Culture

It is not uncommon to find aluminum in municipal water systems. It's part of a treatment chemical used in some water treatment processes. Recently, however, it has been discovered in lead scale, deposits that form on lead water pipes.

The aluminum presence in pipes is both unsurprising and, in the quantities researchers saw in water pipes, not a health concern, according to Daniel Giammar, the Walter E. Browne Professor of Environmental Engineering in the McKelvey School of Engineering at Washington University in St. Louis. But no one had looked at how it might affect the larger municipal system.

In particular, Giammar wanted to find out, "What is that aluminum doing to the behavior of the lead in the scale?" As long as the lead is bound to the scale, it doesn't enter the water system.

Giammar and a team ran several experiments and found that, in a lab setting, aluminum does have a small but important effect on lead's solubility under certain conditions. Their results were published in late April in Environmental Science & Technology. The paper was selected as "ACS Editor's Choice" by the American Chemical Society, which makes it available to the public for free.

The experiments were carried out in large part by visiting PhD student Guiwei Li, who was able to complete the work during his brief stay at Washington University before returning to the Chinese Academy of Sciences.

In simplified models, the researchers took a look at how phosphate, aluminum and a combination of the two, affected a strip of lead in a jar of water with a composition close to that of water found in many water systems. The aim: to better understand lead's solubility, or the amount that would dissolve and make its way into the water when impacted by those chemicals.

In the jar in which only aluminum was added, there was no effect on the solubility of the lead strip; lead had dissolved into the water at a concentration of about 100 micrograms per liter.

In the jar in which only phosphate was added, the concentration of lead in the water decreased from about 100 micrograms per liter to less than one.

In the jar in which both aluminum and phosphate were added, the concentration of lead in the water decreased from about 100 micrograms per liter to about 10 micrograms per liter.

Ten micrograms of lead per liter of water is still below drinking water standards, Giammar said, but it's still more lead in the water than was seen in the jar without aluminum. "This tells us what our next experiment should be," he said. His lab will do these experiments with real lead pipes, as they have done in the past.

"This showed us things that were surprising," he said. "Some people would have thought that aluminum wasn't doing anything because it's inert. But then in our work, we saw that it actually affects lead solubility."

Below please find a summary and link(s) of new coronavirus-related content published today in Annals of Internal Medicine. The summary below is not intended to substitute for the full article as a source of information. A collection of coronavirus-related content is free to the public at http://go.annals.org/coronavirus.

1. Tocilizumab for Hemophagocytic Syndrome in a Kidney Transplant Recipient with COVID-19

Studies suggest that many patients with COVID-19 and acute respiratory distress syndrome experience a cytokine storm characterized by fever; hyperferritinemia; and a massive release of inflammatory cytokines, including interleukin-6, tumor necrosis factor-α, and monocyte chemoattractant proteins. These findings led to the hypothesis that biological agents targeting specific cytokine or inflammatory pathways may improve the respiratory outcomes of patients with the most severe forms of COVID-19. Researchers from the University Hospital of Toulouse; Toulouse, France, tested this hypothesis on a severely ill patient on a ventilator for COVID-19. They treated the patient with tocilizumab as salvage therapy, instead of etoposide, and the patient improved dramatically. Read the full text: https://www.acpjournals.org/doi/10.7326/L20-0419.

Media contacts: A PDF for this article is not yet available. Please click the link to read full text. The lead author, Stanislas Faguer, MD, PhD, can be reached at faguer.s@chu-toulouse.fr.

Humans have been wondering whether we alone in the universe since antiquity.

We know from the geological record that life started relatively quickly, as soon our planet's environment was stable enough to support it. We also know that the first multicellular organism, which eventually produced today's technological civilization, took far longer to evolve, approximately 4 billion years.

But despite knowing when life first appeared on Earth, scientists still do not understand how life occurred, which has important implications for the likelihood of finding life elsewhere in the universe.

In a new paper published in the Proceeding of the National Academy of Sciences today, David Kipping, an assistant professor in Columbia's Department of Astronomy, shows how an analysis using a statistical technique called Bayesian inference could shed light on how complex extraterrestrial life might evolve in alien worlds.

"The rapid emergence of life and the late evolution of humanity, in the context of the timeline of evolution, are certainly suggestive," Kipping said. "But in this study it's possible to actually quantify what the facts tell us."

To conduct his analysis, Kipping used the chronology of the earliest evidence for life and the evolution of humanity. He asked how often we would expect life and intelligence to re-emerge if Earth's history were to repeat, re-running the clock over and over again.

He framed the problem in terms of four possible answers: Life is common and often develops intelligence, life is rare but often develops intelligence, life is common and rarely develops intelligence and, finally, life is rare and rarely develops intelligence.

This method of Bayesian statistical inference--used to update the probability for a hypothesis as evidence or information becomes available--states prior beliefs about the system being modeled, which are then combined with data to cast probabilities of outcomes.

"The technique is akin to betting odds," Kipping said. "It encourages the repeated testing of new evidence against your position, in essence a positive feedback loop of refining your estimates of likelihood of an event."

