lroot on August 11th, 2017


Sunbathers may want to avoid midnight snacks before catching some rays.

A study in mice from the O’Donnell Brain Institute and UC Irvine shows that eating at abnormal times disrupts the biological clock of the skin, including the daytime potency of an enzyme that protects against the sun’s harmful ultraviolet radiation.

Although further research is needed, the finding indicates that people who eat late at night may be more vulnerable to sunburn and longer term effects such as skin aging and skin cancer, said Dr. Joseph S. Takahashi, Chairman of Neuroscience at UT Southwestern Medical Center’s Peter O’Donnell Jr. Brain Institute.

“This finding is surprising. I did not think the skin was paying attention to when we are eating,” said Dr. Takahashi, also an Investigator with the Howard Hughes Medical Institute.

The study showed that mice given food only during the day an abnormal eating time for the otherwise nocturnal animals sustained more skin damage when exposed to ultraviolet B (UVB) light during the day than during the night. This outcome occurred, at least in part, because an enzyme that repairs UV-damaged skin xeroderma pigmentosum group A (XPA) shifted its daily cycle to be less active in the day.

Mice that fed only during their usual evening times did not show altered XPA cycles and were less susceptible to daytime UV rays.

“It is likely that if you have a normal eating schedule, then you will be better protected from UV during the daytime,” said Dr. Takahashi, holder of the Loyd B. Sands Distinguished Chair in Neuroscience. “If you have an abnormal eating schedule, that could cause a harmful shift in your skin clock, like it did in the mouse.”

Previous studies have demonstrated strong roles for the body’s circadian rhythms in skin biology. However, little had been understood about what controls the skin’s daily clock.

The latest research published in Cell Reports documents the vital role of feeding times, a factor that scientists focused on because it had already been known to affect the daily cycles of metabolic organs such as the liver.

The study found that besides disrupting XPA cycles, changing eating schedules could affect the expression of about 10 percent of the skin’s genes.

However, more research is needed to better understand the links between eating patterns and UV damage in people, particularly how XPA cycles are affected, said Dr. Bogi Andersen of University of California, Irvine, who led the collaborative study with Dr. Takahashi.

“It’s hard to translate these findings to humans at this point,” said Dr. Andersen, Professor of Biological Chemistry. “But it’s fascinating to me that the skin would be sensitive to the timing of food intake.”

Dr. Takahashi, noted for his landmark discovery of the Clock gene regulating circadian rhythms, is researching other ways in which eating schedules affect the biological clock. A study earlier this year reinforced the idea that the time of day food is eaten is more critical to weight loss than the amount of calories ingested. He is now conducting long-term research measuring how feeding affects aging and longevity.

Reference: 1Hong Wang, Elyse van Spyk, Qiang Liu, Mikhail Geyfman, Michael L. Salmans, Vivek Kumar, Alexander Ihler, Ning Li, Joseph S. Takahashi, Bogi Andersen. Time-Restricted Feeding Shifts the Skin Circadian Clock and Alters UVB-Induced DNA Damage. Cell Reports, 2017; 20 (5): 1061 DOI: 10.1016/j.celrep.2017.07.022

lroot on August 7th, 2017


Researchers at The Ohio State University Wexner Medical Center and Ohio State’s College of Engineering have developed a new technology, Tissue Nanotransfection (TNT), that can generate any cell type of interest for treatment within the patient’s own body. This technology may be used to repair injured tissue or restore function of aging tissue, including organs, blood vessels and nerve cells. Results of the regenerative medicine study were published in the journal Nature Nanotechnology.

“By using our novel nanochip technology, injured or compromised organs can be replaced. We have shown that skin is a fertile land where we can grow the elements of any organ that is declining,” said Dr. Chandan Sen, director of Ohio State’s Center for Regenerative Medicine & Cell Based Therapies, who co-led the study with L. James Lee, professor of chemical and biomolecular engineering with Ohio State’s College of Engineering in collaboration with Ohio State’s Nanoscale Science and Engineering Center.

Researchers studied mice and pigs in these experiments. In the study, researchers were able to reprogram skin cells to become vascular cells in badly injured legs that lacked blood flow. Within one week, active blood vessels appeared in the injured leg, and by the second week, the leg was saved. In lab tests, this technology was also shown to reprogram skin cells in the live body into nerve cells that were injected into brain-injured mice to help them recover from stroke.

