if they have other major health problems. For some of these patients, however, a reduced-intensity allogeneic stem cell transplant may be a treatment option.
In order to determine if a patient is a good candidate for a stem cell transplantation, the patient’s healthcare team will consider
- The patient’s general health and medical condition
- The type and stage of cancer or disease
- Prior treatment history
- The likelihood that the disease will respond to the transplant
- The availability of a suitable donor or the ability to use the patient’s own stem cells.
The risks of stem cell transplantation have decreased with the passing of each decade. Ongoing research is likely to continue to improve the procedure. For some diseases and patients, however, effective new drugs and new types of therapies may be better treatment options than stem cell transplantation. Doctors and their patients will consider many factors when deciding whether stem cell transplantation is the best treatment option.
Treatments classed as regenerative medicine help our natural healing processes work more rapidly and more effectively. These technologies can enable regeneration in missing or damaged tissue that would not ordinarily regrow, producing at least partial regeneration, and in some promising animal studies complete regeneration.
Strategies presently either under development, in clinical trials, or available via medical tourism include stem cell transplants, manipulation of a patient's own stem cells, and the use of implanted scaffold materials that emit biochemical signals to spur stem cells into action. In the field of tissue engineering, researchers have generated sections of tissue outside the body for transplant, using the patient's own cells to minimize the possibility of transplant rejection. Regenerative therapies have been demonstrated in the laboratory to at least partially heal broken bones, bad burns, blindness, deafness, heart damage, worn joints, nerve damage, the lost brain cells of Parkinson's disease, and a range of other conditions. Less complex organs such as the bladder and the trachea have been constructed from a patient's cells and scaffolds and successfully transplanted.
Work continues to bring these advances to patients. Many forms of treatment are offered outside the US and have been for a decade or more in some cases, while within the US just a few of the simple forms of stem cell transplant have managed to pass the gauntlet of the FDA in the past few years.
Some of the most impressive demonstrations of regenerative medicine since the turn of the century have used varying forms of stem cells - embryonic, adult, and most recently induced pluripotent stem cells - to trigger healing in the patient. Most of the earlier successful clinical applications were aimed at the alleviation of life-threatening heart conditions. However, varying degrees of effectiveness have also been demonstrated for the repair of damage in other organs, such as joints, the liver, kidneys, nerves, and so forth.
Stem cells are unprogrammed cells in the human body that can continue dividing forever and can change into other types of cells. Because stem cells can become bone, muscle, cartilage and other specialized types of cells, they have the potential to treat many diseases, including Parkinson's, Alzheimer's, diabetes and cancer. They are found in embryos at very early stages of development (embyonic stem cells) and in some adult organs, such as bone marrow and brain (adult stem cells). You can find more information on stem cells at the following sites:
Embryonic and adult stem cells appear to have different effects, limitations and abilities. The current scientific consensus is that adult stem cells are limited in their utility, and that both embryonic and adult stem cell research will be required to develop cures for severe and degenerative diseases. Researchers are also making rapid progress in reprogramming stem cells and creating embryonic-like stem cells from ordinary cells.
Progress in Stem Cell Research
Stem cell research is a growing, well-funded field, and as a result it is also a hot topic in the press. Not a week goes by without the announcement of a new and amazing advance, but these days most simply slip by without comment. The pace of progress is rapid, and so what would have been trumpeted in the popular science press a decade ago is now routine, carried out in scores of laboratories worldwide.
The first crop of simple stem cell therapies for regenerative medicine has reached widespread availability in the developed world. "Simple," because these therapies are on the level of transfusions. In most cases stem cells are obtained from the patient, then grown in a cell culture and the greatly expanded number of cells injected back into the body. New medicine doesn't get much simpler than that in this day and age. This is merely the start of a revolution in medicine, however, one will grow to become as large and as influential on health as the advent of blood transfusion or the control of common infectious diseases.
If you read enough of the literature, stem cells from your own body begin to sound like a miracle cure-all: extract them, culture them, return them to the body, and injured tissue begins to heal. It isn't anywhere near that straightforward, however, and this throwaway summary hides the many years of hard work by thousands of scientists required to bring us to this point, as well as the further years of hard work that lie ahead. Research continues, with a tone of excitement coming from the scientific community. They know they are onto something big.
