Strides made toward drug therapy for inherited kidney disease

ScienceDaily (Oct. 27, 2011) — Scientists at UC Santa Barbara have discovered that patients with an inherited kidney disease may be helped by a drug that is currently available for other uses. The findings are published in this week's issue of the Proceedings of the National Academy of Sciences.

Over 600,000 people in the U.S., and 12 million worldwide, are affected by the inherited kidney disease known as autosomal-dominant polycystic kidney disease (ADPKD). The disease is characterized by the proliferation of thousands of cysts that eventually debilitate the kidneys, causing kidney failure in half of all patients by the time they reach age 50. ADPKD is one of the leading causes of renal failure in the U.S.

"Currently, no treatment exists to prevent or slow cyst formation, and most ADPKD patients require kidney transplants or lifelong dialysis for survival," said Thomas Weimbs, director of the laboratory at UCSB where the discovery was made. Weimbs is an associate professor in the Department of Molecular, Cellular and Developmental Biology, and in the Neuroscience Research Institute at UCSB.

Recent work in the Weimbs laboratory has revealed a key difference between kidney cysts and normal kidney tissue. They found that the STAT6 signaling pathway -- previously thought to be mainly important in immune cells -- is activated in kidney cysts, while it is dormant in normal kidneys. Cystic kidney cells are locked in a state of continuous activation of this pathway, which leads to the excessive proliferation and cyst growth in ADPKD.

The drug Leflunomide, which is clinically approved for use in rheumatoid arthritis, has previously been shown to inhibit the STAT6 pathway in cells. Weimbs and his team found that Leflunomide is also highly effective in reducing kidney cyst growth in a mouse model of ADPKD.

"These results suggest that the STAT6 pathway is a promising drug target for possible future therapy of ADPKD," said Weimbs. "This possibility is particularly exciting because drugs that inhibit the STAT6 pathway already exist, or are in active development."

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E. E. Olsan, S. Mukherjee, B. Wulkersdorfer, J. M. Shillingford, A. J. Giovannone, G. Todorov, X. Song, Y. Pei, T. Weimbs. Signal transducer and activator of transcription-6 (STAT6) inhibition suppresses renal cyst growth in polycystic kidney disease. Proceedings of the National Academy of Sciences, 2011; DOI: 10.1073/pnas.1111966108

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Less invasive anesthetic methods better for endovascular aneurysm repair

ScienceDaily (Oct. 27, 2011) — Researchers have identified a safer, more cost effective way to provide anesthesia for patients undergoing endovascular repair of an abdominal aortic aneurysm -- a common, often asymptomatic condition that, if not found and treated, can be deadly.

A new study done by investigators at Wake Forest Baptist Medical Center found that using less invasive spinal, epidural and local/monitored anesthesia care (MAC) is better than general anesthesia for elective endovascular repair of infrarenal abdominal aortic aneurysms (EVAR).

Details of the research appear in the November issue of the Journal of Vascular Surgery, the official publication of the Society for Vascular Surgery.

Aortic aneurysms are abnormal bulges, or "ballooning" in the walls of the aorta, the body's largest artery. Roughly the diameter of a garden hose, this artery brings oxygen-rich blood from the heart to the rest of the body. It extends from the heart down through the chest and abdominal region, where it divides into a blood vessel that supplies each leg. Although an aneurysm can develop anywhere along the aorta, most occur in the section running through the abdomen (abdominal aneurysms). An infrarenal abdominal aortic aneurysm is one that occurs in the belly, below the kidney arteries.

Occasionally an aneurysm may occur because of an area of weakness within the artery wall. An aortic aneurysm is serious because it may rupture, causing life-threatening internal bleeding. The risk of an aneurysm rupturing increases as the aneurysm gets larger. Each year, approximately 15,000 Americans die of a ruptured aortic aneurysm, however the condition is usually asymptomatic until the point of rupture. As such, most aortic aneurysms are unexpectedly identified while a patient is having a computed tomography (CT) scan or ultrasound done for another condition. Men over the age of 65 with a history of ever smoking can have an ultrasound done to specifically screen for aneurysms as part of a "Welcome-to-Medicare" visit with their physician. When detected in time, an aortic aneurysm can usually be repaired with surgery.