From these four hypotheses, Kipping used Bayesian mathematical formulas to weigh the models against one another. "In Bayesian inference, prior probability distributions always need to be selected," Kipping said. "But a key result here is that when one compares the rare-life versus common-life scenarios, the common-life scenario is always at least nine times more likely than the rare one."

The analysis is based on evidence that life emerged within 300 million years of the formation of the Earth's oceans as found in carbon-13-depleted zircon deposits, a very fast start in the context of Earth's lifetime. Kipping emphasizes that the ratio is at least 9:1 or higher, depending on the true value of how often intelligence develops.

Kipping's conclusion is that if planets with similar conditions and evolutionary time lines to Earth are common, then the analysis suggests that life should have little problem spontaneously emerging on other planets. And what are the odds that these extraterrestrial lives could be complex, differentiated and intelligent? Here, Kipping's inquiry is less assured, finding just 3:2 odds in favor of intelligent life.

This result stems from humanity's relatively late appearance in Earth's habitable window, suggesting that its development was neither an easy nor ensured process. "If we played Earth's history again, the emergence of intelligence is actually somewhat unlikely," he said.

Kipping points out that the odds in the study aren't overwhelming, being quite close to 50:50, and the findings should be treated as no more than a gentle nudge toward a hypothesis.

"The analysis can't provide certainties or guarantees, only statistical probabilities based on what happened here on Earth," Kipping said. "Yet encouragingly, the case for a universe teeming with life emerges as the favored bet. The search for intelligent life in worlds beyond Earth should be by no means discouraged."

In the latest CUNY SPH COVID-19 tracking survey, New Yorkers gave convincing evidence that the city is not yet testing enough people and set high expectations for the safety measures they feel are necessary for them to return to work outside their homes. They are also uncertain about reopening public schools, colleges or universities in the fall. These are the major findings of the ninth city and statewide tracking survey from the CUNY Graduate School of Public Health & Health Policy (CUNY SPH), conducted May 15-17.

Almost a quarter (23%) of New York residents reported that one or more persons in their household has been sick with fever or symptoms consistent with COVID-19 since the coronavirus struck, but only half of those people were tested and more than three quarters of them tested positive for COVID-19.

There were stark differences based on race and ethnicity: one or more people were sick at home in 36% of Hispanic/Latinx households compared to 23% of Caucasian, 13% African American and 12% Asian ones. Of those who were tested for coronavirus, the highest percentage of people testing positive were Hispanic/Latinx (a startling 90%), followed by African Americans (65%), Caucasians (58%) and Asians (50%).

"These results indicate that at present we are still testing only the sickest New Yorkers," said Dr. Ayman El-Mohandes, Dean of CUNY SPH. "If our goal is to reopen the city safely, most of those tested should be testing negative, which would mean that the spread of the virus is on the decline. We cannot open up until we ramp up our testing of people without symptoms, and conduct thorough follow-up contact tracing."

Despite the decline in confirmed cases and hospitalizations in the city, New Yorkers' concerns about the virus remain high. Just more than half (51%) of residents believe that they are at high or very high risk of contracting COVID-19. Almost seven out of ten (69%) are either opposed to or uncertain about reopening public schools in the fall.

Before the virus struck, 26% of employed New Yorkers were working from home. That number has shot up to 70% since the epidemic, and 40% of people who are currently working from home say they would prefer to continue doing so for the foreseeable future. The majority of respondents working from home now are Asian (54%) or Caucasian (51%) compared to African American (35%) and Hispanic/Latinx (23%). Working at home also correlates with educational level. Of those who have undergraduate or post-graduate degrees, more than 60% are working from home, compared to 30% with some college and 22% with high school educations.

When this subgroup was asked why they would not want to return to work outside the home, their primary concern (76%) was fear of bringing the virus home to their families, while 69% reported anxiety about using public transportation like buses and subways. A similar number (68%) said they feared getting sick themselves.

The survey also asked all respondents what precautions they felt needed to be in place to make them feel safer at work. The greatest number (84%) said that the availability of a vaccine or medicine against coronavirus or regular sanitization of the workplace would make them more confident, followed closely (82%) by requiring that face masks be worn at work at all times. Further preferences for workplace precautions were also favored by substantial majorities:

79% wanted people who enter building/workplace to report any symptoms

77% wanted greater spacing between people

77% wanted workplace testing and tracing

72% wanted people's temperatures to be taken as they entered the building

Many New Yorkers are uncertain about their future work. More than one in five (21%) believe there will no longer be a demand for their product or service when the economy reopens. About one in four who lost their jobs or were furloughed as a result of the epidemic plan to change their career path.

Of the 22% of New Yorkers who reported being furloughed or laid off, three in five (61%) said they had filed applications for unemployment benefits. Of those that applied, half (50%) are still waiting for their first check, 41% have received benefits and 9% were rejected.