“This is difficult to imagine, but it is achievable, successfully working about 98 percent of the time. With this technology, we can convert skin cells into elements of any organ with just one touch. This process only takes less than a second and is non-invasive, and then you’re off. The chip does not stay with you, and the reprogramming of the cell starts. Our technology keeps the cells in the body under immune surveillance, so immune suppression is not necessary,” said Sen, who also is executive director of Ohio State’s Comprehensive Wound Center.

TNT technology has two major components: First is a nanotechnology-based chip designed to deliver cargo to adult cells in the live body. Second is the design of specific biological cargo for cell conversion. This cargo, when delivered using the chip, converts an adult cell from one type to another, said first author Daniel Gallego-Perez, an assistant professor of biomedical engineering and general surgery who also was a postdoctoral researcher in both Sen’s and Lee’s laboratories.

TNT doesn’t require any laboratory-based procedures and may be implemented at the point of care. The procedure is also non-invasive. The cargo is delivered by zapping the device with a small electrical charge that’s barely felt by the patient.

“The concept is very simple,” Lee said. “As a matter of fact, we were even surprised how it worked so well. In my lab, we have ongoing research trying to understand the mechanism and do even better. So, this is the beginning, more to come.”

Researchers plan to start clinical trials next year to test this technology in humans, Sen said.

Reference: Daniel Gallego-Perez, Durba Pal, Subhadip Ghatak, Veysi Malkoc, Natalia Higuita-Castro, Surya Gnyawali, Lingqian Chang, Wei-Ching Liao, Junfeng Shi, Mithun Sinha, Kanhaiya Singh, Erin Steen, Alec Sunyecz, Richard Stewart, Jordan Moore, Thomas Ziebro, Robert G. Northcutt, Michael Homsy, Paul Bertani, Wu Lu, Sashwati Roy, Savita Khanna, Cameron Rink, Vishnu Baba Sundaresan, Jose J. Otero, L. James Lee, Chandan K. Sen. Topical tissue nano-transfection mediates non-viral stroma reprogramming and rescue. Nature Nanotechnology, 2017; DOI: 10.1038/nnano.2017.134

lroot on August 2nd, 2017

Brain Training

Like much of the rest of the body, the brain loses flexibility with age, impacting the ability to learn, remember, and adapt. Now, scientists at University of Utah Health report they can rejuvenate the plasticity of the mouse brain, specifically in the visual cortex, increasing its ability to change in response to experience. Manipulating a single gene triggers the shift, revealing it as a potential target for new treatments that could recover the brain’s youthful potential. The research was published online in the Proceedings of the National Academy of Sciences (PNAS) on August 8.

“It’s exciting because it suggests that by just manipulating one gene in adult brains, we can boost brain plasticity,” says lead investigator Jason Shepherd, Ph.D., Associate Professor of Neurobiology and Anatomy at University of Utah Health.

“This has implications for potentially reducing normal cognitive decline with aging, or boosting recovery from brain injury after stroke or traumatic brain injury,” he says. Additional research will need to be done to determine whether plasticity in humans and mice is regulated in the same way.

The dramatic way in which the brain changes over time has long captured the imagination of scientists. A “critical window” of brain plasticity explains why certain eye conditions such as lazy eye can be corrected during early childhood but not later in life. The phenomenon has raised the questions: What ordinarily keeps the window open? And, once it’s shut, can plasticity be restored?

Earlier work that Shepherd carried out in collaboration with Mark Bear, Ph.D., a professor at the Massachusetts Institute of Technology and co-author of the current study, showed that the critical window never opens in mice lacking a gene called Arc. Temporarily closing a single eye of a young mouse for a few days deprives the visual cortex of normal input, and the neurons’ electrophysiological response to visual experience changes. By contrast, young mice without Arc cannot adapt to the new experience in the same way.

“Given our previous studies, we wondered whether Arc is essential for controlling the critical period of plasticity during normal brain development,” says Shepherd.

If there is no visual plasticity without Arc, the thinking goes, then perhaps the gene plays a role in keeping the “critical window” open.