Creating Recellularized Organs
Researchers have found what may be a shortcut to the growth of replacement organs from a patient's own stem cells. Called recellularization or decellularization, the process takes a human or animal donor organ and chemically strips the cells from it, leaving only the scaffolding of the extracellular matrix behind. Stem cells from the recipient are then used to repopulate the scaffold, and following the chemical instructions issued by the matrix they create a functioning organ ready for transplant that has little to no risk of rejection.
Since pigs could be used as a source of organs for transplantation, being of about the right size, decellularization is one potential way to eliminate donor organ shortages. The use of animal organs is still some years away from practical implementation, however. Human transplants have moved ahead, and in recent years decellularization has been used in the transplantation of tracheas and bladders in clinical trials. Meanwhile in the laboratory researchers have successfully transplanted decellularized lungs, kidneys, and hearts in mice and rats.
Ultimately decellularization is a stepping stone technology. It is necessary and useful because researchers cannot yet create an entirely artificial scaffold for a complex organ such as a kidney or a heart, complete with all of the chemical cues, fine structure, and mesh of capillaries necessary for its full function. That will become possible, however, at which point donor organs will no longer be needed.
Rejuvenating Aged Stem Cells
Stem cells in the adult body gradually relinquish their job of repair and maintenance with age, eventually causing tissue and organ failure. Based on the past decade of research, this occurs because stem cells become dormant in increasing numbers as rising levels of age-related cellular damage change the mix of chemical signals propagating through tissues. This reaction probably reduces the chances of cancer due to a damaged stem cell running amok, but at the cost of failing tissues. Researchers have found that by restoring signals to a more youthful mix, such as through infusing old tissue with young blood, aged stem cell populations can be restored to action and some of the impact of aging on our tissues might be reversed.
In recent years some of these stem cell activating signals have been identified. Researchers already regularly manipulate the genes and biochemistry of stem cells taken from patients for use in trials of new therapies: there is every reason to expect that future medicine will involve the repair and restoration of aged stem cells either prior to transplant or for existing cell populations within the body.
Regenerative Medicine and Human Longevity
Regenerative medicine will help to produce extended healthy longevity. In the decades ahead clinics will be able to repair some of the mechanical damage caused by aging, such as occurs in worn joints, but more importantly also reverse the decline in function of our stem cells, restoring stem cell maintenance tissue by tissue and organ by organ. At worst a regenerative treatment would be the replacement of a failing organ with a tissue engineered organ built to order from the patient's own cells, thus requiring major surgery, and at best such a treatment would adjust the cells within the failing organ, instructing them to repair the damage, with no surgery needed.
Aging damages every part of our bodies, however, including the stem cells required for regenerative therapies! Thus regenerative medicine on its own is not the full solution to aging: researchers must also address the root causes of age-related degeneration, the damage that accumulates within the molecular machinery of cells, and the metabolic waste products that accumulate in and around cells.
To add to this list, clinics must also become capable of reliably preventing and defeating cancer in all its forms, and also able to repair age-related damage to the brain in situ. Increasing risk of cancer with age cannot be prevented with regenerative medicine, and the brain cannot be removed and replaced with a new tissue engineered organ as will be the case for a liver or even a heart.
All in all these tasks will be a mammoth undertaking. Nonetheless, like all great advances in medicine, this is a worthy and noble cause. Today, hundreds of millions of people live in pain and suffering, and will eventually die, as a result of degenerative conditions of aging, many of which will be alleviated or even cured with near future advances in regenerative medicine. We stand within reach of the means to prevent all this death and anguish. We should rise to this challenge by supporting the researchers and research programs most likely to lead to meaningful progress.
Last updated: May 10th 2014.
When will this so called ''future'' medicine be available for the people who need it now? Are millions of people gonna be dead before the ''future'' medicine comes?
i agree with carlos, this medicine will never be out until, the stupid united states government lets these kinds of medicines into american culture, there are 100's and 1000's of people dying everyday, because of diseases and these medicines have not even made their way into USA, once i grow up and become someone, i will finish what the united states never started. i will upgrade this medicine and find a cure for the horrible diseases that people suffer from. where there's a will there's a way!!
The medical community doesn't want to heal. That takes money out of their pockets. It's all just a money-making scam, not life-saving. My 21yr. old suffered a spinal cord injury. I believe that they could use his "still young" stem cells and help the spinal cord regrow. How long will it take them to figure it out? As long as they keep getting big bucks for NOT figuring it out.
If interested in making this happen in our lifetimes, consider sending this letter, which I sent to my congressman and senators a few years ago:
Thank you for your work on the stimulus plan. Today the markets are the biggest challenge to our economy. Looking forward, spending will be our greatest problem, in particular Social Security and Medicare. Republicans would eliminate them, if they could. Democrats would tax more to try to make them solvent. Most Americans want neither solution.
