Orthopaedic researchers are one step closer to preventing life-long arm and leg deformities from childhood fractures that do not heal properly.
A new study led by the University of South Australia and published in the journal Bone, sheds light on the role that a protein plays in this process.
Lead author Dr Michelle Su says that because children’s bones are still growing, an injury to the growth plate can lead to a limb in a shortened position, compared to the unaffected side.
“Cartilage tissue near the ends of long bones is known as the growth plate that is responsible for bone growth in children and, unfortunately, 30 per cent of childhood and teen fractures involve this growth plate which is highly susceptible to injuries,” Dr Su says.
Instead of the rubbery cartilage tissue regenerating, bone tissue lodges in and around the injury site, causing different limb lengths and angulations.
Researchers from Adelaide, Perth and Shanghai used a rat model to investigate the role of this protein called bone morphogenetic protein (BMP). Dr Su says scientists are aware of the importance of BMP in bone development and normal bone fracture healing, but little is known about its role in growth plate repair.
The researchers found that levels of BMP were greater at the injured growth plate, and that inhibiting BMP suppressed growth plate bony repair and prevented degeneration of the surrounding uninjured region.
“This finding could be the first step in creating a biological treatment in place of correcting deformities by surgery, which can be complicated, extremely invasive and often ineffective,” Dr Su says.
Surgery involves inserting pins, plates, wires or screws to correct the damaged limbs, with a long period of recovery, which is not 100 per cent guaranteed.
“Further studies are needed to pinpoint the exact BMP members and other signalling components that are involved in causing the growth plate dysrepair,” she adds.
Falls account for close to half (46 per cent) or around 30,000 hospitalised injury cases involving children every year in Australia, according to the Australian Institute of Health and Welfare.
Overall, boys are 1.5 times more likely to sustain fractures than girls, but this varies with age — from 1.3 times for those aged between 0-4 and 1.8 times for those aged 10-14 years.
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Materials provided by University of South Australia. Note: Content may be edited for style and length.

Supersized alcopops are ready-to-drink flavored alcoholic beverages with high alcohol content that are disproportionately consumed by underage drinkers. There can be up to 5.5 standard alcoholic drinks in a single 24 ounce can, so consuming only one can of supersized alcopop is considered binge drinking, and consuming two cans can cause alcohol poisoning. Still, these products remain under-regulated and are available inexpensively at gas stations and convenience stores, where they are more readily accessible by underage youth.
New research led by George Mason University’s College of Health and Human Services found that nearly one-half (46.3 %) of all calls to U.S. poison control centers involving supersized alcopop consumption were made for consumers below the legal drinking age. Additionally, in every year studied, the proportion of calls for supersized alcopops among underage drinkers greatly exceeded the proportion of calls that were for underage drinkers for other types of alcohol.
Dr. Matthew Rossheim, an expert on supersized alcopop consumption and related health outcomes, led the study published in Drug and Alcohol Dependence. This study is the first report of clinical data within the last decade to examine negative effects from supersized alcopop consumption.
“A number of studies we’ve conducted have shown that supersized alcopops are commonly consumed by underage drinkers, which often results in serious negative consequences,” explains Rossheim. “Our latest data show a clear trend of supersized alcopop consumption among underage young people requiring poison center services. In this way, supersized alcopops appear to pose a distinct threat to youth.”
Rossheim and colleagues from the National Capital Poison Center and Emory University analyzed data from the National Poison Data System repository of calls to U.S. poison control centers from 2010 through 2019. This included 1,719 calls for consumption of supersized alcopops, many of whom consumed these products in combination with other substances. Acute care facilities such as emergency departments served as the management site for most calls (67.4 %), with another 14.3% referred to acute care.
While the large majority of consumption (more than 80%) was intentional for most age groups, 91% of the calls for children 0-11 years old who consumed supersized alcopops were for unintentional consumption. This suggests that the packaging and flavoring of these products can be attractive to children who do not understand how much alcohol these products contain or that they contain any alcohol at all.
“Better regulation and policies are urgently needed. Limiting their alcohol content and retail availability are immediate steps regulators must take in order to protect our youth.”
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Materials provided by George Mason University. Original written by Danielle Hawkins. Note: Content may be edited for style and length.