In support of the idea, the new investigation finds that in the mouse visual cortex, Arc rises and falls in parallel with visual plasticity. The two peak in teen mice and fall sharply by middle-age, suggesting they are linked.

The researchers probed the connection further in two more ways. First, in collaboration with co-author Harohiko Bito, Ph.D., a professor at the University of Tokyo, they tested mice that have a strong supply of Arc throughout life. At middle-age, these mice responded to visual deprivation as robustly as their juvenile counterparts. By prolonging Arc’s availability, the window of plasticity remained open for longer.

Manipulating Arc is not the first treatment to prolong plasticity. Chronically treating mice with an antidepressant, fluoxetine, and raising rodents in a stimulating environment with toys and plenty of social interaction, are among other paradigms that do the same.

But the second set of experiments raised the bar higher. Viruses were used to deliver Arc to middle age mice, after the critical window had closed. Following the intervention, these older mice responded to visual deprivation as a youngster woulds. In this case even though the window had already shut, Arc enabled it to open once again.

“It was incredible to see that in adult mice, who have gone through normal development and aging, simply overexpressing Arc with a virus restored plasticity,” says co-first author Kyle Jenks, a graduate student in Shepherd’s lab.

The prevailing notion of how plasticity declines is that as the brain develops, inhibitory neurons mature and become stronger. Shepherd explains that he believes their findings add a new dimension for how critical periods of learning are regulated.

“Increased inhibition in the brain makes it harder to express activity-dependent genes, like Arc, in response to experience or learning,” he says. “And that leads to decreased brain plasticity.”

Normally, Arc is rapidly activated in response to stimuli and is involved in shuttling neurotransmitter receptors out of synapses that neurons use to communicate with one another. Additional research will need to be done to understand precisely how manipulating Arc boosts plasticity.

Whether Arc is involved in regulating the plasticity of other neurological functions mediated by other brain structures, like learning, memory, or repair, remains to be tested but will be examined in the future, says Shepherd.

Reference: Kyle R. Jenks, Taekeun Kim, Elissa D. Pastuzyn, Hiroyuki Okuno, Andrew V. Taibi, Haruhiko Bito, Mark F. Bear, and Jason D. Shepherd. Arc restores juvenile plasticity in adult mouse visual cortex. Proceedings of the National Academy of Sciences, August 2017 DOI: 10.1073/pnas.1700866114

Green Tea

A study published online in The FASEB Journal, involving mice, suggests that EGCG (epigallocatechin-3-gallate), the most abundant catechin and biologically active component in green tea, could help insulin resistance and improve cognition. Previous research pointed to the potential of EGCG to help a variety of human conditions, yet until now, EGCG’s impact on insulin resistance and cognition triggered in the brain remained unclear.

“Green tea is the second most consumed beverage in the world after water, and is grown in at least 30 countries,” said Xuebo Liu, Ph.D., a researcher at the College of Food Science and Engineering, Northwest A&F University, in Yangling, China. The ancient habit of drinking green tea may be beneficial when it comes to combatting obesity, insulin resistance, and improving memory.

Liu and colleagues divided 3-month-old male C57BL/6J mice into three groups based on diet: 1) a control group fed with a standard diet, 2) a group fed with an HFFD diet (high-fat and high-fructose diet), and 3) a group fed with an HFFD diet and 2 grams of EGCG per liter of drinking water. For 16 weeks, researchers monitored the mice and found that those fed with HFFD had a higher final body weight than the control mice, and a significantly higher final body weight than the HFFD+EGCG mice. In performing a Morris water maze test, researchers found that mice in the HFFD group took longer to find the platform compared to mice in the control group. The HFFD+EGCG group had a significantly lower escape latency and escape distance than the HFFD group on each test day. When the hidden platform was removed to perform a probe trial, HFFD-treated mice spent less time in the target quadrant when compared with control mice, with fewer platform crossings. The HFFD+EGCG group exhibited a significant increase in the average time spent in the target quadrant and had greater numbers of platform crossings, showing that EGCG could improve HFFD-induced memory impairment.

“Many reports, anecdotal and to some extent research-based, are now greatly strengthened by this more penetrating study,” said Thoru Pederson, Ph.D., Editor-in-Chief of The FASEB Journal.


