The findings will be published online Sept. 17 in JAMA Network Open.

“We wanted to understand the spectrum of allergies to the new vaccines and understand what was causing them,” said the study’s senior author, Kari Nadeau, MD, PhD, the Naddisy Foundation Professor in Pediatric Food Allergy, Immunology, and Asthma.

The study analyzed 22 potential allergic reactions to the first 39,000 doses of Pfizer and Moderna COVID-19 vaccines given to health care providers at Stanford soon after the vaccines received emergency use authorization from the Food and Drug Administration.

Most of those in the study who developed reactions were allergic to an ingredient that helps stabilize the COVID-19 vaccines; they did not show allergies to the vaccine components that provide immunity to the SARS-CoV-2 virus. Furthermore, these allergic reactions occurred via an indirect activation of allergy pathways, which makes them easier to mitigate than many allergic responses.

“It’s nice to know these reactions are manageable,” said Nadeau, who directs the Sean N. Parker Center for Allergy and Asthma Research at Stanford. “Having an allergic reaction to these new vaccines is uncommon, and if it does happen, there’s a way to manage it.”

The study’s lead author is former postdoctoral scholar Christopher Warren, PhD, now an assistant professor at Northwestern University Feinberg School of Medicine.

The research also suggests how vaccine manufacturers can reformulate the vaccines to make them less likely to trigger allergic responses, Nadeau said.

Delivery of protein-making instructions

The mRNA-based COVID-19 vaccines provide immunity via small pieces of messenger RNA that encode molecular instructions for making proteins. Because the mRNA in the vaccines is fragile, it is encased in bubbles of lipids — fatty substances — and sugars for stability. When the vaccine is injected into someone’s arm, the mRNA can enter nearby muscle and immune cells, which then manufacture noninfectious proteins resembling those on the surface of the SARS-CoV-2 virus. The proteins trigger an immune response that allows the person’s immune system to recognize and defend against the virus.

Estimated rates of severe vaccine-related anaphylaxis — allergic reactions bad enough to require hospitalization — are 4.7 and 2.5 cases per million doses for the Pfizer and Moderna vaccines, respectively, according to the federal Vaccine Adverse Event Reporting System. However, the federal system doesn’t capture all allergic reactions to vaccines, tending to miss those that are mild or moderate.

For a more complete understanding of allergic reactions to the new vaccines — how common they are, as well as how severe — the research team examined the medical records of health care workers who received 38,895 doses of mRNA-based COVID-19 vaccines at Stanford Medicine between Dec. 18, 2020, and Jan. 26, 2021. The vaccinations included 31,635 doses of the Pfizer vaccine and 7,260 doses of the Moderna vaccine.

The researchers searched vaccine recipients’ medical records for treatment of allergic reactions and identified which reactions were linked to the vaccines. Twenty-two recipients, 20 of them women, had possible allergic reactions, meaning specific symptoms starting within three hours of receiving the shots. The researchers looked for the following symptoms in recipients’ medical records: hives; swelling of the mouth, lips, tongue or throat; shortness of breath, wheezing or chest tightness; or changes in blood pressure or loss of consciousness. Only 17 of the 22 recipients had reactions that met diagnostic criteria for an allergic reaction. Three recipients received epinephrine, usually given for stronger anaphylaxis. All 22 fully recovered.

Of the 22 recipients, 15 had physician-documented histories of prior allergic reactions, including 10 to antibiotics, nine to foods and eight to nonantibiotic medications. (Some recipients had more than one type of allergy.)

The researchers performed follow-up laboratory testing on 11 individuals to determine what type of allergic reaction they had, as well as what triggered their allergy: Was it one of the inert sugar or lipid ingredients in the bubble, or something else in the vaccine?

The study participants underwent skin-prick tests, in which a clinician injected small amounts of potential allergens — the lipids, sugars (polyethylene glycol or polysorbates) or entire vaccine — into the skin. Skin-prick testing detects allergic reactions mediated by a form of antibody known as immunoglobin E, or IgE; these reactions are generally associated with the severest allergies.

None of the recipients reacted on skin-prick tests to the inert ingredients in the vaccines, and just one recipient’s skin reacted to the whole COVID-19 vaccine. Follow-up blood tests showed that the vaccine recipients did not have significant levels of IgE antibodies against the vaccine ingredients.