Testing and vaccination — these are the pillars on which humanity is trying to get a grip on the Coronavirus pandemic. Although it is taking longer than many had expected, it is believed that it is only a matter of time before we are all vaccinated and thus protected. However, time is also working for the virus, which has now mutated several times, with variants B.1.1.7 from the United Kingdom, B.1.351 from South Africa and P.1 from Brazil spreading rapidly. These viruses have mutations in the so-called spike protein, the structure on the surface of the virus that is responsible for attachment to host cells. At the same time, the spike protein is also the major target of the immune response. Antibodies generated in response to SARS-CoV-2 infection or vaccination bind to the spike protein, thereby blocking the virus.
A team led by Markus Hoffmann and Stefan Pöhlmann of the German Primate Center — Leibniz Institute for Primate Research and Jan Münch of the Ulm University Medical Centre has found that the SARS-CoV-2 variants B.1.351 and P.1 are no longer inhibited by an antibody used for COVID-19 therapy. In addition, these variants are less efficiently inhibited by antibodies from recovered patients and vaccinated individuals. Thus, convalescence from COVID-19 as well as vaccination may offer only incomplete protection against these mutant viruses (Cell).
SARS-CoV-2 viruses invade lung cells in order to multiply. For the virus to enter a cell, it must first attach to the cell surface. For this, the virus uses its so-called spike protein, which is located on the viral envelope. The spike protein is also the target for therapies and vaccines aimed at preventing the virus from replicating in the body.
At the beginning of the pandemic, SARS-CoV-2 was relatively stable, but recently several viral variants have been detected and are spreading rapidly. Variants B.1.1.7, B.1.351, and P.1, which first appeared in the United Kingdom, South Africa, and Brazil, respectively, have mutations in the spike protein and some are located in areas targeted by currently used antiviral agents and vaccines. “This is worrisome because the rapid spread of variants that might not be efficiently inhibited by antibodies could undermine our current vaccination strategy,” says Stefan Pöhlmann, an infection biologist at the German Primate Center in Göttingen. Therefore, the team led by Pöhlmann and Münch investigated how effectively the mutant viruses are inhibited by drugs and antibodies.
“We found that certain antiviral agents that block host cell entry and are in (pre)clinical development inhibit the mutant viruses just as well as the original virus. Variant B1.1.7, which is currently spreading rapidly in Germany, was also efficiently inhibited by antibodies, including antibodies induced by vaccination. In contrast, an antibody used for COVID-19 therapy did not inhibit variants B.1.351 and P.1. Moreover, these variants were less well inhibited by antibodies from convalescent or vaccinated individuals, they partially bypassed the neutralizing effect of the antibodies,” says Jan Münch.
The use of the currently available vaccines makes sense and a rapid expansion of the vaccination efforts in Germany is desirable. However, it is possible that vaccination or recovery from COVID-19 may offer reduced protection from SARS-CoV-2 variants B.1.351 and P.1.” Clinical studies must now show the extent to which this fear is true.
“Our findings show that it is important to limit the spread of the virus as much as possible until widespread vaccination is feasible. Otherwise, we risk the emergence of new variants that cannot be effectively controlled by the currently available vaccines,” says Markus Hoffmann, first author of the study.
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Materials provided by Deutsches Primatenzentrum (DPZ)/German Primate Center. Note: Content may be edited for style and length.

Humans are born with tens of thousands of hematopoietic stem cells (HSCs) that collectively ensure lifelong production of blood and immune cells that protect us from infections. HSCs can either duplicate to produce more stem cell progeny or differentiate to produce distinct immune cell lineages, an extremely critical decision that ensures that the body achieves the fine balance between having enough immune cells to fight invaders while still retaining enough HSCs to maintain future blood production. As we age, HSCs accumulate mutations that lead to the emergence of genetically distinct subpopulations. This common phenomenon known as clonal hematopoiesis (CH) is known to start in early fifties and is frequently associated with loss of function mutations in the DNMT3A gene. CH is associated with a significantly higher risk of blood cancers, cardiovascular disease, stroke and all-cause mortality.
A study led by Dr. Katherine King, associate professor at Baylor College of Medicine and Texas Children’s Hospital, shows for the first time that long-term infection and chronic inflammation drive CH mediated by the loss of Dnmt3a function. In addition, the study offers key insights into the mechanism by which chronic inflammation leads to CH and demonstrates the critical role of DNMT3a in regulating normal HSC responses to infections. The study was published in the journal Cell Stem Cell.