Scientists at Albert Einstein College of Medicine have found that stem cells in the brain’s hypothalamus govern how fast aging occurs in the body. The finding, made in mice, could lead to new strategies for warding off age-related diseases and extending lifespan. The paper was published in Nature.

The hypothalamus was known to regulate important processes including growth, development, reproduction and metabolism. In a 2013 Nature paper, Einstein researchers made the surprising finding that the hypothalamus also regulates aging throughout the body. Now, the scientists have pinpointed the cells in the hypothalamus that control aging: a tiny population of adult neural stem cells, which were known to be responsible for forming new brain neurons.

“Our research shows that the number of hypothalamic neural stem cells naturally declines over the life of the animal, and this decline accelerates aging,” says senior author Dongsheng Cai, M.D., Ph.D., (professor of molecular pharmacology at Einstein. “But we also found that the effects of this loss are reversible. By replenishing these stem cells or the molecules they produce, it’s possible to slow and even reverse various aspects of aging throughout the body.”

In studying whether stem cells in the hypothalamus held the key to aging, the researchers first looked at the fate of those cells as healthy mice got older. The number of hypothalamic stem cells began to diminish when the animals reached about 10 months, which is several months before the usual signs of aging start appearing. “By old age which is about two years in mice most of those cells were gone,” says Dr. Cai.

The researchers next wanted to learn whether this progressive loss of stem cells was actually causing aging and was not just associated with it. So they observed what happened when they selectively disrupted the hypothalamic stem cells in middle-aged mice. “This disruption greatly accelerated aging compared with control mice, and those animals with disrupted stem cells died earlier than normal,” says Dr. Cai.

Could adding stem cells to the hypothalamus counteract aging? To answer that question, the researchers injected hypothalamic stem cells into the brains of middle-aged mice whose stem cells had been destroyed as well as into the brains of normal old mice. In both groups of animals, the treatment slowed or reversed various measures of aging.

Dr. Cai and his colleagues found that the hypothalamic stem cells appear to exert their anti-aging effects by releasing molecules called microRNAs (miRNAs). They are not involved in protein synthesis but instead play key roles in regulating gene expression. miRNAs are packaged inside tiny particles called exosomes, which hypothalamic stem cells release into the cerebrospinal fluid of mice.

The researchers extracted miRNA-containing exosomes from hypothalamic stem cells and injected them into the cerebrospinal fluid of two groups of mice: middle-aged mice whose hypothalamic stem cells had been destroyed and normal middle-aged mice. This treatment significantly slowed aging in both groups of animals as measured by tissue analysis and behavioral testing that involved assessing changes in the animals’ muscle endurance, coordination, social behavior and cognitive ability.

The researchers are now trying to identify the particular populations of microRNAs and perhaps other factors secreted by these stem cells that are responsible for these anti-aging effects a first step toward possibly slowing the aging process and treating age-related diseases.

Abstract: “It has been proposed that the hypothalamus helps to control ageing, but the mechanisms responsible remain unclear. Here we develop several mouse models in which hypothalamic stem/progenitor cells that co-express Sox2 and Bmi1 are ablated, as we observed that ageing in mice started with a substantial loss of these hypothalamic cells. Each mouse model consistently displayed acceleration of ageing-like physiological changes or a shortened lifespan. Conversely, ageing retardation and lifespan extension were achieved in mid-aged mice that were locally implanted with healthy hypothalamic stem/progenitor cells that had been genetically engineered to survive in the ageing-related hypothalamic inflammatory microenvironment. Mechanistically, hypothalamic stem/progenitor cells contributed greatly to exosomal microRNAs (miRNAs) in the cerebrospinal fluid, and these exosomal miRNAs declined during ageing, whereas central treatment with healthy hypothalamic stem/progenitor cell-secreted exosomes led to the slowing of ageing. In conclusion, ageing speed is substantially controlled by hypothalamic stem cells, partially through the release of exosomal miRNAs.”