Since the skin tests did not explain the mechanism of recipients’ allergic reactions, the investigators proceeded to another type of diagnostic test. Vaccine recipients provided blood samples for tests of allergic activation of immune cells known as basophils. The blood samples from 10 of the 11 participants showed a reaction to the inert ingredient polyethylene glycol (PEG), which is used in both the Pfizer and Moderna vaccines. In addition, all 11 recipients had basophil activation in response to the whole mRNA vaccine when it was mixed with their own basophils.

All 11 subjects had high levels of IgG antibodies against PEG in their blood; IgG antibodies help activate basophils under some conditions, and this finding suggests the individuals were likely sensitive to PEG before receiving their vaccines.

“What’s important is what we didn’t find, as much as what we did find,” Nadeau said. “It does not seem that the mRNA itself causes the allergic reactions.”

In addition, the data suggest that reactions to the COVID-19 vaccines were generally not the most severe form of allergic reaction, which is good news in terms of vaccine safety, she said. Allergic reactions mediated by IgG and basophils can be managed with antihistamines, fluids, corticosteroids and close observation, meaning that many individuals who have had a reaction to their first vaccine dose can safely receive a second dose under medical supervision.

PEG is widely used as a stabilizer in household products, cosmetics and medications, with women more likely to be exposed to large quantities of the substance, possibly explaining why more vaccine allergies have been seen among women. (Repeated exposures to a substance can sometimes sensitize the immune system and provoke allergies.) Because most reactions were to PEG rather than the vaccine’s active ingredients, it is likely that vaccine manufacturers can reformulate the vaccines with different stabilizers that are less likely to cause allergies, Nadeau said.

The study’s other Stanford authors are research assistants Theo Snow, Alexandra Lee, Mihir Shah, Eric Smith, Evan Do and Iris Chang; Andra Blomkalns, MD, professor of emergency medicine; Brooke Betts, PharmD, clinical pharmacist; medical student Anthony Buzzanco; graduate student Joseph Gonzalez; Sharon Chinthrajah, MD, associate professor of medicine and of pediatrics; lab manager Diane Dunham; Grace Lee, MD, professor of pediatrics; Ruth O’Hara, MD, PhD, dean of research and professor of psychiatry and behavioral sciences; Helen Park, PharmD, clinical pharmacist at the Veterans’ Affairs Palo Alto Health Care System; Lisa Schilling, RN, MPH, vice president of quality, safety and clinical effectiveness and chief quality officer with Stanford Health Care; Sayantani Sindher, MD, clinical associate professor of medicine and of pediatrics; Deepak Sisodiya, PharmD, administrative director of pharmacy services at Stanford Health Care; Mindy Tsai, DMSc, senior research scientist in pathology; and Stephen Galli, MD, professor of pathology and of microbiology and immunology.

Nadeau is a member of the Stanford Institute for Immunology, Transplantation and Infection; senior fellow at the Stanford Woods Institute for the Environment; a fellow at the Stanford Center for Innovation and Global Health; and member of the Bill Lane Center for the American West at Stanford. Nadeau and Galli are members of Stanford Bio-X. Nadeau, O’Hara and Galli are members of the Stanford Cardiovascular Institute. Nadeau and O’Hara are members of the Wu Tsai Neurosciences Institute at Stanford. O’Hara, Nadeau, Chinthrajah, Grace Lee, Sindher and Galli are members of the Stanford Maternal and Child Health Research Institute. Galli is a member of the Stanford Cancer Institute.

Researchers from the Swiss Institute of Allergy and Asthma Research at the University of Zurich; the Department of National Heart and Lung Institute at Imperial College London; and the Centre in Allergic Mechanisms of Asthma, London, also contributed to this research.

The research was supported by the Asthma and Allergic Diseases Cooperative Research Centers (grant U19AI104209), the National Institutes of Health (grant R01AI140134), the National Institute of Allergy and Infectious Disease SARS Vaccine study (grant UM1AI10956508), the Parker Foundation, the Crown Foundation and the Sunshine Foundation.

The researchers studied the impact of deleting specific proteins in immune cells that were responsible for controlling the ability of cells to silence or switch off genes.