Seventeen percent (17%) of our respondents classified themselves as self-employed or small business owners. Of those, 42% report applying for an SBA Economic Injury Disaster Loan or Paycheck Protection Program. Nearly everyone that applied was accepted, and two-thirds (67%) said they had received their loans. An additional 16% reported that they received their loans but will return the money, since they were unable to meet the conditions. A further 16% are waiting to hear the status of their applications.

The complete survey results and related commentary can be found at https://sph.cuny.edu/research/covid-19-tracking-survey/week-10 and JHC Impact, an initiative of the Journal of Health Communication: International Perspectives.

Survey methodology:

The CUNY Graduate School of Public Health and Health Policy (CUNY SPH) survey was conducted by Emerson College Polling from May 15-17, 2020 (week 10). This tracking effort started March 13-15 (week 1), and continued with questions fielded March 20-22 (week 2) and March 27-29 (week 3), April 3-5, 2020 (week 4), April 10-12, 2020 (week 5), April 17-29 (week 6), April 24-26, 2020 (week 7), May 1-3, 2020 (week 8).

The sample for the NY Statewide and New York City results were both, n=1,000, with a Credibility Interval (CI) similar to a poll's margin of error (MOE) of +/- 3 percentage points. The data sets were weighted by gender, age, ethnicity, education and region based on the 2018 1-year American Community Survey model. It is important to remember that subsets based on gender, age, ethnicity and region carry with them higher margins of error, as the sample size is reduced. In the New York City results, data was collected using an Interactive Voice Response (IVR) system of landlines (n=475), SMS-to-online (n=327) and an online panel provided by MTurk and Survey Monkey (n=197). In the Statewide results, data was collected using an Interactive Voice Response (IVR) system of landlines (n=469), SMS-to-online (n=319) and an online panel provided by MTurk and Survey Monkey (n=212).

In the statewide survey regions were broken out into the following:

Region 1: Long Island 14.7% (USC1-4), Shirley, Seaford, Glen Cove, Garden City

Region 2: NYC 45.3% (USC 5-16) Queens, Brooklyn, Manhattan, Staten Island, Bronx

Region 3: Upstate 40% (USC 17-27): Albany, Harrison, Carmel, Rhinebeck, Amsterdam, Schuylerville, Utica, Corning, Irondequoit, Buffalo, Rochester

LA JOLLA--(May 18, 2020) Many cancer medications fail to effectively target the most commonly mutated cancer genes in humans, called RAS. Now, Salk Professor Geoffrey Wahl and a team of scientists have uncovered details into how normal RAS interacts with mutated RAS and other proteins in living cells for the first time. The findings, published in The Proceedings of the National Academy of Sciences on May 18, 2020, could aid in the development of better RAS-targeted cancer therapeutics.

"RAS proteins have been studied for decades because the RAS gene is changed (mutated) in so many cancers, yet there are still new things to be learned as we develop more sophisticated tools to study the problem," says Wahl, co-corresponding author, professor in Salk's Gene Expression Laboratory and holder of the Daniel and Martina Lewis Chair. "We have identified a new mechanism for regulating RAS enzyme activity that will help inform therapeutic strategies for inhibiting the mutated RAS proteins involved in cancer."

The family of RAS genes helps to regulate cell communication ("signaling") and growth. However, prior research suggests mutated RAS deviates from normal RAS in its ability to regulate processes that drive tumor growth across multiple types of cancer, including the majority of pancreatic cancers. Scientists have long attempted to target cancer-related RAS activity but this has proved very difficult. Efforts to understand which proteins normal and mutated RAS interact with in the cell have also given contradictory answers due to the difficulty of replicating the cellular environment in a test tube. And while previous studies have suggested that normal RAS proteins can bind to mutated RAS proteins to suppress tumor growth, exactly how these interactions happened was unknown.

"We improved upon an existing genetic technology developed by our lab, which allows us to study RAS protein interactions instantaneously in living cells," says Yao-Cheng (Leo) Li, Salk project scientist who led this study. "The key to understanding the function of RAS is being able to accurately analyze protein interactions on the cell membrane. This new technology allows us to do that."

Similar to watching a soccer team effortlessly execute a complicated play, the team used their high-powered genetic tool (which enables interacting proteins to light up, like fireflies) to examine how RAS interacted with other proteins, as well as with its mutated form, within living cells. They found that close proximity on the cell membrane was required for one RAS protein to interact with other RAS proteins, behavior the team coined "membrane association facilitated interactions" (MAFI). The cell membrane is required for RAS interactions with itself and some other proteins that localize to the same place on the cell membrane, which is why such interactions were not previously found in test tube studies.

The team also unexpectedly discovered a new mechanism for regulating the quantity of RAS proteins in the cell. They found that if they positioned a small fragment of a protein that interacts strongly with RAS on the membrane, MAFI would enable this protein to bind RAS very tightly, and this could inhibit RAS function better, creating an inactive RAS complex. The cell has a mechanism for detecting and eliminating inactive RAS complexes using small structures called lysosomes to perform this "housecleaning." Because the cell died as a result of eliminating the RAS proteins, this new and unexpected finding may aid in the development of new cancer therapeutics.