Infrarenal abdominal aortic aneurysms make up about 95 percent or more of abdominal aortic aneurysms and, while they occur in both sexes, they are most prevalent in men older than 60, affecting about 3 percent of this population, explained study co-author Matthew S. Edwards, B.A., M.S., M.D., a professor of vascular and endovascular surgery and public health sciences at Wake Forest Baptist.

"That's a lot of people," Edwards said. "If aortic aneurysms aren't repaired, they can burst and 80 to 90 percent of people who have a ruptured aortic aneurysm die. It's necessary for those who are suitable candidates for surgery to have their aneurysms repaired."

EVAR has completely revolutionized the care of aneurysms, allowing doctors to do repairs through two small incisions in the groin, Edwards said. It is currently the most common procedure for repairing aortic aneurysms in the United States. Historic trends have led to general anesthesia being the most common mode of anesthesia used for this procedure, but it is sometimes associated with the development of pneumonia, the need for a breathing tube and other pulmonary complications, he explained.

Other anesthetic techniques can also be used, such as local anesthesia, local anesthesia plus sedation (called "monitored" or "MAC"), spinal anesthesia and epidural anesthesia. According to this study, these other methods result in a shortened hospital stay and fewer pulmonary complications.

"In our study, general anesthesia was associated with increased postoperative length of stay (LOS) and increased complications involving the lungs when compared to the other anesthetic methods," Edwards said.

The researchers collected data on 6,009 patients who had elective EVAR performed between 2005 to 2008 at one of 221 North American hospitals. General anesthesia was used in 4,868 of the cases, while 419 patients had spinal anesthesia during their procedure; 331 had epidural anesthesia; and 391 had local/MAC. Emergency cases and patients who had other procedures being done at the same time that required general anesthesia were excluded from the study.

The team then reviewed the data to evaluate rates of mortality, morbidity and length of stay (LOS), or how long the patient remained in the hospital after the procedure.

The researchers found that general anesthesia was associated with an increase in pulmonary complications when compared to spinal and local/MAC anesthesia. Use of general anesthesia also was associated with a 10 percent increase in LOS for general when compared to spinal anesthesia, and a 20 percent increase when compared to general versus local/MAC anesthesia. Trends toward increased pulmonary complications and LOS were not observed for general versus epidural anesthesia. No significant association between anesthesia type and mortality was observed.

"Our study data suggest that increasing the use of less invasive anesthetic techniques, when appropriate, may limit postoperative complications in EVAR patients," Edwards said.

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Matthew S. Edwards, Jeanette S. Andrews, Angela F. Edwards, Racheed J. Ghanami, Matthew A. Corriere, Philip P. Goodney, Christopher J. Godshall, Kimberley J. Hansen. Results of endovascular aortic aneurysm repair with general, regional, and local/monitored anesthesia care in the American College of Surgeons National Surgical Quality Improvement Program database. Journal of Vascular Surgery, 2011; 54 (5): 1273 DOI: 10.1016/j.jvs.2011.04.054

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Governments must plan for migration in response to climate change, researchers say

ScienceDaily (Oct. 27, 2011) — Governments around the world must be prepared for mass migrations caused by rising global temperatures or face the possibility of calamitous results, say University of Florida scientists on a research team reporting in the Oct. 28 edition of Science.

If global temperatures increase by only a few of degrees by 2100, as predicted by the U.N. Intergovernmental Panel on Climate Change, people around the world will be forced to migrate. But transplanting populations from one location to another is a complicated proposition that has left millions of people impoverished in recent years. The researchers say that a word of caution is in order and that governments should take care to understand the ramifications of forced migration.

A consortium of 12 scientists from around the world, including two UF researchers, gathered last year at the Rockefeller Foundation's Bellagio Center to review 50 years of research related to population resettlement following natural disasters or the installation of infrastructure development projects such as dams and pipelines. The group determined that resettlement efforts in the past have left communities in ruin, and that policy makers need to use lessons from the past to protect people who are forced to relocate because of climate change.

"The effects of climate change are likely to be experienced by as many people as disasters," UF anthropologist Anthony Oliver-Smith said. "More people than ever may be moving in response to intense storms, increased flooding and drought that makes living untenable in their current location."