They were surprised to find that one population of ‘sentinel’ immune cells was affected by deletion of a component of the machinery, causing the cells to disappear from skin and lungs completely. This suggests that drugs which inhibit this component to treat diseases, such as cancer, could have unintended consequences for the immune system.

The research was led by Dr Yifan Zhan, Dr Yuxia Zhang, Mr Shengbo Zhang, Dr Michael Chopin, Professor Stephen Nutt and colleagues, and was published in Science Immunology.

A complex issue

The research team studied the role of the polycomb repressive complex 2 (PRC2) in frontline responder immune cells.

Dr Chopin said the PRC2 was responsible for ‘switching off’ genes, including in immune cells, which was essential for maintaining their numbers and normal function.

“Our laboratory investigates gene regulation, or the molecular processes inside cells that control how and when the genes encoded by our DNA are used,” he said.

“We studied the function of the PRC2 in two immune cell populations that form the first line of defence against infection. These cells provide a critical immune barrier to the external environment, protecting the skin and lungs from microbial invasion.”

The research team removed two components of the complex, an enzyme called EZH2 and a structural protein called Suz12, to see how it impacted immune cell development, populations and function.

Deleting EZH2 had no impact on the biology or function of either cell population — with the cells still able to respond to viral infection effectively.

“We surprised to find that the immune cells were largely unaffected by deleting EZH2,” Dr Chopin said.

In contrast, when Suz12 was deleted, certain populations of macrophages, such as those that reside in our skin and lungs, completely disappeared.

“These tissue-resident macrophages are responsible for detecting and ridding the body of a variety of infiltrating bacteria and virus-infected cells, and alerting the body that it is under attack by stimulating the production of inflammatory signals,” Dr Chopin said.

“Tissue-resident macrophages have the unique property of being able to independently maintain their numbers throughout adult life. Our research highlights a key role for Suz12 and PRC2 in controlling this regulatory program of these immune cells.”

Unexpected effects

Professor Nutt said it was important to understand the potential knock-on effects of drugs that interfere with the proteins that switch genes off.

“PRC2 has been implicated in many cancers, such as lymphoma. There is significant work being undertaken around the world to develop drugs that target components of the complex to treat cancer.

He said at least one drug already approved for treating a rare type of sarcoma inhibited components of the complex.

“We need to study more closely whether drugs that inhibit the function of EZH2 and Suz12 could have unintended consequences for the immune system,” he said.

On the flipside, Professor Nutt said, it was also important to understand what redundancies exist that might prevent drugs having their desired effect.

“The current belief is that inhibiting EZH2 will dampen the immune response, for example if you are wanting to treat immune or inflammatory diseases,” Professor Nutt said. “Our research shows that, at least with these specific frontline immune cells, that are active early in infection and trigger other elements of the immune system, that is unlikely to be the case.”

Professor Nutt said the research was part of the team’s broader focus on gene regulation at a molecular level.

“The normal function of the cells in our bodies relies on each cell’s ability to use the appropriate combination of genes from the tens of thousands of genes encoded in our DNA in the right place and at the right time,” he said.

“The molecular controls that prevent genes from being used are essential to life.”

The research was supported by the Australian National Health and Medical Research Council, WEHI Innovation Grant and the Victorian Government.

In Singapore, the prevalence of childhood SLE has been reported to be 14.2 per 100,000 children, while that of adult SLE is 40 per 100,000 adult population. Cognitive dysfunction is common in patients with SLE. Earlier studies have shown that 25% of SLE patients were found to have cognitive dysfunction, compared to 7.3% in age- and gender-matched healthy individuals. Common cognitive dysfunction demonstrated by SLE patients includes impairment of simple reaction time, sustained and selected attention, memory search, working memory, and short-term memory for learnt associations, which result in reduced health-related quality of life and a negative impact on vocational capability.

The neural mechanism leading to cognitive dysfunction in patients with SLE remains unknown. Researchers at the NUS Yong Loo Lin School of Medicine attempted to unravel such mechanisms by adopting non-invasive diffusion magnetic resonance imaging (MRI) to study the brains of SLE patients, particularly the white matter, coupled with computerised neuropsychological assessment. White matter lies beneath the grey matter cortex in the human brain and comprises millions of bundles of nerve fibres that transmit signals to different brain regions.