Reference: Yalin Zhang, Min Soo Kim, Baosen Jia, Jingqi Yan, Juan Pablo Zuniga-Hertz, Cheng Han, Dongsheng Cai. Hypothalamic stem cells control ageing speed partly through exosomal miRNAs. Nature, 2017; DOI: 10.1038/nature23282

lroot on July 2nd, 2017

Blood Vessels

Stem cell biologists have tried unsuccessfully for years to produce cells that will give rise to functional arteries. Now new techniques developed at the Morgridge Institute for Research and the University of Wisconsin in Madison have produced, for the first time, functional arterial cells at both the quality and scale to be relevant for modeling and clinical application.

Reporting in the July 10 issue of the journal Proceedings of the National Academy of Sciences, scientists in the lab of stem cell pioneer James Thomson describe methods for generating and characterizing arterial endothelial cells which are the cells that initiate artery development and exhibit many of the specific functions required by the body.

Further, these cells contributed both to new artery formation. “No one has been able to make those kinds of cells efficiently before,” says Jue Zhang, a Morgridge assistant scientist and lead author. “The key finding here is a way to make arterial endothelial cells more functional and clinically useful.”

The Thomson lab has made arterial engineering one of its top research priorities. New techniques have produced, for the first time, functional arterial cells at both the quality and scale to be relevant for modeling and clinical application.

The challenge is that generic endothelial cells are relatively easy to create, but they lack true arterial properties and thus have little clinical value, Zhang says.

The research team applied two pioneering technologies to the project. First, they used single-cell RNA sequencing to identify the signaling pathways critical for arterial endothelial cell differentiation. They found about 40 genes of optimal relevance. Second, they used CRISPR-Cas9 gene editing technology that allowed them to create reporter cell lines to monitor arterial differentiation in real time.

“With this technology, you can test the function of these candidate genes and measure what percentage of cells are generating into our target arterial cells,” says Zhang.

The research group developed a protocol around five key growth factors that make the strongest contributions to arterial cell development. They also identified some very common growth factors used in stem cell science, such as insulin, that surprisingly inhibit arterial endothelial cell differentiation.

“Our ultimate goal is to apply this improved cell derivation process to the formation of functional arteries that can be used in cardiovascular surgery,” says Thomson, director of regenerative biology at Morgridge and a UW–Madison professor of cell and regenerative biology. “This work provides valuable proof that we can eventually get a reliable source for functional arterial endothelial cells and make arteries that perform and behave like the real thing.”

Thomson’s team, along with many UW–Madison collaborators, is in the first year of a seven-year project supported by the National Institutes of Health on the feasibility of developing artery banks suitable for use in human transplantation.

“Now that we have a method to create these cells, we hope to continue the effort using a more universal donor cell line,” says Zhang. The lab will focus on cells banked from a unique population of people who are genetically compatible donors for a majority of the population.

Reference: Zhang, J., Chu, L., Hou, Z., Schwartz, M. P., Hacker, T., Vickerman, V., Thomson, J. A. (2017). Functional characterization of human pluripotent stem cell-derived arterial endothelial cells. Proceedings of the National Academy of Sciences, 201702295. doi:10.1073/pnas.1702295114

Adult Stem Cells

Whether using embryonic or adult stem cells, coercing these master cells to convert to the desired target cell and reproduce flawlessly is difficult. Now an international team of researchers has a two-part system that can convert the cells to the targets and then remove the remnants of that conversion, leaving only the desired DNA behind to duplicate.

“One difficulty with human pluripotent stem cells is that you can’t use them directly,” said Xiaojun Lian, assistant professor of biomechanical engineering, biology and a member of the Huck Institutes of the Life Sciences, Penn State. They need to be the right type of differentiated cells for each tissue in the body.

Normally, pluripotent stem cells induced from both adult and embryonic cells receive a chemical signal to change from a stem cell to a functional cell. Pluripotent stem cells can change to any cell in the human body. However, this natural cell change is part of a complex series of triggers controlled by DNA. Researchers have in the past inserted DNA into the pluripotent cells to convert them, but remnants of the inserted DNA remain.

In this current work, published in a recent issue of Scientific Reports, the researchers are not incorporating a piece of DNA that will tell the cells to convert, but DNA that will make the cell glow green when illuminated by a blue light. This marker allows the researchers to see that the DNA plasmid is incorporated into the cell, and that it is completely gone upon removal. A plasmid is a circular piece of DNA that contains functional DNA fragments that control gene expression in cells.