"These findings define new mechanisms of RAS signaling regulation" says Nikki Lytle, an author of the paper and Salk postdoctoral fellow. "This provides an unexpected model for RAS suppression, which could lead to new strategies for targeting mutated RAS in the future."

In the future, the researchers hope their discovery can be utilized to develop a new class of RAS-targeted therapeutics, which may require drug delivery through cutting-edge approaches involving nanoparticles or viruses that can target malignant cells.

In an upcoming study to be published in Gastroenterology, researchers at the Icahn School of Medicine at Mount Sinai and the University of North Carolina School of Medicine report on the clinical course of COVID-19 and risk factors for adverse outcomes in a large cohort of patients with IBD collected through an international registry.

When the Covid epidemic started to unfold around the country, the researchers collaborated to form an international registry of patients who have Inflammatory Bowel Disease (IBD) and COVID-19. The registry, Surveillance Epidemiology of Coronavirus Under Research Exclusion for Inflammatory Bowel Disease (SECURE-IBD), to date includes 528 patients from 33 countries.

"We established the registry to better characterize the clinical course of COVID-19 within the IBD patient population and evaluate the association between demographics, clinical characteristics, and IBD treatments on COVID-19 outcomes," says study co-author, Erica Brenner, MD, Pediatric Gastroenterology Fellow, UNC Children's Hospital.

The researchers conclude that increasing age, comorbidities, and corticosteroids are associated with severe COVID-19 among IBD patients, although a causal relationship cannot be definitively established. Notably, TNF antagonists do not appear to be associated with severe COVID-19.

"One of our main takeaways for the IBD patient population is that maintaining remission with steroid-sparing treatments will be important through this pandemic. Our finding that TNF antagonist therapy is not associated with severe COVID-19 is reassuring news in light of the large number of patients who require this therapy, currently the most commonly prescribed biologic therapy for IBD patients," says study co-author, Ryan Ungaro, MD, Assistant Professor, Icahn School of Medicine at Mount Sinai and a gastroenterologist with Mount Sinai Hospital's Feinstein IBD Center.

What The Study Did: National health care survey data were used to assess the amount of money spent on primary care relative to other areas of health care spending in the U.S. from 2002 to 2016.

Authors: Andrew W. Bazemore, M.D., M.P.H., of the American Board of Family Medicine in Washington, is the corresponding author.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/

(doi:10.1001/jamainternmed.2020.1360)

Editor's Note: Please see the article for additional information, including other authors, author contributions and affiliations, conflicts of interest and financial disclosures, and funding and support.

What The Study Did: Researchers compared the risk of suicide by firearm based on sociodemographic characteristics of U.S. adults.

Authors: Mark Olfson, M.D., M.P.H., of Columbia University in New York, is the corresponding author.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/

(doi:10.1001/jamainternmed.2020.1334)

Editor's Note: The article includes funding/support disclosures. Please see the article for additional information, including other authors, author contributions and affiliations, conflicts of interest and financial disclosures, and funding and support.

Crown-of-thorns starfish are on the menu for many more fish species than previously suspected, an investigation using fish poo and gut goo reveals.

The finding suggests that some fish, including popular eating and aquarium species, might have a role to play in keeping the destructive pest population under control.

The native starfish (Acanthaster solaris) is responsible for widespread damage to the Great Barrier Reef. Since 1962 its population has surged to plague proportions on three occasions, each time causing the loss of large amounts of hard coral. A fourth outbreak is currently underway.

Increasing the amount of predation on starfish has long been touted as a potential solution to preventing outbreaks. However, aside from a mollusc called the Giant Triton (Charonia tritonis), identifying what eats it has been a challenging task.

Now, a team of scientists led by Dr Frederieke Kroon from the Australian Institute of Marine Science in Townsville, Australia, has applied a genetic marker unique for crown-of-thorns, developed at AIMS, to detect the presence of starfish DNA in fish poo and gut contents.

Over three years, Dr Kroon's team used it on samples taken from 678 fish from 101 species, comprising 21 families, gathered from reefs experiencing varying levels of starfish outbreak.

"Our results strongly indicate that direct fish predation on crown-of-thorns may well be more common than is currently appreciated," said Dr Kroon.

The study, published in the journal Scientific Reports, confirms that at least 18 coral reef fish species - including Spangled Emperor (Lethrinus nebulosus), Redthroat Emperor (Lethrinus miniatus) and Blackspotted Puffer (Arothron nigropunctatus) - consume young or adult starfish on the reef.

Among the species were nine which had not been previously reported to feed on crown-of-thorns. These include the Neon Damsel (Pomacentrus coelistis), Redspot Emperor (Lethrinus lentjan), and the Blackspot Snapper (Lutjanus fulviflama).

"Our findings might also solve a mystery - why reef areas that are closed to commercial and recreational fishing tend to have fewer starfish than areas where fishing is allowed," said Dr Kroon.

She and colleagues from AIMS worked with researchers from CSIRO Land and Water and managers from the Great Barrier Reef Marine Park Authority to conduct the study.