“Previously, we showed that chronic infection significantly impairs the ability of wild-type HSCs to remain in a quiescent stem cell state. Prolonged (lasting several months) exposure to a systemic bacterial infection promoted extensive differentiation of HSCs. While this produced sufficient immune cells to fight the infection, it also reduced the number of bone marrow HSCs by 90%,” King said. “In contrast, HSCs in mice lacking Dnmt3a gene did not differentiate much. In fact, they underwent self-renewal to produce more HSCs. We undertook the current study to test our prediction that defective differentiation and increased duplication of Dnmt3a HSCs allows them to overtake and outcompete normal HSCs when fighting chronic infections or facing long-term inflammatory conditions.”
To test their hypothesis, researchers used a combination of experimental and mathematical modeling experiments to test how HSCs from Dnmt3a mutant mice respond to long-term infection and chronic inflammation. For experimental validation, they generated mosaic mice that were generated by transplanting a mixture of whole bone marrow from Dnmt3a-mutant mice and normal mice into irradiated mice, which allowed them to track how each subpopulation of HSC contracts or grows relative to one another over time when infected for several months with Mycobacterium avium bacteria.
Using this model that mimics chronic infection in humans, they found long-term infection caused specific expansion of Dnmt3a-loss of function HSCs along with a concomitant reduction in their ability to differentiate into immune cells, which is contrary to the behavior exhibited by normal HSCs to chronic infection. Moreover, compared to the normal HSCs, Dnmt3a HSCs were more resistant to exhaustion and were less sensitive to stress-induced apoptosis (‘cell death’) upon chronic infection. Collectively, this indicates how a minor population of Dnmt3a HSCs could eventually overtake a major population of normal HSCs in the presence of chronic infection.
A number of viral or bacterial infections and chronic inflammatory stress conditions including tuberculosis, hepatitis, herpetic infections, and inflammatory bowel disease trigger the release of interferon gamma (IFN?) by the immune system, which in turn, initiates a cascade of protective immune responses. The team found that compared to wild-type HSCs, Dnmt3a-loss of function HSCs exhibited an entirely opposite set of cellular responses and global changes in gene expression patterns in response to IFN?, which tended towards preserving or even increasing the numbers of stem cells at the expense of mounting an effective response against imminent invaders or stress.
“We are excited by the findings of this study which opens several areas of future investigations. We have shown for the first time how chronic inflammation due to long-term infections or autoimmune conditions such as rheumatoid arthritis, ulcerative colitis or Crohn’s disease dampen the body’s immune response as we age. Moreover, it sheds light on the critically important role of DNMT3a in modulating immune responses during chronic infection or stress and also explains how aging and inflammation are linked to blood cancers,” King concluded.
Other authors involved in the study are Daniel Hormaechea-Agulla, Katie Matatall, Duy Le, Grant Challen, and Marek Kimmel. They are affiliated with one or more institutions: Baylor College of Medicine, Rice University, Silesian University of Technology, and Washington University School of Medicine. Grants from the National Institutes of Health, Dan L. Duncan Cancer Center, and Polish National Science Center supported this work.
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Materials provided by Texas Children’s Hospital. Note: Content may be edited for style and length.

Fish oil supplements are a billion-dollar industry built on a foundation of purported, but not proven, health benefits. Now, new research from a team led by a University of Georgia scientist indicates that taking fish oil only provides health benefits if you have the right genetic makeup.
The study, led by Kaixiong Ye and published in PLOS Genetics, focused on fish oil (and the omega-3 fatty acids it contains) and its effect on triglycerides, a type of fat in the blood and a biomarker for cardiovascular disease.
“We’ve known for a few decades that a higher level of omega-3 fatty acids in the blood is associated with a lower risk of heart disease,” said Ye, assistant professor of genetics in the Franklin College of Arts and Sciences. “What we found is that fish oil supplementation is not good for everyone; it depends on your genotype. If you have a specific genetic background, then fish oil supplementation will help lower your triglycerides. But if you do not have that right genotype, taking a fish oil supplement actually increases your triglycerides.”