The alternative solution requires rethinking demographics, and some scientific investment.
The reason 65 was the age set for retirement during the New Deal was because most workers died before 64 in the 1920’s. Life was harder. Most jobs involved heavy physical labor. Healthcare was poorer.
Today’s entitlement problem is not a financial problem. It’s a demographics problem. Today’s average life expectancy is 78 and rising. Healthcare’s better. Work’s less strenuous. But most Americans resist retiring at 78 because they believe old age will rob them of the strength to work that long. But as more retirees are supported by fewer workers, the system will fail.
The alternative is to cure the diseases of old age so people can work at 80 as though they were 60 again. Much work has been started on this, but a concerted effort to finish it is needed now to make a difference in solving the coming entitlement crisis.
Below is a partial list of people working on the problem.
With enough government support, a sustained scientific effort, like that of the space program, could yield substantial benefits before the worst of the demographic pressures hit. Pooling and coordinating the effort in one place, perhaps UVA or Virginia Tech, will provide a focus for information services to persuade an aging work force that working longer and maintaining a good quality of life are compatible.
Ciao e Buona Fortuna,
-Cynthia Kenyon, Hillblom Center for the biology of Aging, San Francisco
-David Scaddon, M.D. & Anthony Komaroff, M.D., Harvard Medical School
-Brian Kennedy & Matt Kaeberlain, University of Washington, Seattle
-T. Keith Blackwell, Harvard Medical School
-Nir Barzilai, Institute for Aging, Albert Einstein College of Medicine, NY,NY
-Thomas Rando, Stanford University
-D. Leanne Jones, Salk Institute for Biological Studies, La Jolla, CA
-Norman Sharpless, University of North Carolina, Chapel Hill
-Woodring Wright, University of Texas Southwestern Medical Center, Dallas
-Hemachandra Reddy, Oregon Health & Science University, Beaverton
-Mark Mattson, National Institute on Aging, Baltimore
-Gencia Corp, UVA, Charlottesville, VA
I wonder if it would be possible to stimulate/genetically alter our bone marrow to constantly produce stem cells and then have these stem cells transported round the body via the circulatory system. If so, then maybe old, damaged cells would be constantly replaced by fresh, new cells, completely free of damage or mutation.
This is truly incredible. To even take a glimpse at what life would be like if people could live indefinitely, so long as trauma is not experienced. We need to create a greater acceptance of this life saving study, and teach those who appose it that it is for the good of everyone and all of mankind. The only possible issue I see with this is when the world's population quadruples every year. Either way, I only see good things coming from stem cell research.
". sound like a miracle cure-all extract them, culture them, return them to the body, and injured tissue begins to heal. It isn't anywhere near that simple. " No, actually it IS that simple. The comments above about the government not wanting people to be cured is absolutely true. Sick people spend a lot of money on drugs. The government will find a way to profit from stem cell therapy, or they won't allow it. Give them time to figure out a scam. In the meantime, if you are ill, go to Panama or another country that has verifiable results from their stem cell therapy. Most of the clinics in Mexico are a bit suspicious, so research carefully and choose wisely.
In Germany, they are using stem cells from patients own body, harvesting them and then injecting them into the patients spinal fluid or brain tissue of stroke victims. Some of them had their stroke 10 years ago. Many of them are now walking due to this cutting edge therapy. Like Carlos Angulo said, "When will this so called 'future' medicine be available for the people who need it now". I had a stroke in 2007 and I wish the US had this therapy now. If this does become available in the US, I doubt if anyone but the rich could afford the treatment. Right now it costs about $60,000 to have the treatment done in Germany and stay there in what is described as a 4 star hotel for approximately 4-10 days. The only thing I don't know is what it would cost to fly to Germany. Actually it would probably be worth going to Germany. As I said, it will be too expensive when it becomes available in the US and insurance probably won't pay for the therapy. I guess we have to go to Germany to obtain this therapy. When will the US catch up to all that Europe has to offer now?
Is regenerative medicine play God or good science? And how do we even know that people want regenerative medicine if there is no data to prove that congressmen should fund it?
I harvested my adult peripherical blood, hoping there are some good stem cells still there, since I am a healthy 72 year old female, and stored it in a cryogenic lab, awaiting expected progress in biogenetic engineering that could give me healthy longevity. This is the least invasive way, of several options of harvesting stem cells, that might serve us well in a not too distant future. Of course, the younger you are, the better, but this field is so new!