"This innovative research sheds new light on the extent that coral reef fishes eat crown-of-thorns starfish," said Mr Darren Cameron, co-author of the paper, and Director of the COTS Control Program at the Great Barrier Reef Marine Park Authority.

"A number of the fish species shown to feed on these starfish are caught by commercial and recreational fisheries, highlighting the importance of marine park zoning and effective fisheries management in controlling crown-of-thorns starfish across the Great Barrier Reef."

When there's a vexing problem to be solved, people sometimes offer metaphorical advice such as "stretching the mind" or engaging in "flexible" thinking, but in confronting a problem facing many biomedical research labs, a team of MIT researchers has engineered a solution that is much more literal. To make imaging cells and molecules in brain and other large tissues easier while also making samples tough enough for years of handling in the lab, they have come up with a chemical process that makes tissue stretchable, compressible and pretty much indestructible.

"ELAST" technology, described in a new paper in Nature Methods, provides scientists a very fast way to fluorescently label cells, proteins, genetic material and other molecules within brains, kidneys, lungs, hearts and other organs. That's because when such tissues can be stretched out or squished down thin, labeling probes can infuse them far more rapidly. Several demonstrations in the paper show that even after repeated expansions or compressions to speed up labeling, tissues snap back to their original form unaltered except for the new labels.

The lab of Kwanghun Chung, an associate professor of chemical engineering and a member of MIT's Institute for Medical Engineering and Science, and Picower Institute for Learning and Memory, developed ELAST amid work on a five-year project, funded by the National Institutes of Health, to make the most comprehensive map yet of the entire human brain. That requires being able to label and scan every fine cellular and molecular detail in the thickest slabs possible to preserve 3D structure. It also means the lab must be able to keep samples perfectly intact for years, even as they must accomplish numerous individual rounds of labeling quickly and efficiently. Each round of labeling - maybe a particular kind of neuron one day, or a key protein the next - will tell them something new about how the brain is structured and how it works.

"When people donate their brain, it is like they are donating a library," said Chung. "Each one contains a library worth of information. You cannot access all the books in the library at the same time. We have to repeatedly be able to access the library without damaging it. Each of these brains is an extremely precious resource."

Former lab postdoc Taeyun Ku, now an assistant professor at the Korea Advanced Institute of Science and Technology, is the study's lead author. He said the particular difficulty of working with human tissues, which of course are much larger than those of lab animals like mice, inspired him to take this new engineering approach. Late one night in the lab around Christmas 2017, he said, he was mulling over how to transform tissue for quicker labeling and began to tinker with repeated compression of an elastic gel.

"We changed our way of thinking: biological tissue doesn't need to be very biological," Ku said. "If our goal is not to image living events but to image appearances, we can change the material type of the tissue while maintaining the appearances. Our work shows how higher-level engineering of the brain enables us to better look into what inside the brain."

Entangled links

The team's efforts to engineer ELAST came down to finding the right formulation of a gel-like chemical called polyacrylamide. In the past Chung has used the substance in a different formulation with crosslinking chemicals to make tissues strong but fairly brittle, said study co-author Webster Guan, a chemical engineering graduate student. When that formulation infused the tissues, cells and molecules would become directly attached to a grid-like mesh.

In the new formulation, the team used a high concentration of acrylamide with much less crosslinker and initiator. The result was an entanglement of long polymer chains with links that are able to slip around, giving the gel a structural integrity but with much more flexibility. Moreover, rather than attaching to the chains, Guan said, the cells and molecules of the tissue just become entangled within it, adding further to the ability of the acrylamide-infused tissues to withstand stretching or squashing without anything becoming torn or permanently displaced in the process.

In the study the team reports stretching human or mouse brain tissues to twice their width and length simultaneously or compressing their thickness by 10 times with virtually no distortion after returning to their regular size.

"These results demonstrate that ELAST enables fully reversible tissue shape transformation while preserving structural and molecular information in the tissue," they wrote.

Fully integrating the polyacrylamide into a large amount of tissue to achieve the elasticity can take as long as 21 days, they report, but from then on, any individual labeling step, such as labeling a particular kind of cell to determine its abundance, or a specific protein to see where it is expressed, can proceed far more quickly than with prior methods.

In one case, by repeatedly compressing a 5-milimeter thick cross section of a human brain, the team needed only 24 hours to label it all the way through. For comparison, back in 2013 when Chung and colleagues debuted "CLARITY," a method of making brain tissue transparent and fixing it with an acrylamide gel, they needed 24 hours to label a slice only a tenth as thick. Because labeling time is estimated by squaring the depth that probes must penetrate, calculations suggest labeling with ELAST proceeds 100 times faster than with CLARITY.

Though Chung's lab mostly focuses on brains, the applicability to other organs can aid in other cell mapping efforts, Chung said. He added that even if labeling tissue isn't a goal at all, having an easy new way to make a durable, elastic gel could have other applications, for instance in creating soft robotics. Resources for learning more about ELAST are available at Chung's website.

The mystery of some lava-like flows on Mars has been solved by scientists who say they are caused not by lava but by mud.