Ye’s team, including first author and graduate student Michael Francis, examined four blood lipids (fats) — high-density lipoprotein, low-density lipoprotein, total cholesterol and triglycerides — that are biomarkers for cardiovascular disease. The data for their sample of 70,000 individuals was taken from UK Biobank, a large-scale cohort study collecting genetic and health information from half a million participants.
The team divided the sample into two groups, those taking fish oil supplements (about 11,000) and those not taking fish oil supplements. Then they performed a genome-wide scan for each group, testing for 8 million genetic variants to compare. After running over 64 million tests, their results revealed a significant genetic variant at gene GJB2. Individuals with the AG genotype who took fish oil decreased their triglycerides. Individuals with the AA genotype who took fish oil slightly increased their triglycerides. (A third possible genotype, GG, was not evident in enough study volunteers to draw conclusions.)
Determining your genotype is not as far-fetched as it sounds, thanks to direct-to-consumer genetic testing companies. Companies may not report that specific genetic variant yet, but a tech-savvy consumer should be able to download the raw data and look at the specific position to discover the genotype, according to Ye. The ID for the variant is rs112803755 (A >G).
The study’s findings may also shed light on previous trials, most of which found that fish oil provides no benefit in preventing cardiovascular disease.
“One possible explanation is that those clinical trials didn’t consider the genotypes of the participants,” Ye said. “Some participants may benefit, and some may not, so if you mix them together and do the analysis, you do not see the impact.”
Now that Ye has identified a specific gene that can modify an individual’s response to fish oil supplementation, his next step will be directly testing the effects of fish oil on cardiovascular disease.
“Personalizing and optimizing fish oil supplementation recommendations based on a person’s unique genetic composition can improve our understanding of nutrition,” he said, “and lead to significant improvements in human health and well-being.”
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Materials provided by University of Georgia. Original written by Allyson Mann. Note: Content may be edited for style and length.

In “Hooked,” Michael Moss explores how no addictive drug can fire up the reward circuitry in our brains as rapidly as our favorite foods.In a legal proceeding two decades ago, Michael Szymanczyk, the chief executive of the tobacco giant Philip Morris, was asked to define addiction. “My definition of addiction is a repetitive behavior that some people find difficult to quit,” he responded.Mr. Szymanczyk was speaking in the context of smoking. But a fascinating new book by Michael Moss, an investigative journalist and best-selling author, argues that the tobacco executive’s definition of addiction could apply to our relationship with another group of products that Philip Morris sold and manufactured for decades: highly processed foods.In his new book, “Hooked,” Mr. Moss explores the science behind addiction and builds a case that food companies have painstakingly engineered processed foods to hijack the reward circuitry in our brains, causing us to overeat and helping to fuel a global epidemic of obesity and chronic disease. Mr. Moss suggests that processed foods like cheeseburgers, potato chips and ice cream are not only addictive, but that they can be even more addictive than alcohol, tobacco and drugs. The book draws on internal industry documents and interviews with industry insiders to argue that some food companies in the past couple of decades became aware of the addictive nature of their products and took drastic steps to avoid accountability, such as shutting down important research into sugary foods and spearheading laws preventing people from suing food companies for damages.PenguinRandomHouseIn another cynical move, Mr. Moss writes, food companies beginning in the late 1970s started buying a slew of popular diet companies, allowing them to profit off our attempts to lose the weight we gained from eating their products. Heinz, the processed food giant, bought Weight Watchers in 1978 for $72 million. Unilever, which sells Klondike bars and Ben & Jerry’s ice cream, paid $2.3 billion for SlimFast in 2000. Nestle, which makes chocolate bars and Hot Pockets, purchased Jenny Craig in 2006 for $600 million. And in 2010 the private equity firm that owns Cinnabon and Carvel ice cream purchased Atkins Nutritionals, the company that sells low-carb bars, shakes and snacks. Most of these diet brands were later sold to other parent companies.