“We wanted to explore the limits for turning the conversion on and off and to have the ability to control the level of expression and removal of DNA after conversion,” said Lauren N. Randolph, doctoral student in bioengineering, Penn State.

Previous approaches incorporated the appropriate DNA to switch on the conversions, but did not completely remove all the DNA inserted.

The researchers are using a Tet-On 3G inducible PiggyBac system that is a plasmid they named XLone to achieve insertion, activation and removal. The PiggyBac portion of the system includes the DNA to insert that DNA into the cell’s DNA. The Tet-On 3G portion contains the necessary signaling information. This system also makes the cells more sensitive to doxycycline, which is the drug used to initiate the conversion.

“We are using abundant multiple copies of the plasmid to increase the likelihood that it gets in and does what it is supposed to do and actually follows through reproduction of the cells,” said Lian.

If only one or a few plasmids are inserted into the cell, the new DNA could just be silenced. Insertion of multiple plasmids assures that at least one will function.

“The first advantage with our system is that it does not have any leakage expression,” said Randolph. “If we don’t induce the system with doxycycline, we get nothing.”

The second advantage is that once the cells are reproducing as heart cells or nerve cells, the plasmid can be removed and the cells continue to reproduce without any remnant of the plasmid system.

While the researchers are currently aiming to understand and study gene function and directed cell differentiation in human stem cells, eventually they would like to be able to create cell-based therapies.

Reference: Lauren N. Randolph, Xiaoping Bao, Chikai Zhou, Xiaojun Lian. An all-in-one, Tet-On 3G inducible PiggyBac system for human pluripotent stem cells and derivatives. Scientific Reports, 2017; 7 (1) DOI: 10.1038/s41598-017-01684-6

lroot on June 29th, 2017

Fit 70 Year Old

Is 70 the new 60? A new Stony Brook University-led study to be published in PLOS ONE uses new measures of aging to scientifically illustrate that one’s actual age is not necessarily the best measure of human aging itself, but rather aging should be based on the number of years people are likely to live in a given country in the 21st Century.

The study combines the new measures of aging with probabilistic projections from the United Nations and predicts an end to population aging in the U.S. and other countries before the end of the century. Population aging when the median age rises in a country because of increasing life expectancy and lower fertility rates is a concern for countries because of the perception that population aging leads to declining numbers of working age people and additional social burdens.

According to Warren Sanderson, Professor of Economics at Stony Brook University and the lead author, this study’s projections imply that as life expectancies increase people are generally healthier with better cognition at older ages and countries can adjust public policies appropriately as to population aging.

Population aging could peak by 2040 in Germany and by 2070 in China, according to the study, which combines measures of aging with probabilistic population projections from the UN. In the USA, the study shows very little population aging at all in the coming century.

Traditional population projections categorize “old age” as a simple cutoff at age 65. But as life expectancies have increased, so too have the years that people remain healthy, active, and productive. In the last decade, IIASA researchers have published a large body of research showing that the very boundary of “old age” should shift with changes in life expectancy, and have introduced new measures of aging that are based on population characteristics, giving a more comprehensive view of population aging.

The study combines these new measures with UN probabilistic population projections to produce a new set of age structure projections for four countries: China, Germany, Iran, and the USA.

“Both of these demographic techniques are relatively new, and together they give us a very different, and more nuanced picture of what the future of aging might look like,” says Professor Sanderson, also a researcher at IIASA. He wrote the article with Sergei Scherbov, leader of the Re-Aging Project at IIASA, and Patrick Gerland, chief of the mortality section of the Population Division of the United Nations.

One of the measures used in the paper looks at life expectancy as well as years lived to adjust the definition of old age. Probabilistic projections produce a range of thousands of potential scenarios, so that they can show a range of possibilities of aging outcomes.

For China, Germany, and the USA, the study showed that population aging would peak and begin declining well before the end of the century. Iran, which had an extremely rapid fall in fertility rate in the last 20 years, has an unstable age distribution and the results for the country were highly uncertain.

“We chose these four countries for analysis because they have very different population structures and projections, and so they allow us to test this methodology across a range of possible scenarios,” summarizes Scherbov.