"Sometimes the problem is simply a lack of regard for the people ostensibly in the way of progress," said Oliver-Smith, an emeritus professor who has researched issues surrounding forced migration for more than 30 years. But resettlements frequently fail because the complexity of the task is underestimated. "Transplanting a population and its culture from one location to another is a complex process -- as complicated as brain surgery," he said.

"It's going to be a matter of planning ahead now," said Burt Singer, a courtesy faculty member at the UF Emerging Pathogens Institute who worked with the research group. He too has studied issues related to population resettlement for decades.

Singer said that regulatory efforts promoted by the International Finance Corporation, the corporate lending arm of the World Bank, are helping to ensure the well-being of resettled communities in some cases. But as more people are relocated -- especially very poor people with no resources -- financing resettlement operations in the wake of a changing climate could become a real challenge.

Planning and paying for resettlement is only part of the challenge, Oliver-Smith said. "You need informed, capable decision makers to carry out these plans," he said. A lack of training and information can derail the best-laid plans. He said the World Bank increasingly turns to anthropologists to help them evaluate projects and outcomes of resettlement.

"It is a moral imperative," Oliver-Smith said. Also, a simple cost-benefit analysis shows that doing resettlement poorly adds to costs in the future. Wasted resources and the costs of malnutrition, declining health, infant and elder mortality, and the destruction of families and social networks should be included in the total cost of a failed resettlement, he said.

Oliver-Smith said the cautionary tales of past failures yield valuable lessons for future policy makers, namely because they point out many of the potential pitfalls than can beset resettlement projects. But they also underscore the fact that there is a heavy price paid by resettled people, even in the best-case scenarios.

In the coming years, he said, many projects such as hydroelectric dams and biofuel plantations will be proposed in the name of climate change, but moving people to accommodate these projects may not be the simple solution that policy makers sometimes assume.

A clear-eyed review of the true costs of forced migration could alert governments to the complexities and risks of resettlement.

"If brain surgeons had the sort of success rate that we have had with resettling populations, very few people would opt for brain surgery," he said.

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The above story is reprinted from materials provided by University of Florida. The original article was written by Donna Hesterman.

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A. de Sherbinin, M. Castro, F. Gemenne, M. M. Cernea, S. Adamo, P. M. Fearnside, G. Krieger, S. Lahmani, A. Oliver-Smith, A. Pankhurst, T. Scudder, B. Singer, Y. Tan, G. Wannier, P. Boncour, C. Ehrhart, G. Hugo, B. Pandey, and G. Shi. Preparing for Resettlement Associated with Climate Change. Science, 2011; 334 (6055): 456-457 DOI: 10.1126/science.1208821

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Step toward unraveling Alzheimer's disease

ScienceDaily (Oct. 27, 2011) — Scientists outline new methods for better understanding links between specific proteins and the risks associated with Alzheimer's disease in an article co-authored by University of Alabama researchers and publishing in Science Express.

In experiments using a series of model organisms, including yeast, microscopic roundworms and rats, the researchers show how basic mechanisms inside cells are disrupted when a specific human protein, known as the amyloid beta peptide, fails to properly fold. This study also shows the role a second protein, referred to by the scientists as PICALM, can play in modifying the problem.

"By using these yeast models, in combination with worms, we really are hopeful of finding a way by which we can understand and maybe combat Alzheimer's disease more rapidly," said Dr. Guy Caldwell, professor of biological sciences at The University of Alabama and one of three UA-authors on the Science article.

The research involved scientists from several universities and research institutes, including the Whitehead Institute and Massachusetts Institute of Technology, where the lead author, Dr. Sebastian Treusch, is affiliated. Treusch works in the lab of Dr. Susan Lindquist, a renowned expert in cell biology and collaborator with Caldwell on a grant from the Howard Hughes Medical Institute that funded part of this research.

While the repeated misfoldings of amyloid beta peptides within the human brain were previously known to trigger the death of neurons, resulting in Alzheimer's, Caldwell says the underlying mechanisms of toxicity weren't as well understood.

