Teacher:In this task, you are given a text of many news articles seperated by special token "|||||". Your task is to summarize them.
Teacher: Now, understand the problem? Solve this instance: Signs of aging have been partially reversed in mice, according to research led by scientists at the Salk Institute for Biological Studies. The study indicates that rejuvenation, long considered science fiction, may one day become reality. 
  
 Mice genetically engineered to replicate progeria, a disease of accelerated aging, lived 30 percent longer after receiving the treatment. And normally aged mice experienced improvement in pancreatic and muscle function, along with better wound healing. 
  
 The results suggest that aging in humans may likewise be a plastic process that can be controlled, said noted stem cell scientist Juan Carlos Izpisúa Belmonte, who led the study along with Salk Institute colleague Alejandro Ocampo. 
  
 The study, published Thursday in the journal Cell, is a proof of principle, the scientists cautioned. Years of research lie ahead before any therapy can be tried in people. The complete study can be found at j.mp/belmonteaging. 
  
 The researchers accomplished this feat in mice genetically engineered to make four proteins that reprogram adult cells to an embryonic-like state. 
  
 A decade ago, the Japanese researcher Shinya Yamanaka used these proteins -- Oct4, Sox2, Klf4, and c-Myc -- to make what are called induced pluripotent stem cells, or IPS cells. These act very much like embryonic stem cells, but can be made from common adult cells such as those in skin. Pluripotent means the cells can become nearly any type of cell in the body. In 2012, Yamanaka shared a Nobel Prize for his work. 
  
 Two groups of mice were tested. One were mice that were normally aged to 12 months (most breeds of mice can naturally live to about 18 months to 2 years). 
  
 The second consisted of mice genetically engineered to model a fatal childhood disease, Hutchinson-Gilford progeria syndrome. This disease is characterized by heart disease, joint stiffness, hair loss and other conditions generally experienced by older people. Those affected usually die before adulthood. 
  
 A full reprogramming would have been fatal to the mice, because the adult cells would have lost their function. However, the scientists engineered the mice to produce these “Yamanaka factors” only when given the antibiotic doxycycline, providing an on-off switch. 
  
 When the mice were exposed to the Yamanaka factors for two days a week, every week, they experienced changes in the DNA that removed some of the characteristic “epigenetic” marks of aging. These marks are chemical groups added to or removed from the core DNA molecule. These modifications or their removal turn genes off and on, but don’t change their underlying sequence. 
  
 Signs of safety 
  
 Izpisúa Belmonte said the improvement in the progeria model mice is notable because the treatment didn’t repair the mutation in the DNA, but only altered the epigenetic pattern of gene activation to more closely resemble that of younger cells. 
  
 Also notably, the animals didn’t develop tumors, a known risk with cellular reprogramming, said Pradeep Reddy, another Salk researcher and study co-author. 
  
 Izpisúa Belmonte said reprogramming works in discrete stages, so a brief exposure doesn’t erase the cells’ identity, but rolls them back to a more youthful state 
  
 “We know from in vitro studies that the factors need to be there for more time to induce full reprogramming,” he said. “So the cells never go back to a pluripotent state.” 
  
 Amy Firth, a stem cell researcher at the University of Southern California, said the work is “exciting.” 
  
 “I used to work at the Salk Institute as a postdoc, so I was very familiar with Juan Carlos Izpisúa Belmonte’s research,” said Firth, assistant professor of medicine at the Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC. “It’s great to see some new data.” 
  
 The study is solid, because the researchers approached the issue from several different avenues to demonstrate rejuvenation through the reprogramming factors, Firth said. 
  
 The researchers not only demonstrated rejuvenation in cells, but went to whole animals to demonstrate actual benefit, she said. 
  
 Kristin Baldwin, a stem cell scientist at The Scripps Research Institute, reacted similarly to Firth in describing the Salk team's feat. 
  
 "It's an exciting, remarkable study, showing that you can in vivo tinker with the marks of aging a little bit ... so that you do seem to improve the function of the cells," said Baldwin, an investigator at TSRI's Dorris Neuroscience Center. 
  
 Baldwin said she and colleagues approached the aging problem from the opposite direction in a study published Dec. 12 in the journal Nature Biotechnology. It’s available at j.mp/ipsaging. 
  
 That study examined epigenetic markers of age in artificial embryonic stem cells. Called induced pluripotent stem cells, they are created from adult or "somatic" cells in the body, such as from skin and blood. These IPS cells act much like human embryonic stem cells, but weren’t derived from a human embryo. 
  
 Researchers in that study found the age markers were retained to varying degrees in IPS cells, suggesting they might not be fully restored to a youthful state. This means some of these cells might not be well suited for therapy, such as replacing a patient’s injured or diseased tissues. 
  
 Baldwin said the problems can be dealt with by careful screening of IPS cells. If one lineage of cells is unsuitable, scientists can create another set of cells, and continue until they find an acceptable line. 
  
 Other factors in aging 
  
 Aging involves other changes besides the epigenetic ones, Baldwin and Izpisúa Belmonte said. These include DNA damage from radiation or mutagenic chemicals, shortening of the protective chromosome ends called telomeres, and the accumulation of cellular debris. 
  
 What the study helps demonstrate is that a substantial amount of aging appears linked to these epigenetic changes, Izpisúa Belmonte said. 
  
 "The caveat, which is what we showed in our study, is that they're not going to be able to reverse the somatic mutations that are accumulating during aging," Baldwin said. "Nobody knows how much of those contribute to the negative effects of aging.” ||||| The aging process is clocklike in the sense that a steady accumulation of changes eventually degrades the efficiency of the body’s cells. In one of the deepest mysteries of biology, the clock’s hands are always set back to zero at conception: However old the parents and their reproductive cells, a fertilized egg is free of all marks of age. 
  