“The food industry blocked us in the courts from filing lawsuits claiming addiction; they started controlling the science in problematic ways, and they took control of the diet industry,” Mr. Moss said in an interview. “I’ve been crawling through the underbelly of the processed food industry for 10 years and I continue to be stunned by the depths of the deviousness of their strategy to not just tap into our basic instincts, but to exploit our attempts to gain control of our habits.”A former reporter for The New York Times and recipient of the Pulitzer Prize, Mr. Moss first delved into the world of the processed food industry in 2013 with the publication of “Salt Sugar Fat.” The book explained how companies formulate junk foods to achieve a “bliss point” that makes them irresistible and market those products using tactics borrowed from the tobacco industry. Yet after writing the book, Mr. Moss was not convinced that processed foods could be addictive.“I had tried to avoid the word addiction when I was writing ‘Salt Sugar Fat,’” he said. “I thought it was totally ludicrous. How anyone could compare Twinkies to crack cocaine was beyond me.”But as he dug into the science that shows how processed foods affect the brain, he was swayed. One crucial element that influences the addictive nature of a substance and whether or not we consume it compulsively is how quickly it excites the brain. The faster it hits our reward circuitry, the stronger its impact. That is why smoking crack cocaine is more powerful than ingesting cocaine through the nose, and smoking cigarettes produces greater feelings of reward than wearing a nicotine patch: Smoking reduces the time it takes for drugs to hit the brain.But no addictive drug can fire up the reward circuitry in our brains as rapidly as our favorite foods, Mr. Moss writes. “The smoke from cigarettes takes 10 seconds to stir the brain, but a touch of sugar on the tongue will do so in a little more than a half second, or six hundred milliseconds, to be precise,” he writes. “That’s nearly 20 times faster than cigarettes.”This puts the term “fast food” in a new light. “Measured in milliseconds, and the power to addict, nothing is faster than processed food in rousing the brain,” he added.Mr. Moss explains that even people in the tobacco industry took note of the powerful lure of processed foods. In the 1980s, Philip Morris acquired Kraft and General Foods, making it the largest manufacturer of processed foods in the country, with products like Kool-Aid, Cocoa Pebbles, Capri Sun and Oreo cookies. But the company’s former general counsel and vice president, Steven C. Parrish, confided that he found it troubling that it was easier for him to quit the company’s cigarettes than its chocolate cookies. “I’m dangerous around a bag of chips or Doritos or Oreos,” he told Mr. Moss. “I’d avoid even opening a bag of Oreos because instead of eating one or two, I would eat half the bag.”As litigation against tobacco companies gained ground in the 1990s, one of the industry’s defenses was that cigarettes were no more addictive than Twinkies. It may have been on to something. Philip Morris routinely surveyed the public to gather legal and marketing intelligence, Mr. Moss writes, and one particular survey in 1988 asked people to name things that they thought were addictive and then rate them on a scale of 1 to 10, with 10 being the most addictive.“Smoking was given an 8.5, nearly on par with heroin,” Mr. Moss writes. “But overeating, at 7.3, was not far behind, scoring higher than beer, tranquilizers and sleeping pills. This statistic was used to buttress the company’s argument that cigarettes might not be exactly innocent, but they were a vice on the order of potato chips and, as such, were manageable.”But processed foods are not tobacco, and many people, including some experts, dismiss the notion that they are addictive. Mr. Moss suggests that this reluctance is in part a result of misconceptions about what addiction entails. For one, a substance does not have to hook everyone for it to be addictive. Studies show that most people who drink or use cocaine do not become dependent. Nor does everyone who smokes or uses painkillers become addicted. It is also the case that the symptoms of addiction can vary from one person to the next and from one drug to another. Painful withdrawals were once considered hallmarks of addiction. But some drugs that we know to be addictive, such as cocaine, would fail to meet that definition because they do not provoke “the body-wrenching havoc” that withdrawal from barbiturates and other addictive drugs can cause.The American Psychiatric Association now lists 11 criteria that are used to diagnose what it calls a substance use disorder, which can range from mild to severe, depending on how many symptoms a person exhibits. Among those symptoms are cravings, an inability to cut back despite wanting to, and continuing to use the substance despite it causing harm. Mr. Moss said that people who struggle with processed food can try simple strategies to conquer routine cravings, like going for a walk, calling a friend or snacking on healthy alternatives like a handful of nuts. But for some people, more extreme measures may be necessary.“It depends where you are on the spectrum,” he said. “I know people who can’t touch a grain of sugar without losing control. They would drive to the supermarket and by the time they got home their car would be littered with empty wrappers. For them, complete abstention is the solution.”