Abstract: “We merge two methodologies, prospective measures of population aging and probabilistic population forecasts. We compare the speed of change and variability in forecasts of the old age dependency ratio and the prospective old age dependency ratio as well as the same comparison for the median age and the prospective median age. While conventional measures of population aging are computed on the basis of the number of years people have already lived, prospective measures are computed also taking account of the expected number of years they have left to live. Those remaining life expectancies change over time and differ from place to place. We compare the probabilistic distributions of the conventional and prospective measures using examples from China, Germany, Iran, and the United States. The changes over time and the variability of the prospective indicators are smaller than those that are observed in the conventional ones. A wide variety of new results emerge from the combination of methodologies. For example, for Germany, Iran, and the United States the likelihood that the prospective median age of the population in 2098 will be lower than it is today is close to 100 percent.”

Reference: Warren C. Sanderson, Sergei Scherbov, Patrick Gerland. Probabilistic population aging. PLOS ONE, 2017; 12 (6): e0179171 DOI: 10.1371/journal.pone.0179171

lroot on June 28th, 2017

Infinity Symbol

Emma Morano passed away last April. At 117 years old, the Italian woman was the oldest known living human being.

Super centenarians, such as Morano and Jeanne Calment of France, who famously lived to be 122 years old, continue to fascinate scientists and have led them to wonder just how long humans can live. A study published in Nature last October concluded that the upper limit of human age is peaking at around 115 years.

Now, however, a new study in Nature by McGill University biologists Bryan G. Hughes and Siegfried Hekimi comes to a starkly different conclusion. By analyzing the lifespan of the longest-living individuals from the USA, the UK, France and Japan for each year since 1968, Hekimi and Hughes found no evidence for such a limit, and if such a maximum exists, it has yet to be reached or identified, Hekimi says.

Far into the foreseeable future

“We just don’t know what the age limit might be. In fact, by extending trend lines, we can show that maximum and average lifespans, could continue to increase far into the foreseeable future,” Hekimi says. Many people are aware of what has happened with average lifespans. In 1920, for example, the average newborn Canadian could expect to live 60 years; a Canadian born in 1980 could expect 76 years, and today, life expectancy has jumped to 82 years. Maximum lifespan seems to follow the same trend.

It’s impossible to predict what future lifespans in humans might look like, Hekimi says. Some scientists argue that technology, medical interventions, and improvements in living conditions could all push back the upper limit.

“It’s hard to guess,” Hekimi adds. “Three hundred years ago, many people lived only short lives. If we would have told them that one day most humans might live up to 100, they would have said we were crazy.”

Reference: Bryan G. Hughes, Siegfried Hekimi. Many possible maximum lifespan trajectories. Nature, 2017; 546 (7660): E8 DOI: 10.1038/nature22786

lroot on June 15th, 2017

Toxins in Your Tap Water

America has a drinking water crisis. An NRDC study has found that contaminants that may harm human health are found in tap water in every state in the nation. This is a problem even for people who don’t drink tap water since water borne toxins can be absorbed through the skin and lungs while bathing and into food if used for cooking.

Established in 1974, the Safe Drinking Water Act is one of the bedrock environmental laws in the United States, consisting of rules that regulate about 100 contaminants found in drinking water. NRDC has documented serious problems with our outdated and deteriorating water infrastructure, widespread violations and inadequate enforcement of the Safe Drinking Water Act for more than 25 years.

The study shows that in 2015 alone, there were more than 80,000 reported violations of the Safe Drinking Water Act by community water systems. Nearly 77 million people were served by more than 18,000 of these systems with violations in 2015. These violations included exceeding health-based standards, failing to properly test water for contaminants, and failing to report contamination to state authorities or the public. What’s worse, 2015 saw more than 12,000 health-based violations in some 5,000 community water systems serving more than 27 million people.

In 2016, the publication “What’s in Your Water: Flint and Beyond” detailed the lead crisis in Flint, Michigan, and contextualized a larger, national crisis around lead in drinking water. The new study picks up where that one left off, detailing a stunning number of violations of the Safe Drinking Water Act around the nation.

1. Combined Disinfectants and Disinfection Byproducts

Exposure to these contaminants can lead to cancer and may be linked to reproductive impacts such as miscarriages and birth defects. In 2015, there were 11,311 violations (4,591 health-based) at community water systems serving 25,173,431 people (12,584,936 health-based). Formal enforcement measures were taken in 12.4 percent of all cases and 23.0 percent of health-based cases.