Led jointly by Associate Professor Juan Helen Zhou, from the Centre for Sleep and Cognition and Deputy Director for the Centre for Translational Magnetic Resonance Research at NUS Medicine, and Associate Professor Anselm Mak, a clinician scientist with the Division of Rheumatology at the Department of Medicine, the group investigated brain white matter free water changes in SLE. White matter free water refers to water molecules surrounding white matter in the brain that are able to diffuse unhindered

In the paper published in Rheumatology, a Tier 1 journal in the field of Rheumatology with the Oxford University Press, they compared the free-water signals in SLE patients without clinically overt neuropsychiatric manifestations with a group of matched healthy participants using the novel free water diffusion MRI technique. They discovered that patients with SLE had significantly higher white matter free water than their healthy counterparts, suggesting possible microvascular degradation and/or inflammation. Such increases in free water were significantly related to cognitive dysfunction, especially sustained attention, as well as cumulative dosage of medical steroids.

“The clinical implications of the study would indicate to physicians that steroids should be judiciously prescribed, aiming for the lowest possible dose for the shortest possible duration. While systemic use of steroids will continue to be the mainstay of treatment for moderate to severe SLE-related inflammation, there are other therapeutic options that could produce similar results: these should be considered first in order to reduce steroid use or shorten the necessary course,” said Assoc Prof Anselm Mak.

He also added that there are other SLE manifestations that could be symptomatically treated without the prescription of steroids. For example, non-steroidal anti-inflammatory drugs could be used for milder inflammation, topical treatment for hair loss and topical analgesics for oral ulcers.

SLE patients on long-term steroid treatments should also be regularly assessed and monitored for cognitive dysfunction. The researchers noted that the use of the Automated Neuropsychiatric Assessment Matrix (ANAM), which has been validated for use in adult and paediatric SLE patients, is an efficient and effective tool for these regular evaluations.

Further research will have to be conducted to find out if a reduction of steroid dosage would be related to reduction of white matter free water that would lead to an improvement to cognitive function in SLE patients. The team is also keen to further investigate the mechanism of the increase in white matter free water underlying cognitive decline using multimodal imaging, behavioral, and blood assays in SLE patients longitudinally.

Under the guidance of Mechanical Engineering Professor Hod Lipson, the “Digital Food” team of his Creative Machines Lab has been building a fully autonomous digital personal chef. Lipson’s group has been developing 3D-printed foods since 2007. Since then, food printing has progressed to multi-ingredient prints and has been explored by researchers and a few commercial companies.

“We noted that, while printers can produce ingredients to a millimeter-precision, there is no heating method with this same degree of resolution,” said Jonathan Blutinger, a PhD in Lipson’s lab who led the project. “Cooking is essential for nutrition, flavor, and texture development in many foods, and we wondered if we could develop a method with lasers to precisely control these attributes.”

In a new study published Sept. 1, 2021, by npj Science of Food, the team explored various modalities of cooking by exposing blue light (445 nm) and infrared light (980 nm and 10.6 μm) to chicken, which they used as a model food system. They printed chicken samples (3 mm thick by ~1in² area) as a test bed and assessed a range of parameters including cooking depth, color development, moisture retention, and flavor differences between laser-cooked and stove-cooked meat. They discovered that laser-cooked meat shrinks 50% less, retains double the moisture content, and shows similar flavor development to conventionally cooked meat.

“In fact, our two blind taste-testers preferred laser-cooked meat to the conventionally cooked samples, which shows promise for this burgeoning technology,” Blutinger said.

While Lipson and Blutinger are excited about the possibilities of this new technology, whose hardware and software components are fairly low-tech, they note that there is not yet a sustainable ecosystem to support it. Lipson states that “what we still don’t have is what we call ‘Food CAD,’ sort of the Photoshop of food. We need a high level software that enables people who are not programmers or software developers to design the foods they want. And then we need a place where people can share digital recipes, like we share music.”

Still, says Blutinger, “Food is something that we all interact with and personalize on a daily basis — it seems only natural to infuse software into our cooking to make meal creation more customizable.”

Video on Robots that Cook: precision cooking with multiwavelength lasers: https://www.youtube.com/watch?v=jct3f92rIOE&t=42s

Story Source:

Materials provided by Columbia University School of Engineering and Applied Science. Original written by Holly Evarts. Note: Content may be edited for style and length.