There are tens of thousands of these landforms on the Martian surface, often situated where there are massive channels scoured into the surface by ancient liquids flowing downstream.

These channels are extremely long, extending many hundreds of kilometres in length and usually more than dozens of kilometres wide. They are believed to be the result of massive floods involving huge bodies of water comparable to the largest floods ever known to have occurred on Earth. When the water seeps into the subsurface it can emerge again as mud.

A European team of researchers has now simulated the movement of mud on the surface of Mars, with the results published in Nature Geoscience.

The research was led by the Institute of Geophysics at the Czech Academy of Sciences, and involved Lancaster University, the Open University and the Rutherford Appleton Laboratory in the UK, CNRS in France, DLR and Münster University in Germany, and CEED in Norway.

Using the Mars Chamber at the Open University, the scientists recreated the surface temperature and atmospheric pressure on Mars as part of a simulation of conditions on both Earth and Mars.

Lionel Wilson, Emeritus Professor of Earth and Planetary Sciences at Lancaster University, said: "We performed experiments in a vacuum chamber to simulate the release of mud on Mars. This is of interest because we see many flow-like features on Mars in spacecraft images, but they have not yet been visited by any of the roving vehicles on the surface and there is some ambiguity about whether they are flows of lava or mud."

The scientists performed experiments at low pressure and at extremely cold temperatures (-20°C) to recreate the Martian environment. They found that free flowing mud under Martian conditions behaves differently from on Earth, because of rapid freezing and the formation of an icy crust. This is because water is not stable and begins to boil and evaporate. The evaporation removes latent heat from the mud, eventually causing it to freeze.

Under Martian conditions, the experimental mud flows formed similar shapes to "pahoehoe" lava frequently occurring on Hawaii or Iceland on Earth, which cools down to form smooth undulating surfaces. In the experiment, this happened when liquid mud spilled from ruptures in the frozen crust, then refroze.

However, under terrestrial atmospheric pressure, the experimental mud flows did not form lava shapes, did not expand, and had no icy crust, even under very cold conditions.

This "sedimentary volcanism" has also been proposed for the dwarf planet Ceres which lies in the asteroid belt between Mars and Jupiter and may have a muddy water ocean beneath an icy crust.

Dr Petr Brož, the leading author of the study, said: "We suggest that mud volcanism can explain the formation of some lava-like flow morphologies on Mars, and that similar processes may apply to eruptions of mud on icy bodies in the outer Solar System, like on Ceres."

CAMBIDGE, MA -- MIT neuroscientists have discovered that an enzyme called HDAC1 is critical for repairing age-related DNA damage to genes involved in memory and other cognitive functions. This enzyme is often diminished in both Alzheimer's patients and normally aging adults.

In a study of mice, the researchers showed that when HDAC1 is lost, a specific type of DNA damage builds up as the mice age. They also showed that they could reverse this damage and improve cognitive function with a drug that activates HDAC1.

The study suggests that restoring HDAC1 could have positive benefits for both Alzheimer's patients and people who suffer from age-related cognitive decline, the researchers say.

"It seems that HDAC1 is really an anti-aging molecule," says Li-Huei Tsai, the director of MIT's Picower Institute for Learning and Memory and the senior author of the study. "I think this is a very broadly applicable basic biology finding, because nearly all of the human neurodegenerative diseases only happen during aging. I would speculate that activating HDAC1 is beneficial in many conditions."

Picower Institute research scientist Ping-Chieh Pao is the lead author of the study, which appears today in Nature Communications.

DNA repair and aging

There are several members of the HDAC family of enzymes, and their primary function is to modify histones -- proteins around which DNA is spooled. These modifications control gene expression by blocking genes in certain stretches of DNA from being copied into RNA.

In 2013, Tsai's lab published two papers that linked HDAC1 to DNA repair in neurons. In the current paper, the researchers explored what happens when HDAC1-mediated repair fails to occur. To do that, they engineered mice in which they could knock out HDAC1 specifically in neurons and another type of brain cells called astrocytes.

For the first several months of the mice's lives, there were no discernable differences in their DNA damage levels or behavior, compared to normal mice. However, as the mice aged, differences became more apparent. DNA damage began to accumulate in the HDAC1-deficient mice, and they also lost some of their ability to modulate synaptic plasticity -- changes in the strength of the connections between neurons. The older mice lacking HCAC1 also showed impairments in tests of memory and spatial navigation.

The researchers found that HDAC1 loss led to a specific type of DNA damage called 8-oxo-guanine lesions, which are a signature of oxidative DNA damage. Studies of Alzheimer's patients have also shown high levels of this type of DNA damage, which is often caused by accumulation of harmful metabolic byproducts. The brain's ability to clear these byproducts often diminishes with age.

An enzyme called OGG1 is responsible for repairing this type of oxidative DNA damage, and the researchers found that HDAC1 is needed to activate OGG1. When HDAC1 is missing, OGG1 fails to turn on and DNA damage goes unrepaired. Many of the genes that the researchers found to be most susceptible to this type of damage encode ion channels, which are critical for the function of synapses.