2. Total Coliform

The presence of coliforms in drinking water indicates that possible presence of organisms that can cause diarrhea, cramps, nausea, and headaches in otherwise-healthy people. These impacts can be much more serious and even life-threatening for children, the elderly, and immune-compromised people. In 2015, there were 10,261 violations (2,574 health-based) at community water systems serving 17,768,807 people (10,118,586 health-based). Formal enforcement was taken in 8.8 percent of cases (and 8.3 percent of health-based cases).

3. Combined Surface, Ground Water, and Filter Backwash Rules

Exposure to some of these pathogens, such as Cryptosporidium or Giardia, can cause severe gastrointestinal distress, nausea, and diarrhea. They can cause serious, life-threatening infections for the very young, elderly, and immune-compromised. In 2015 there were 5,979 violations (1,790 health-based) at community water systems serving 17,312,604 people (5,336,435 health-based). Formal enforcement was taken in 13.7 percent of cases (28.2 percent of health-based cases).

4. Nitrites and Nitrates

Exposure can lead to blue baby syndrome in infants (potentially leading to death in extreme cases), developmental effects, and cardiovascular disease. In extreme cases, blue baby syndrome can be severe and lead to death. In 2015, there were 1,529 violations (459 health-based) at community water systems serving 3,867,431 people (1,364,494 health-based). Formal enforcement action was taken in 11.3 percent of all cases (and 27.9 percent of health-based cases).

5. Lead and Copper

Exposure to lead is particularly toxic to children and can cause serious, irreversible damage to their developing brains and nervous systems. Lead exposure can also cause miscarriages and stillbirths in pregnant women, as well as fertility issues, cardiovascular and kidney effects, cognitive dysfunction, and elevated blood pressure in healthy adults. In 2015, there were 8,044 violations (303 health-based) by systems serving 18,350,633 people (582,302 health-based). Formal enforcement action was taken in 12.0 percent of the cases (and in 14.2 percent of health-based cases).

6. Radionuclides

Exposure can lead to cancers and compromised kidney function. In 2015, there were 2,297 violations (962 health-based) in community water systems serving 1,471,364 people (445,969 health-based). Formal enforcement was taken in 11.7 percent of all cases (and 16.1 percent of health-based cases).

7. Arsenic

A known human carcinogen, exposure can lead to cancers, development effects, pulmonary disease, or cardiovascular disease. In 2015, there were 1,537 violations (1,135 health-based) at community water systems serving 1,842,594 people (358,323 health-based). Formal enforcement was taken in 28.9 percent of cases (37.1 percent of health-based cases).

8. Synthetic Organic Contaminants

Exposure can lead to cancers, developmental effects, central nervous system and reproductive difficulties, endocrine issues, or liver and kidney problems. In 2015 there were 6,864 violations (17 health-based) serving 2,669,594 people (301,099 health-based). Formal enforcement action was taken in 7.3 percent of cases (and 5.9 percent of health-based cases).

9. Inorganic Contaminants

Exposure can lead to increased cholesterol, kidney damage, hair loss, skin irritation, and cancer. In 2015, there were 1,505 violations (291 health-based) in community water systems serving 1,312,643 people (83,033 health-based). Formal enforcement was taken in 5.2 percent of cases (15.1 percent of health-based cases).

10. Volatile Organic Contaminants

Exposure can lead to cancers; developmental, skin, and reproductive issues; and cardiovascular problems. Exposure can also cause adverse effects on the liver, kidneys, and immune and nervous systems. In 2015 there were 10,383 violations (15 of them health-based) at community water systems serving 3,451,072 people (5,276 health-based). Formal enforcement was taken in 6.1 percent of cases (and 26.7 percent of health-based cases).

11. Public Notification

All community water systems are required to directly deliver information about their drinking water quality to each customer once a year. In 2015 there were 13, 202 violations by community water systems serving 8,381,050 people. Formal enforcement action was taken in 10.3 percent of cases.

The take away from this is to either install a water purifier or use natural spring water. Purifiers are also available for showers and are typically installed between the shower head and pipe.