Properly functioning cells must efficiently deliver proteins and chemicals to other parts of the cell, Caldwell said. This research shows how the amyloid beta peptide interrupts a specific cellular pathway called endocytosis, preventing the delivery of other needed proteins to other parts of the cell.

"Understanding what is going wrong inside a cell, or what pathways or proteins might be directly linked to the mechanisms that are involved in Alzheimer's, is really a much more fruitful strategy for drug development."

Information drawn from the brains of deceased Alzheimer's patients, who previously donated their bodies to science, was also significant in the effort, Caldwell said.

Rapid advances in DNA sequencing methods and human genetic population studies are generating an overwhelming number of leads for researchers; those genetic studies, taken in combination with advantageous attributes of simple organisms, can reveal basic functions of genes and proteins and can be an insightful combination, Caldwell says.

"What this paper shows is that simple systems, like yeast and worms, can be engineered to discern mechanisms that might be associated with complex human diseases, and, by that, we may accelerate the path of discovery for advancing therapeutics for those diseases."

UA's lead author is Dr. Shusei Hamamichi, a former post-doctoral researcher in the Caldwell lab who earned his doctorate at UA while working alongside Caldwell and Dr. Kim Caldwell, also a co-author of the paper and an associate professor of biological sciences at UA.

In the paper's conclusion, the researchers describe the potential significance of the development in light of the challenges faced in understanding and treating Alzheimer's disease.

"The treatments available for AD are few and their efficacy limited," the scientists wrote. "Determining how best to rescue neuronal function in the context of the whole brain is a problem of staggering proportions."

"On a personal level," Caldwell said, "so many of us have been affected by family or loved ones who have suffered from Alzheimer's. It's a great privilege for us to be able to contribute to the respective avenues of our understanding of the disease. It's a devastating disorder. The societal cost of Alzheimer's disease is tremendous."

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Sebastian Treusch, Shusei Hamamichi, Jessica L. Goodman, Kent E. S. Matlack, Chee Yeun Chung, Valeriya Baru, Joshua M. Shulman, Antonio Parrado, Brooke J. Bevis, Julie S. Valastyan, Haesun Han, Malin Lindhagen-Persson, Eric M. Reiman, Denis A. Evans, David A. Bennett, Anders Olofsson, Philip L. Dejager, Rudolph E. Tanzi, Kim A. Caldwell, Guy A. Caldwell, Susan Lindquist. Functional Links Between Aß Toxicity, Endocytic Trafficking, and Alzheimer’s Disease Risk Factors in Yeast. Science, 2011; DOI: 10.1126/science.1213210

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NASA launches multi-talented Earth-observing satellite

ScienceDaily (Oct. 28, 2011) — NASA's newest Earth-observing satellite soared into space early Oct. 28, 2011 aboard a Delta II rocket after liftoff at 5:48 a.m. EDT from Space Launch Complex 2 at Vandenberg Air Force Base in California.

NASA's National Polar-orbiting Operational Environmental Satellite System Preparatory Project, or NPP, successfully separated from the Delta II 58 minutes after launch, and the first signal was acquired by the Tracking and Data Relay Satellite System. NPP's solar array deployed 67 minutes after launch to provide the satellite with electrical power. NPP is on course to reach its sun-synchronous polar orbit 512 miles (824 km) above Earth.

"NPP is critical to our understanding of Earth's processes and changes," said NASA Deputy Administrator Lori Garver. "Its impact will be global and builds on 40 years of work to understand our complex planet from space. NPP is part of an extremely strong slate of current and future innovative NASA science missions that will help us win the future as we make new discoveries."

NPP carries five science instruments, including four new state-of-the-art sensors, which will provide critical data to help scientists understand the dynamics of long-term climate patterns and help meteorologists improve short-term weather forecasts. The mission will extend more than 30 key long-term datasets NASA has been tracking, including measurements of the ozone layer, land cover, and ice cover.

NPP serves as a bridge mission between NASA's Earth Observing System (EOS) of satellites and the next-generation Joint Polar Satellite System, a National Oceanic and Atmospheric Administration (NOAA) program that will also collect weather and climate data.