Targeting neurodegeneration

Several years ago, Tsai and Stephen Haggarty of Harvard Medical School, who is also an author of the new study, screened libraries of small molecules in search of potential drug compounds that activate or inhibit members of the HDAC family. In the new paper, Tsai and Pao used one of these drugs, called exifone, to see if they could reverse the age-related DNA damage they saw in mice lacking HDAC1.

The researchers used exifone to treat two different mouse models of Alzheimer's, as well as healthy older mice. In all cases, they found that the drug reduced the levels of oxidative DNA damage in the brain and improved the mice's cognitive functions, including memory.

Exifone was approved in the 1980s in Europe to treat dementia but was later taken off the market because it caused liver damage in some patients. Tsai says she is optimistic that other, safer HDAC1-activating drugs could be worth pursuing as potential treatments for both age-related cognitive decline and Alzheimer's disease.

"This study really positions HDAC1 as a potential new drug target for age-related phenotypes, as well as neurodegeneration-associated pathology and phenotypes," she says.

Tsai's lab is now exploring whether DNA damage and HDAC1 also play a role in the formation of Tau tangles -- misfolded proteins in the brain that are a signature of Alzheimer's and other neurodegenerative diseases.

A squad of climate-related factors is responsible for the massive Australian coral bleaching event of 2016. If we're counting culprits: it's two by sea, one by land.

First, El Niño brought warmer water to the Coral Sea in 2016, threatening Australia's Great Barrier Reef's corals. Long-term global warming meant even more heat in the region, according to a new CIRES assessment. And in a final blow that year, a terrestrial heatwave swept over the coast, blanketing the reef system well into the winter, Karnauskas found. The final toll: more than half the coral in some parts of the Great Barrier Reef died.

"When the Great Barrier Reef bleached severely back in 2016, it earned global attention," said Kris Karnauskas, CIRES Fellow, associate professor of atmospheric and oceanic sciences at the University of Colorado Boulder and author on the study out today in Geophysical Research Letters. "Some speculated it was global warming, others thought it was El Niño, but the actual role of those two forces have not really been disentangled. As a physical climate scientist with a bias for the ocean, I thought I should dig in."

Karnauskas dissected the reasons behind the excessively warm water in Northern Australia's Coral Sea--water warm enough to "bleach" and kill coral, especially in the northern Great Barrier Reef. Karnauskas used satellite observations and a mathematical technique to fingerprint what phenomena led to what amount of warming, and when. It was the interaction of two key things, he found, that caused the coral-killing heat: A marine heatwave followed by a terrestrial one, both exacerbated by global warming.

First came a marine heatwave. It was El Niño that initially caused a spike in sea surface temperature by shifting sun-blocking clouds away from the region, but global warming trends increased its intensity and extended it by several months by raising the background temperature. Then, a landborne heatwave moved across eastern Australia and spilled out over the ocean just as the first phase of the marine heatwave was ending.

"It turns out that El Niño did play a role, and the eventual warmth was certainly higher because of the long-term trend, but the reason it lasted so long was actually this terrestrial heatwave lurking over eastern Australia until the marine warming event was just finally waning, and then: bang, the heatwave leaked out over the coastline," Karnauskas said. "That warm air over the ocean changed the way heat is exchanged between the ocean and atmosphere, keeping the ocean warm and bleaching for an extra month or so."

Increased water temperatures off the northeastern Australian coast triggered mass death of corals on an unprecedented scale. The hot water persisted for months, and caused extensive damage to the ecosystem--drastically changing the species composition of the region.

"This new finding reveals that climate variability and change can lead to marine impacts in surprising, compounding ways, including heatwaves both on land and in the ocean," said Karnauskas. "From heatwaves to hurricanes, we need to double down on efforts to understand the complexities of how anthropogenic climate change will influence extreme events in the future."

Neural networks in the visual cortex of the brain do a remarkable job of transforming the patterns of light that fall onto the retina into the vivid sensory experience that we call sight. A critical element of this encoding process depends on neurons that respond selectively to different features in the visual scene. Edges and their orientation in space carry an enormous amount of information about the visual environment, and individual neurons in the visual cortex encode this information by responding selectively to a narrow range of edge orientations; some responding maximally to vertical or horizontal, and others to different orientations in between. But neurons in visual cortex face another challenge in representing visual information: They must bring together the signals that originate from the left and right eyes to create a single unified binocular representation. The association of the inputs from the two eyes occurs in the visual cortex and we know that this is achieved with a high degree of precision such that individual neurons respond selectively to the same orientation with stimulation of either the left or right eye. What has been missing is a clear understanding of the developmental mechanisms that are responsible for uniting the inputs from the two eyes, a gap in knowledge that led Max Planck Florida researchers to a series of experiments that have revealed a critical role for early visual experience in guiding the formation of a unified binocular representation.