A new analysis suggests that schools and colleges, large companies and other organizations that want to keep themselves safe with frequent mass testing should think beyond their own personnel.By dedicating a substantial portion of their tests to people in the surrounding community, they can reduce the number of Covid-19 cases among their members by as much as 25 percent, researchers report in a new paper, which has not yet been published in a scientific journal.“It’s natural in an outbreak for people to become self-serving, self-focused,” said Dr. Pardis Sabeti, a computational biologist at Harvard University and the Broad Institute who led the analysis. But she added, “If you’ve been in enough outbreaks, you just understand that testing in a box doesn’t makes sense. These things are communicable, and they’re coming in from the community.”The study has “really profound implications, especially if others can replicate it,” said David O’Connor, a virologist at the University of Wisconsin, Madison, who was not involved in the analysis but reviewed a draft of the paper.Early in the pandemic, when testing resources were in short supply, many colleges proposed intensive, expensive testing regimens focused entirely on their own campuses. When they sought Dr. Sabeti’s advice, she said, she told them they ought to test friends, relatives and neighbors of their students and employees as well.It was not an easy idea to sell without data on its effectiveness, so Dr. Sabeti and her colleagues developed an epidemiological model to simulate how a virus might spread through a midsize institution, Colorado Mesa University, and what would happen under different testing policies. They found that allocating some tests to community contacts would significantly reduce the expected number of Covid cases on campus.C.M.U. now offers free tests to all of its students’ self-reported contacts, and runs a testing site that is open to local residents, according to Amy Bronson, a co-chair of the university’s Covid-19 task force and an author of the paper.And in November, the University of California, Davis, began offering free coronavirus tests to anyone who lives or works in that city.“A virus does not respect geographic boundaries,” said Brad Pollock, an epidemiologist at U.C. Davis who directs the project. “It is ludicrous to think that you can get control of an acute infectious respiratory disease like Covid-19, in a city like Davis that hosts a very large university, without coordinated public health measures that connect both the university and the community.”

A 10-week muscle-building and dietary program involving 50 middle-aged adults found no evidence that eating a high-protein diet increased strength or muscle mass more than consuming a moderate amount of protein while training. The intervention involved a standard strength-training protocol with sessions three times per week. None of the participants had previous weightlifting experience.
Published in the American Journal of Physiology: Endocrinology and Metabolism, the study is one of the most comprehensive investigations of the health effects of diet and resistance training in middle-aged adults, the researchers say. Participants were 40-64 years of age.
The team assessed participants’ strength, lean-body mass, blood pressure, glucose tolerance and several other health measures before and after the program. They randomized participants into moderate- and high-protein diet groups. To standardize protein intake, the researchers fed each person a freshly cooked, minced beef steak and carbohydrate beverage after every training session. They also sent participants home with an isolated-protein drink to be consumed every evening throughout the 10 weeks of the study.
“The moderate-protein group consumed about 1.2 grams of protein per kilogram of body weight per day, and the high-protein group consumed roughly 1.6 grams per kilogram per day,” said Colleen McKenna, a graduate student in the division of nutritional sciences and registered dietician at the University of Illinois Urbana-Champaign who led the study with U. of I. kinesiology and community health professor Nicholas Burd. The team kept calories equivalent in the meals provided to the two groups with additions of beef tallow and dextrose.
The study subjects kept food diaries and McKenna counseled them every other week about their eating habits and protein intake.
In an effort led by U. of I. food science and human nutrition professor Hannah Holscher, the team also analyzed gut microbes in fecal samples collected at the beginning of the intervention, after the first week — during which participants adjusted to the new diet but did not engage in physical training — and at the end of the 10 weeks. Previous studies have found that diet alone or endurance exercise alone can alter the composition of microbes in the digestive tract.

One-third of the Earth’s surface is covered by more than 11,000 grass species — including crops like wheat, corn, rice and sugar cane that account for the bulk of the world’s agricultural food production and important biofuels. But grass is so common that few people realize how diverse and important it really is.
Research published today in the journal Nature provides insights that scientists could use not only to improve crop design but also to more accurately model the effects of climate change. It also offers new clues that could help scientists use leaf fossils to better interpret the climate of the ancient past.
The study’s senior author is Lawren Sack, a UCLA professor of ecology and evolutionary biology and one of the world’s most influential scientific researchers.