I definitely think that regenerative medicine will help us to see the light at the end of the dark tunnel we call despair and possible death. It will also possibly give us all a much better future and help us understand genetic engineering.
Is the stem cell therapy good only for the young? Anything for the old ones?
I have already saved my peripheral HSC about 5 years ago and had one reinfusion which 'cured my neuropathic pain from my cervical spondylosis. I still have a few bags of stem cells that I would reinfuse in the near future for antiaging purpose. I hope to coinfuse allogenic cord derived MSC with my own HSC . Any comments on this?
any reserch done on arthrogryposis? The knees and arms and hands are affected.
i agree with you guys too about that medicine stuff that you guys were talking about.
Is there a stem cell study to regrow nerves in the prostate area?
What would happen if this medicine were to say, mix with the cells of bacteria and/or viruses? Would it make them unstoppable if not appropriately tested? I believe that we need to find a way to access a higher part of our brain to create our own regenerative cells that could heal different types of wounds and in some cases, sickness
can we regenerate the toes which has fully imputed.
hi just thought i should tell you that you have spelt ageing wrong x
In response to Mr. Chua:
I would like to know where Peter Chua got his treatment. I've suffered from cervical spondylosis for over forty years. I don't even know where to begin getting stem cell therapy.
peter chua (first wrote) at April 1, 2012 8:39 PM
I have already saved my peripheral HSC about 5 years ago and had one reinfusion which 'cured my neuropathic pain from my cervical spondylosis. I still have a few bags of stem cells that I would reinfuse in the near future for antiaging purpose. I hope to coinfuse allogenic cord derived MSC with my own HSC . Any comments on this?
I would like to know how possible for a spinal cord injuries of incomplete or complete T12-L1 get cure through stem cells Regeneration?
is there any good places that do stem cell therapy for penis damaged by priapism
To answer how possible for a spinal cord injuries of incomplete or complete T12-L1 get cure through stem cells Regeneration, the difficulty is with the loss of spinal fluid flow in the damaged area of the spinal cord. If the damaged are of the spinal cord has been deprived of spinal fluid, it will atrophy. There are only two fluids in the body that cannot be reproduced or synthesized at the present time: Spinal fluid and Retinal fluid. If there were a way to synthesize spinal fluid, many spinal cord injury patients could have the damaged area of the spinal cord repaired or replaced and then have synthetic fluid placed in the area that has been deprived of fluid however, as we have no artificial or synthetic fluid with which to place in the new spinal apparatus, the flow of fluid will not occur as it does naturally. It is not the same process as replacing a blood vessel and re-establishing the flow of blood throughout a limb. This is what makes spinal injuries so devastating and difficult to reverse.
It appears you can spell ageing or aging either way, both are correct. At any rate very interesting article.
Since this technology, stem cell, is not available in the United States (aging process) where does one have to go out of the U.S. for treatment.
I have been keeping up with this research myself. I am 28 my mother is still around and most my aunts as well. I am hoping this regenerative medicine against aging will be around for their lifetime as well as mine. I think this will be a big breakthrough for all of us and a way to learn how to make life bearable for all of us. Humanity has came along way from cavemen. Stem cells seem to work for the most part. I read articles about Peter Nygard and Gordie Howe. Very interesting stuff.
ok yes there are 100s and thousands of people dying now. so what. there will still be hundreds and thousands of people dying tomorrow. and people dying 40 years from now. you can't rush delicate stuff like this. or else people mess up and one miss calculation means rapidly reproducing cells which causes tumors and possibly cancer
even the allogeneic transplants had boosted P16. I'm hoping that this is all because of the chemo.
Late answer to Sam above. Using LLLT (Low Level Laser Therapy) on the shins is thought to cause migration of stem cells throughout the body, where they tend to find places they are needed. There is research on repairing the hearts of animals in this fashion.
I would really like to see stem cell therapy or gene replacement therapy be applicable to my younger brother's hearing loss. He has never been able to hear since the day he was born. I strongly believe that he has been forced to settle for his lower-paying job at Syracuse University as a grounds keeper because of his hearing loss. It would be wonderful to see what his actual potential could be. He is 56 years old and has a wife and 2 grown daughters. Just before he was born something happened in his brain. He has nerve deafness and now, related to whatever happened before he was born, he is being treated for epileptic seizures. He is such a good man. This should NOT be happening to him.