The first issue that Max Planck scientists Jeremy Chang, David Whitney, and David Fitzpatrick wanted to address is whether alignment of the inputs from the two eyes requires visual experience. Does the brain use vision to align the representations? They approached this question in the ferret, a species that has a well-organized visual cortex with a repeating modular structure in which nearby neurons have similar orientation preferences, resulting in distinct patterns of activity across the cortical surface for different orientations. This makes it possible to use imaging techniques that detect calcium signals to visualize the different modular patterns of activity that are associated with different orientations.  Prior to the onset of visual experience, they found that monocular stimulation produced activity patterns that had all the hallmarks of the mature visual cortex except one: the modular patterns of activity produced by stimulation of the left eye with a single orientation, were different from the modular patterns produced by the same stimulus orientation presented to the right eye. In other words, our brains are capable of developing orderly network representations of edge orientation in the absence of visual experience, but these networks lack the binocular alignment that is seen in mature animals. Additional experiments allowed the investigators to uncover a dynamic process that occurs over a short period of time (7-10 days) in which visual experience drives the alignment of these early representations. Importantly, the period when visual experience is capable of supporting alignment was found to be limited to the first week after eye opening, making it clear that early visual experience is critical for proper development of the circuits that support binocular vision for the rest of life.

These results suggested that binocular visual experience early in development is likely to be a key factor in the alignment of the network representations of the two eyes.  This led them to wonder what the patterns of activity in visual cortex would look like for simultaneous stimulation of the two eyes early in development before alignment has been achieved. Surprisingly, they found that binocular stimulation led to the appearance of a third modular representation--one that was distinct from the patterns of activity found for stimulation of the two eyes independently. By tracking these three representations across time they discovered that the early binocular representation was more stable than the others, appearing most similar to the mature, unified representation that emerges with visual experience. Thus, the activation of this binocular representation with the onset of binocular visual experience may guide the reorganization process, ensuring that all three representations become aligned as a single coherent network.

Ultimately, these changes in network structure must reflect changes in the response properties of single neurons, and to probe the process of alignment at the cellular scale, they turned to experiments using two-photon imaging that allowed them to visualize the response properties of individual neurons. Consistent with the network representation observations, individual neurons exhibited mismatched orientation preferences for monocular stimulation prior to the onset of visual experience that are rectified by changes in preferred orientation induced by visual experience. The next steps of this project are to investigate network reorganization at the synaptic scale, to identify precisely which components of the cortical network are changing and the mechanisms that enable the change.

A greater understanding of the mechanisms responsible for the experience-dependent alignment of cortical networks is critical for addressing visual disorders that arise from early abnormalities in visual experience such as amblyopia.  But experience-guided alignment of cortical networks is likely critical for a broad range of brain functions--sensory, motor, and cognitive-- that are optimized to support effective navigation and interaction with our world. Identifying those aspects of brain circuitry that depend on early experience for proper alignment, and understanding the underlying alignment mechanisms could offer insights into a host of neurodevelopmental disorders whose causes are still largely unknown.

White blood cells are known to circulate through the entire body inside blood vessels, acting as a surveillance system. However, a specialized group of these cells are permanently present in tissues like the skin, intestine and lungs, protecting against external invaders, such as microbes. But it is largely unknown how these cells are generated. A new study led by Marc Veldhoen, group leader at Instituto de Medicina Molecular João Lobo Antunes (iMM; Portugal) and published this week in the prestigious Nature Immunology*, shows that the local availability of specific molecules is crucial to generate these tissue resident surveillance cells. The impact of these results extends beyond protective immunity in tissues, as these cells are also efficient when elicited after vaccination and yield more effective anti-tumor immunity.

These tissue resident surveillance cells are a specialized group of T-cells, important to directly attack invading microorganisms. "The tissue resident T-cells develop after an initial infection, as part of immunological memory, and provide protection against future infections", explains Cristina Ferreira, first author of the paper.

Now, Marc Veldhoen and his team, have shown that within another population of T-cells, the regulatory T cells, mainly known for their ability to dampen immune responses to avoid damaging our own tissues, there are cells important for the development of these tissue resident T-cells. Using mouse models lacking this population of regulatory T-cells, the team observed that the number of tissue resident T-cells generated and present in the tissues was much lower. "It´s like the "surveillance system" in the gut, where we looked, was shut down. We could observe that a reduced number of the tissue resident T-cells resulted in less protection against invading pathogens", explains Marc Veldhoen.

But what is the role of the regulatory T-cells in the development of the tissue resident T-cells? "What we observed is that the regulatory T-cells are alerted to move to the site of infection, where they promote the local availability of a specific molecule, TGF-beta. According to our results, this is crucial to generate the tissue resident surveillance cells", explains Cristina Ferreira.

"We believe that learning more about how these cells develop might impact not only on how we look at infection conditions, especially in the gut, but also in cancer. It has been shown that the presence of tissue resident T-cells is important for a good outcome in cancer patients and, in animal models, studies have shown that these cells were most efficacious against cancer. Very likely, the reason is that these cells are specialized to penetrate deep into tissues. The more we know about these cells, the better we are equipped to develop ways to boost treatments in diseases, such as breast cancer", adds Marc Veldhoen, on the importance of these discoveries.