Twelve newly sequenced ancient Japanese genomes show that modern day populations do indeed show the genetic signatures of early indigenous Jomon hunter-gatherer-fishers and immigrant Yayoi farmers — but also add a third genetic component that is linked to the Kofun peoples, whose culture spread in Japan between the 3^rd and 7^th centuries.

Rapid cultural transformations

The Japanese archipelago has been occupied by humans for at least 38,000 years but Japan underwent rapid transformations only in the last 3,000 years, first from foraging to wet-rice farming, and then to a technologically advanced imperial state.

The previous, long-standing hypothesis suggested that mainland Japanese populations derive dual-ancestry from the indigenous Jomon hunter-gatherer-fishers, who inhabited the Japanese archipelago from around 16,000 to 3,000 years ago, and later Yayoi farmers, who migrated from the Asian continent and lived in Japan from around 900 BC to 300 AD.

But the 12 newly sequenced ancient Japanese genomes — which came from the bones of people living in pre- and post-farming periods — also identify a later influx of East Asian ancestry during the imperial Kofun period, which lasted from around 300 to 700 AD and which saw the emergence of political centralisation in Japan.

Shigeki Nakagome, Assistant Professor in Psychiatry in Trinity College Dublin’s School of Medicine, led the research, which brought together an interdisciplinary team of researchers from Japan and Ireland. Professor Nakagome said:

“Researchers have been learning more and more about the cultures of the Jomon, Yayoi, and Kofun periods as more and more ancient artefacts show up, but before our research we knew relatively little about the genetic origins and impact of the agricultural transition and later state-formation phase.”

“We now know that the ancestors derived from each of the foraging, agrarian, and state-formation phases made a significant contribution to the formation of Japanese populations today. In short, we have an entirely new tripartite model of Japanese genomic origins — instead of the dual-ancestry model that has been held for a significant time.”

Genomic insights into key Japanese transformations

In addition to the overarching discovery, the analyses also found that the Jomon maintained a small effective population size of around 1,000 over several millennia, with a deep divergence from continental populations dated to 20,000-15,000 years ago — a period which saw Japan become more geographically insular through rising sea-levels.

The Japanese archipelago had become accessible through the Korean Peninsula at the beginning of the Last Glacial Maximum, some 28,000 years ago, enabling movement between. And the widening of the Korea Strait 16,000 to 17,000 years ago due to rising sea-levels may have led to the subsequent isolation of the Jomon lineage from the rest of the continent. These time frames also coincide with the oldest evidence of Jomon pottery production.

“The indigenous Jomon people had their own unique lifestyle and culture within Japan for thousands of years prior to the adoption of rice farming during the subsequent Yayoi period. Our analysis clearly finds them to be a genetically distinct population with an unusually high affinity between all sampled individuals — even those differing by thousands of years in age and excavated from sites on different islands,” explained Niall Cooke, PhD Researcher at Trinity. “These results strongly suggest a prolonged period of isolation from the rest of the continent.”

The spread of agriculture is often marked by population replacement, as documented in the Neolithic transition throughout most of Europe, with only minimal contributions from hunter-gatherer populations observed in many regions. However, the researchers found genetic evidence that the agricultural transition in prehistoric Japan involved the process of assimilation, rather than replacement, with almost equal genetic contributions from the indigenous Jomon and new immigrants associated with wet-rice farming.

Several lines of archaeological evidence support the introduction of new large settlements to Japan, most likely from the southern Korean peninsula, during the Yayoi-Kofun transition. And the analyses provide strong support for the genetic exchange involved in the appearance of new social, cultural, and political traits in this state-formation phase.

“The Japanese archipelago is an especially interesting part of the world to investigate using a time series of ancient samples given its exceptional prehistory of long-standing continuity followed by rapid cultural transformations. Our insights into the complex origins of modern-day Japanese once again shows the power of ancient genomics to uncover new information about human prehistory that could not be seen otherwise,” added Dan Bradley, Professor of Population Genetics in Trinity’s School of Genetics and Microbiology, who co-led the project.

The algorithm, available online in the journal Neurology, uses data from a kind of brain scan known as amyloid positron emission tomography (PET) to gauge brain levels of the key Alzheimer’s protein amyloid beta.