The research determined that grass with narrow leaves and high numbers of veins should be better able to withstand the drier conditions expected in the future. That finding should enable scientists to better predict grass species’ ability to tolerate cold and drought — important for conserving species amidst climate change. It also suggests that scientists who are breeding agricultural grasses to better survive cold climates and drought should turn their focus toward varieties with smaller leaves and more large veins.
From other types of plants, scientists have learned that leaf size is an important factor in how plants adapt to their environments. But until now, it was not known how thousands of species of grass could exist in so many diverse environments, and whether leaf size might play a role.
“Grass leaf blades can vary in size from a few square millimeters for grasses of the high Andes to more than a square meter for tropical bamboos,” Sack said.

Researchers have developed a new microscopy technique that can acquire 3D super-resolution images of subcellular structures from about 100 microns deep inside biological tissue, including the brain. By giving scientists a deeper view into the brain, the method could help reveal subtle changes that occur in neurons over time, during learning, or as result of disease.
The new approach is an extension of stimulated emission depletion (STED) microscopy, a breakthrough technique that achieves nanoscale resolution by overcoming the traditional diffraction limit of optical microscopes. Stefan Hell won the 2014 Nobel Prize in Chemistry for developing this super-resolution imaging technique.
In Optica, The Optical Society’s (OSA) journal for high impact research, the researchers describe how they used their new STED microscope to image, in super-resolution, the 3D structure of dendritic spines deep inside the brain of a living mouse. Dendric spines are tiny protrusions on the dendritic branches of neurons, which receive synaptic inputs from neighboring neurons. They play a crucial role in neuronal activity.
“Our microscope is the first instrument in the world to achieve 3D STED super-resolution deep inside a living animal,” said leader of the research team Joerg Bewersdorf from Yale School of Medicine. “Such advances in deep-tissue imaging technology will allow researchers to directly visualize subcellular structures and dynamics in their native tissue environment,” said Bewersdorf. “The ability to study cellular behavior in this way is critical to gaining a comprehensive understanding of biological phenomena for biomedical research as well as for pharmaceutical development.”
Going deeper
Conventional STED microscopy is most often used to image cultured cell specimens. Using the technique to image thick tissue or living animals is a lot more challenging, especially when the super-resolution benefits of STED are extended to the third dimension for 3D-STED. This limitation occurs because thick and optically dense tissue prevents light from penetrating deeply and from focusing properly, thus impairing the super-resolution capabilities of the STED microscope.
To overcome this challenge, the researchers combined STED microscopy with two-photon excitation (2PE) and adaptive optics. “2PE enables imaging deeper in tissue by using near-infrared wavelengths rather than visible light,” said Mary Grace M. Velasco, first author of the paper. “Infrared light is less susceptible to scattering and, therefore, is better able to penetrate deep into the tissue.”
The researchers also added adaptive optics to their system. “The use of adaptive optics corrects distortions to the shape of light, i.e., the optical aberrations, that arise when imaging in and through tissue,” said Velasco. “During imaging, the adaptive element modifies the light wavefront in the exact opposite way that the tissue in the specimen does. The aberrations from the adaptive element, therefore, cancel out the aberrations from the tissue, creating ideal imaging conditions that allow the STED super-resolution capabilities to be recovered in all three dimensions.”
Seeing changes in the brain
The researchers tested their 3D-2PE-STED technique by first imaging well-characterized structures in cultured cells on a cover slip. Compared to using 2PE alone, 3D-2PE-STED resolved volumes more than 10 times smaller. They also showed that their microscope could resolve the distribution of DNA in the nucleus of mouse skin cells much better than a conventional two-photon microscope.
After these tests, the researchers used their 3D-2PE-STED microscope to image the brain of a living mouse. They zoomed-in on part of a dendrite and resolved the 3D structure of individual spines. They then imaged the same area two days later and showed that the spine structure had indeed changed during this time. The researchers did not observe any changes in the structure of the neurons in their images or in the mice’s behavior that would indicate damage from the imaging. However, they do plan to study this further.
“Dendritic spines are so small that without super-resolution it is difficult to visualize their exact 3D shape, let alone any changes to this shape over time,” said Velasco. “3D-2PE-STED now provides the means to observe these changes and to do so not only in the superficial layers of the brain, but also deeper inside, where more of the interesting connections happen.”
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Materials provided by The Optical Society. Note: Content may be edited for style and length.