Scientists will use NPP data to extend and improve upon EOS data records. These satellites have provided critical insights into the dynamics of the entire Earth system, including clouds, oceans, vegetation, ice, solid Earth and atmosphere. NPP will allow scientists to extend the continuous satellite record needed to detect and quantify global environmental changes.

"The measurements from NPP will benefit science and society for many years to come," said Michael Freilich, director of NASA's Earth Science Division. "NPP will help improve weather forecasts, enable unique scientific insights, and allow more accurate global environmental predictions. I'm confident that the strong partnerships forged in the NPP program between NASA and NOAA, industry, and the research and applications communities will ensure the success of the mission."

The satellite will be operated from the NOAA Satellite Operations Facility in Suitland, Md. NASA will operate NPP for the first three months after launch while the satellite and instrument are checked out. NPP operations will then be turned over to NOAA and the JPSS program for the remainder of the mission.

NPP data will be transmitted once every orbit to a ground station in Svalbard, Norway, and to direct broadcast receivers around the world. The data will be sent back to the United States via fiber optic cable to the NOAA Suitland facility. NPP data is then processed into data records that NASA and NOAA will make available through various data archives.

The Delta II launch vehicle that delivered NPP into orbit also deployed auxiliary payloads within 98 minutes after launch. The five small "CubeSat" research payloads are the third in a series of NASA Educational Launch of Nanosatellite missions, known as ELaNa missions.

The NPP mission is managed by NASA's Goddard Space Flight Center in Greenbelt, Md., for the Earth Science Division of the Science Mission Directorate at NASA Headquarters in Washington. The Joint Polar Satellite System program provides the NPP ground system. NOAA will provide operational support for the mission. Launch management is the responsibility of the NASA Launch Services Program at the Kennedy Space Center in Florida.

For more information about NPP, visit: http://www.nasa.gov/npp

For more information about the ELaNa III mission, visit: http://go.nasa.gov/tgbuVn

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New oncolytic virus shows improved effectiveness in preclinical testing

ScienceDaily (Oct. 27, 2011) — A new fourth-generation oncolytic virus designed to both kill cancer cells and inhibit blood-vessel growth has shown greater effectiveness than earlier versions when tested in animal models of human brain cancer.

Researchers at the Ohio State University Comprehensive Cancer Center -- Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC -- James) are developing the oncolytic virus as a treatment for glioblastoma, the most common and deadly form of brain cancer (average survival: 15 months after diagnosis).

The new oncolytic virus, called 34.5ENVE, improved survival of mice with transplanted human glioblastoma tumors by 50 percent in a majority of cases compared with the previous-generation oncolytic virus.

The study was published online in the journal Molecular Therapy.

"These findings show the amazing therapeutic efficacy of this new oncolytic virus against four different glioblastoma models in animals," says cancer researcher Dr. Balveen Kaur, associate professor of neurological surgery, and a member of the OSUCCC -- James viral oncology research program.

The new oncolytic virus is engineered to replicate in cells that express the protein nestin. First identified as a marker for neuronal stem cells, nestin is also expressed in glioblastoma and other malignancies including gastrointestinal, pancreatic, prostate and breast cancer.

"We believe that nestin-driven oncolytic viruses will prove valuable for the treatment of many types of cancer," Kaur says.

The new oncolytic virus also carries a gene to inhibit tumor blood-vessel growth. That gene, called Vstat120, was added to increase its anti-tumor effectiveness and prolong the virus's presence within tumors.

In this study of eight animals with intracranial tumors, six lived longer than 80 days, and these were later found to be tumor free. By comparison, control mice survived a median of 20 days, and mice treated with a first-, a second-, and a third-generation oncolytic virus survived 33, 34 and 53 days, respectively.

"Magnetic resonance imaging and histological analyses revealed extensive tumor destruction in animals treated with 34.5 ENVE," says Kaur, who is also chief of Ohio State's Dardinger Laboratory of Neurosciences. "We hope that we can soon evaluate the safety of this virus in patients with cancer."

Funding from the National Institute for Neurological Disorders and Stroke, National Cancer Institute and National Research Foundation of Korea supported this research.

Other researchers involved in this study were Ji Young Yoo, Amy Haseley, Anna Bratasz, E. Antonio Chiocca, Jianying Zhang and Kimerly Powell of The Ohio State University.