In those who eventually develop Alzheimer’s dementia, amyloid silently builds up in the brain for up to two decades before the first signs of confusion and forgetfulness appear. Amyloid PET scans already are used widely in Alzheimer’s research, and this algorithm represents a new way of analyzing such scans to approximate when symptoms will arise. Using a person’s age and data from a single amyloid PET scan, the algorithm yields an estimate of how far a person has progressed toward dementia — and how much time is left before cognitive impairment sets in.

“I perform amyloid PET scans for research studies, and when I tell cognitively normal individuals about positive results, the first question is always, ‘How long do I have until I get dementia?’,” said senior author Suzanne Schindler, MD, PhD, an assistant professor of neurology. “Until now, the answer I’d have to give was something like, ‘You have an increased risk of developing dementia in the next five years.’ But what does that mean? Individuals want to know when they are likely to develop symptoms, not just whether they are at higher risk.”

Schindler and colleagues analyzed amyloid PET scans from 236 people participating in Alzheimer’s research studies through Washington University’s Charles F. and Joanne Knight Alzheimer Disease Research Center. The participants were an average of 67 years old at the beginning of the study. All participants underwent at least two brain scans an average of 4½ years apart. The researchers applied a widely used metric known as the standard uptake value ratio (SUVR) to the scans to estimate the amount of amyloid in each participant’s brain at each time point.

The researchers also accessed over 1,300 clinical assessments on 180 of the participants. The assessments typically were performed every one to three years. Most participants were cognitively normal at the start of data collection, so the repeated assessments allowed the researchers to pinpoint when each participant’s cognitive skills began to slip.

Schindler spent years trying to figure out how to use the data in amyloid PET scans to estimate the age at which symptoms would appear. The breakthrough came when she realized that amyloid accumulation has a tipping point and that each individual hits that tipping point at a different age. After this tipping point, amyloid accumulation follows a reliable trajectory.

“You may hit the tipping point when you’re 50; it may happen when you’re 80; it may never happen,” Schindler said. “But once you pass the tipping point, you’re going to accumulate high levels of amyloid that are likely to cause dementia. If we know how much amyloid someone has right now, we can calculate how long ago they hit the tipping point and estimate how much longer it will be until they are likely to develop symptoms.”

People in the study who reached the tipping point at younger ages took longer to develop cognitive symptoms than those who reached it later in life. Participants who hit the tipping point at age 50 typically took nearly 20 years to develop symptoms; those who hit it at age 80 took less than 10 years.

“When we look at the brains of relatively young people who have died with Alzheimer’s, they typically look pretty healthy, other than Alzheimer’s,” Schindler said. “But older people more frequently have damage to the brain from other causes, so their cognitive reserves are lower, and it takes less amyloid to cause impairment.”

The power of this new technique is that it requires just one brain scan, plus the person’s age. With that data, the model can estimate the time to symptom onset, plus or minus several years. In this study, the correlation between the expected age of symptom onset and the true age at diagnosis was better than 0.9 on a scale of 0 (no correlation) to 1 (perfect correlation).

After age, the genetic variant APOE4 is the strongest risk factor for Alzheimer’s dementia. People who carry one copy of the variant are two to three times more likely to develop Alzheimer’s dementia than the general population, and people who carry two copies are 10 times more likely. In this study, people with the high-risk variant hit the tipping point younger, but once that point was passed, they followed the same trajectory as everyone else.

“APOE4 seems to have a seeding effect,” Schindler said. “At very low levels, below the tipping point, you see amyloid rising in people with APOE4 while it’s not changing in people without APOE4. That means APOE4 carriers are going to hit the tipping point sooner. People with two copies of APOE4 hit the tipping point about 10 years earlier than people with no copies. But after that point, we see no difference between the APOE4 carriers and noncarriers.”

At an out-of-pocket cost of about $6,000, amyloid PET brain scans are too expensive for routine clinical use. However, this algorithm could help accelerate the pace of drug development by streamlining clinical trials.

“Most participants in clinical trials designed to prevent or slow Alzheimer’s symptoms do not develop symptoms during the trials,” Schindler said. “That’s a lot of time and effort — for the participants as well as the researchers — that doesn’t yield useful data. If we could do trials only on people who are likely to develop symptoms in the next few years, that would make the process of finding therapies much more efficient.”