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 Ten years ago, the Japanese biologist Shinya Yamanaka amazed researchers by identifying four critical genes that reset the clock of the fertilized egg. The four genes are so powerful that they will reprogram even the genome of skin or intestinal cells back to the embryonic state. Dr. Yamanaka’s method is now routinely used to change adult tissue cells into cells very similar to the embryonic stem cells produced in the first few divisions of a fertilized egg. 
  
 Scientists next began to wonder if the four Yamanaka genes could be applied not just to cells in glassware but to a whole animal. The results were disastrous. As two groups of researchers reported in 2013 and 2014, the animals all died, some because their adult tissue cells had lost their identity and others from cancer. Embryonic cells are primed for rapid growth, which easily becomes uncontrolled. 
  
 But at the Salk Institute, Juan Carlos Izpisua Belmonte had been contemplating a different approach. He has long been interested in regeneration, the phenomenon in which certain animals, like lizards and fish, can regenerate lost tails or limbs. The cells near the lost appendage revert to a stage midway between an embryonic cell, which is open to all fates, and an adult cell, which is committed to being a particular type of cell, before rebuilding the missing limb. 
  
 This partial reprogramming suggested to him that reprogramming is a stepwise process, and that a small dose of the Yamanaka factors might rejuvenate cells without the total reprogramming that converts cells to the embryonic state. 
  
 With Alejandro Ocampo and other Salk researchers, Dr. Izpisua Belmonte has spent five years devising ways to deliver a nonlethal dose of Yamanaka factors to mice. The solution his team developed was to genetically engineer mice with extra copies of the four Yamanaka genes, and to have the genes activated only when the mice received a certain drug in their drinking water, applied just two days a week. 
  
 The Salk team worked first with mice that age prematurely, so as to get quick results. “What we saw is that the animal has fewer signs of aging, healthier organs, and at the end of the experiment we could see they had lived 30 percent longer than control mice,” Dr. Izpisua Belmonte said. 
  
 Photo 
  
 The team also saw improved organ health in normal mice but, because the mice are still living, could not yet say if longevity was extended. 
  
 Dr. Izpisua Belmonte believes these beneficial effects have been obtained by resetting the clock of the aging process. The clock is created by the epigenome, the system of proteins that clads the cell’s DNA and controls which genes are active and which are suppressed. 
  
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 When an egg develops into a whole animal, the epigenome plays a critical role by letting a heart cell, say, activate just the genes specific to its role but switching off all the genes used by other types of cells. This process lets the embryo’s cells differentiate into all the various types of cells required by the adult body. 
  
 The epigenome is also involved throughout life in maintaining each cell and letting it switch genes on and off as required for its housekeeping duties. The epigenome itself is controlled by agents that add or subtract chemical groups, known as marks, to its proteins. 
  
 Only in the last few years have biologists come to realize that the state of the epigenome may be a major cause of aging. If the epigenome is damaged, perhaps by accumulating too many marks, the cell’s efficiency is degraded. 
  
 Dr. Izpisua Belmonte sees the epigenome as being like a manuscript that is continually edited. “At the end of life there are many marks and it is difficult for the cell to read them,” he said. 
  
 What the Yamanaka genes are doing in his mice, he believes, is eliminating the extra marks, thus reverting the cell to a more youthful state. 
  
 The Salk biologists “do indeed provide what I believe to be the first evidence that partial reprogramming of the genome ameliorated symptoms of tissue degeneration and improved regenerative capacity,” Dr. Vijg said. 
  
 But he cautioned the fast-aging mice used in the study might not be fully representative of ordinary aging. 
  
 Dr. Guarente said it was more likely that the Yamanaka genes were not erasing the epigenomic marks directly, but rather were activating the genes which are responsible for the immense health and vitality of embryonic cells. This gene activation is a natural function of the Yamanaka factors. It is these embryonic pro-health genes that are rejuvenating the tissues in the mice, Dr. Guarente suggested, and causing changes in the epigenome through their activity. 
  
 Thomas A. Rando, an expert on stem cells and aging at Stanford, said that it should be possible in theory to uncouple the differentiation program and the aging process, and that “if that’s what’s happening, this is the first demonstration of that.” 
  
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 Dr. Izpisua Belmonte said he was testing drugs to see if he could achieve the same rejuvenation as with the Yamanaka factors. The use of chemicals “will be more translatable to human therapies and clinical applications,” he said. |||||
Student:
In the future, we may be able to treat aging itself, rather than just the diseases that come with it, the Guardian reports. “Our study shows that aging may not have to proceed in one single direction," researcher Juan Carlos Izpisua Belmonte says. "With careful modulation, aging might be reversed.” According to the New York Times, the study—published Thursday in Cell—is science's first attempt at combating aging by rejiggering the genome. In the study, researchers genetically engineered mice to produce four proteins that revert cells back to their embryonic state, the San Diego Union-Tribune reports. They then created an on/off switch for the proteins to keep cells from permanently reverting to their embryonic state and becoming useless. After six weeks of treatment, mice genetically engineered to have the rapid-aging disease progeria lived 30% longer. Mice without progeria had better functioning hearts, pancreases, and muscles, as well as improved healing of wounds, following treatment. Basically, they seemed younger. The study's results were described by outside experts as "exciting" and "huge." While similar treatments for humans are likely at least a decade away, researchers believe they could be used to slow down the body's internal clock and control at least some aspects of aging. They won't, however, "lead to immortality," says Izpisua Belmonte (Meanwhile, optimistic women may live longer.)