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Ji Young Yoo, Amy Haseley, Anna Bratasz, E Antonio Chiocca, Jianying Zhang, Kimerly Powell, Balveen Kaur. Antitumor Efficacy of 34.5ENVE: A Transcriptionally Retargeted and “Vstat120”-expressing Oncolytic Virus. Molecular Therapy, 2011; DOI: 10.1038/mt.2011.208

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Do bacteria age? Biologists discover the answer follows simple economics

ScienceDaily (Oct. 27, 2011) — When a bacterial cell divides into two daughter cells and those two cells divide into four more daughters, then 8, then 16 and so on, the result, biologists have long assumed, is an eternally youthful population of bacteria. Bacteria, in other words, don't age -- at least not in the same way all other organisms do.

But a study conducted by evolutionary biologists at the University of California, San Diego questions that longstanding paradigm. In a paper published in the November 8 issue of the journal Current Biology, they conclude that not only do bacteria age, but that their ability to age allows bacteria to improve the evolutionary fitness of their population by diversifying their reproductive investment between older and more youthful daughters. An advance copy of the study appears this week in the journal's early online edition.

"Aging in organisms is often caused by the accumulation of non-genetic damage, such as proteins that become oxidized over time," said Lin Chao, a professor of biology at UC San Diego who headed the study. "So for a single celled organism that has acquired damage that cannot be repaired, which of the two alternatives is better -- to split the cellular damage in equal amounts between the two daughters or to give one daughter all of the damage and the other none?"

The UC San Diego biologists' answer -- that bacteria appear to give more of the cellular damage to one daughter, the one that has "aged," and less to the other, which the biologists term "rejuvenation" -- resulted from a computer analysis Chao and colleagues Camilla Rang and Annie Peng conducted on two experimental studies. Those studies, published in 2005 and 2010, attempted unsuccessfully to resolve the question of whether bacteria aged. While the 2005 study showed evidence of aging in bacteria, the 2010 study, which used a more sophisticated experimental apparatus and acquired more data than the previous one, suggested that they did not age.

"We analyzed the data from both papers with our computer models and discovered that they were really demonstrating the same thing," said Chao. "In a bacterial population, aging and rejuvenation goes on simultaneously, so depending on how you measure it, you can be misled to believe that there is no aging."

In a separate study, the UC San Diego biologists filmed populations of E. coli bacteria dividing over hundreds of generations and confirmed that the sausage-shaped bacteria divided each time into daughter cells that grew elongated at different rates -- suggesting that one daughter cell was getting all or most of the cellular damage from its mother while the other was getting little or none. Click this link to watch the time-lapse film of one bacterium dividing over 10 generations into 1,000 bacteria in a period of five hours and see if you can see any differences.

"We ran computer models and found that giving one daughter more the damage and the other less always wins from an evolutionary perspective," said Chao. "It's analogous to diversifying your portfolio. If you could invest $1 million at 8 percent, would that provide you with more money than splitting the money and investing $500,000 at 6 percent and $500,000 at 10 percent?"

"After one year it makes no difference," he added. "But after two years, splitting the money into the two accounts earns you more and more money because of the compounding effect of the 10 percent. It turns out that bacteria do the same thing. They give one daughter a fresh start, which is the higher interest-bearing account and the other daughter gets more of the damage."

Although E. coli bacteria appear to divide precisely down the middle into two daughter cells, the discovery that the two daughters eventually grow to different lengths suggests that bacteria do not divide as symmetrically as most biologists have come to believe, but that their division is really "asymmetrical" within the cell.

"There must be an active transport system within the bacterial cell that puts the non-genetic damage into one of the daughter cells," said Chao. "We think evolution drove this asymmetry. If bacteria were symmetrical, there would be no aging. But because you have this asymmetry, one daughter by having more damage has aged, while the other daughter gets a rejuvenated start with less damage."

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The above story is reprinted from materials provided by University of California - San Diego. The original article was written by Kim McDonald.

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Camilla U. Rang, Annie Y. Peng, Lin Chao. Temporal Dynamics of Bacterial Aging and Rejuvenation. Current Biology, 27 October 2011 DOI: 10.1016/j.cub.2011.09.018

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