Now, a new technique for measuring turbulent flows has been developed by an international collaboration of scientists from the Okinawa Institute of Science and Technology Graduate University (OIST) in Japan, along with the University of Genova, Italy, KTH Stockholm, Sweden and ETH Zurich, Switzerland. By using fibers rather than particles — the usual method of measurement — the researchers could get a more detailed picture of turbulent flows. Their method was reported on 17th September in the journal, Physical Review X.

“Turbulence is a very unique and complicated phenomena, it’s even been called the last unsolved problem in classical physics,” said Dr. Stefano Olivieri, a postdoctoral researcher from the Complex Fluids and Flows Unit at OIST, who was an author of the study. “It’s difficult to predict, difficult to simulate, and difficult to measure.”

Measuring turbulent flows is a pressing challenge for physicists for numerous reasons. Not only is turbulence characterized by its chaotic and random nature, but it also occurs across many scales at once. In turbulent flows, the swirling vortices of fluid break down into eddies that are smaller and smaller in scale, until eventually the eddies are so small and viscous that the kinetic energy of the fluid is transferred to the environment as heat.

Currently, the most common way to measure turbulent flows is by tracking the movement of particles, called tracers, that are added to the fluid. These particles are tiny and of similar density to the fluid, and so move at the same speed and in the same direction as the flow.

But in order to observe how each swirl of fluid is moving, looking at how one particle moves isn’t enough. Physicists need to be able to determine how two particles that are a specific distance apart move in relation to each other. The smaller the eddy, the closer together the two particles need to be to characterize the motion of the vortex.

To make matters more challenging, one of the defining features of turbulence is its diffusivity — a turbulent flow will spread apart over time, and so too will the tracers, especially in open flows, like an ocean current. In many cases, tracers can quickly spread too far apart to measure how the eddies are behaving.

“Every tracer particle is moving independently of each other, so you need lots of tracer particles in order to find ones that are the right distance apart,” explained Professor Marco Rosti, who leads the OIST Complex Fluids and Flows Unit.

“And too many tracer particles can actually disrupt the flow,” he added.

To circumvent this issue, the research team developed an innovative and easy solution to the problem: using fibers instead of tracer particles.

The researchers created a computer simulation where fibers of different lengths were added to a turbulent flow. These fibers were rigid, which kept the ends of each fiber a fixed distance apart. By tracking how each fiber moved and rotated within the fluid over time, the researchers were able to build up a picture that encompassed the full scale and structure of the turbulent flow.

“By using rigid fibers, we can measure the difference in the speed and the direction of the flow at two points a fixed distance apart, and we can see how these differences change depending on the scale of the eddy. The shortest fibers also allowed us to accurately measure the rate at which the kinetic energy of the fluid is transferred from the largest to the smallest scales, where it is then dissipated by heat. This value, called the energy dissipation rate, is a crucial quantity in the characterization of turbulent flows,” said Prof. Rosti.

The researchers also performed the same experiment in the laboratory. They manufactured two different fibers, one made from nylon and the other from a polymer called polydimethylsiloxane. The team tested both these fibers by adding them to water tank containing turbulent water and found that the fibers gave similar results to the simulation.

However, using rigid fibers comes with one important caveat, the scientists emphasized, as the overall movement of the fiber ends is restricted.

“Due to the fiber rigidity, the fiber ends can’t move towards each other, even if that’s the direction of the flow. That means that a fiber cannot fully represent the movement of the flow in the same way that tracer particles can,” explained Dr. Olivieri. “So before we even began simulations or lab experiments, we first needed to develop a suitable theory that took these limitations of movement into account. This was perhaps the most challenging part of the project.”

The researchers also measured the same turbulent flow in the laboratory the conventional way, by adding a high concentration of tracer particles to the water tank. The results obtained from the two different methods were similar, verifying that the fiber method and the newly developed theory gave accurate information.

Moving forward, the researchers hope to expand their method to incorporate flexible fibers that have less restriction on how they move. They also plan to develop a theory that can help measure turbulence in more complex non-Newtonian fluids that behave differently from water or air.

“This new technique has a lot of exciting potential, especially for scientists studying turbulence in large, open flows like ocean currents,” said Prof. Rosti. “And being able to easily measure quantities that were previously difficult to obtain moves us one step closer to fully understanding turbulence.”