Publisher Health

A large-scale study of U.S. children and adolescents has found that participation in a team sport is associated with fewer mental health difficulties, but that kids who are exclusively involved in an individual sport — such as tennis or wrestling — may face greater mental health difficulties than kids who do no sports at all. Matt Hoffmann of California State University, U.S.A., and colleagues present these findings in the open-access journal PLOS ONE on June 1, 2022.
Previous research has consistently suggested that youth participation in organized sports might help protect against mental health difficulties. However, some studies have linked youth sports participation to worse mental health, so more detailed research is needed to determine which approaches to sports might be most beneficial.
To shed new light, Hoffmann and colleagues analyzed data on the sports habits and mental health of 11,235 kids aged 9 to 13. Parents and guardians reported on several aspects of the children’s mental health by filling out a form known as the Child Behavior Checklist. The researchers looked for any associations between the mental health data and the kids’ sports habits, while also accounting for other factors that might impact mental health, such as household income and overall physical activity.
In line with the researchers’ expectations, the analysis showed that kids involved in team sports were less likely to have signs of anxiety, depression, withdrawal, social problems, and attention problems.
The researchers also expected individual sports to be associated with fewer mental health difficulties, even if to a lesser extent than for team sports. However, they instead found that children who exclusively played individual sports tended to have greater mental health difficulties than those who did not play sports at all. Nonetheless, for female kids, participation in both team and individual sports was associated with a lower likelihood of rule-breaking behavior than non-sports participation.
Overall, these findings add to a growing body of evidence that playing team sports is positively associated with mental health for children and adolescents. The authors suggest that further research could help clarify the link they observed between individual sports and worse mental health difficulties, and longitudinal observations are needed to investigate any causal relationships between sport participation and mental health.
The authors add: “Children and adolescents who played exclusively team sports, like basketball or soccer, had fewer mental health difficulties than those who did not participate in any organized sports. However, to our surprise, youth who participated in only individual sports, such as gymnastics or tennis, had more mental health difficulties compared to those who did not participate in organized sports.”
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Molecular machines that kill infectious bacteria have been taught to see their mission in a new light.
The latest iteration of nanoscale drills developed at Rice University are activated by visible light rather than ultraviolet (UV), as in earlier versions. These have also proven effective at killing bacteria through tests on real infections.
Six variants of molecular machines were successfully tested by Rice chemist James Tour and his team. All of them punched holes in the membranes of gram-negative and gram-positive bacteria in as little as two minutes. Resistance was futile for bacteria that have no natural defenses against mechanical invaders. That means they are unlikely to develop resistance, potentially offering a strategy to defeat bacteria that have become immune to standard antibacterial treatments over time.
“I tell students that when they are my age, antibiotic-resistant bacteria are going to make COVID look like a walk in the park,” Tour said. “Antibiotics won’t be able to keep 10 million people a year from dying of bacterial infections. But this really stops them.”
The breakthrough study led by Tour and Rice alumni Ana Santos and Dongdong Liu appears in Science Advances.
Because extended exposure to UV can be damaging to humans, the Rice lab has been refining its molecules for years. The new version gets its energy from still-blueish light at 405 nanometers, spinning the molecules’ rotors at 2 to 3 million times per second.

Your virtual visit with your doctor is at 1:00 p.m. It’s now 1:20 p.m. and your physician has not yet logged in. Do you call the clinic? Hang up and log back in? Groan in frustration?
Being stuck in a virtual waiting room and staring at a blank computer or device screen is a huge dissatisfier among telemedicine patients. To respect patients’ time, and provide the optimal experience, UC San Diego Health conducted a 10-week quality improvement study to evaluate how text messaging a link to a patient when their doctor is ready provides a way to connect patients and doctors most efficiently, without relying on the virtual waiting room.
Results of the study published in the May 27 online issue of Quality Management in Health Care.
“Borrowing from the airline and restaurant industries, we tested whether we could contact patients via text to log into their appointment when their doctor is ready. The goal of the feasibility study was to determine if this flexibility lead to improved perception of waiting time and an enhanced experience, while assessing for time saving for both patients and providers,” said Brett C. Meyer, MD, neurologist, co-director of the UC San Diego Heath Stroke Center, and clinical director of telehealth at UC San Diego Health.
“We stepped back and asked, ‘Do we need a virtual waiting room at all? Can we let patients know when their provider is available instead of making them wait online?'” said Emily S. Perrinez, RN, MSN, MPH, study co-author and director of telehealth operations at UC San Diego Health. “The reality is that wait times and lack of timely communication both correlate with patient experience. Real-time text notification that the provider is ready improved patient satisfaction and this experience is the kind of feedback we love to see.”
Twenty-two patients at a stroke clinic participated in the two-and-a-half month study. Patients chose to either receive a text, which included a visit link when their provider was ready for their visit or the standard telehealth routine of logging in at a scheduled time and waiting in front of a camera in a virtual waiting room.

Individuals with HIV who began taking antiretroviral therapy (ART) in the early stages of infection achieved a lengthy period of HIV suppression without ART after receiving two broadly neutralizing anti-HIV antibodies (bNAbs), according to a small study published today in the journal Nature. The findings suggest that combination bNAb therapy might offer a future alternative to daily ART for people living with HIV. The research was conducted by scientists at the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, in collaboration with researchers at the NIH Clinical Center; the Maple Leaf Medical Clinic in Toronto; the Frederick National Laboratory for Cancer Research; Harvard Medical School, Boston; and The Rockefeller University, New York City.
Although oral antiretrovirals are highly effective at keeping HIV levels under control, it can be difficult for some people with HIV to adhere to a daily medication regimen. Additionally, the medicines can present long-term side effects from lifetime usage and create the possibility for the development of drug-resistant virus. In previous research, single bNAbs showed only limited success in keeping virus levels low partly because bNAb-resistant HIV either already existed or emerged in the individual. To address this problem, researchers in the NIAID Laboratory of Immunoregulation tested a dual combination of bNAbs — called 3BNC117 and 10-1074 — targeting different parts of the surface of HIV.
The researchers conducted a two-component clinical trial between September 2018 and January 2021. The first component was a Phase 1 randomized, placebo-controlled trial involving 14 participants with HIV. These individuals had started ART during the early phase of their infection. They were taken off antiretrovirals shortly after receiving their first infusion of the combination bNAbs or placebo. Participants received up to eight bNAb or placebo infusions — two in the first month and once monthly thereafter — for 24 weeks. HIV levels and CD4 T-cell counts were measured every two weeks.
The purpose of the study was to see if treatment with the bNAbs could suppress HIV in the absence of ART. None of the seven participants who received the bNAb treatment had to restart ART before 28 weeks post-infusion compared to six of the seven participants who received placebo. The median duration of time off antiretrovirals was 39.6 weeks (bNAb group) and 9.4 weeks (placebo), respectively.
The second component of the study involved bNAb infusions in a group of 5 study participants who were not taking ART but still maintained low levels of HIV. In this smaller group, only two of the five study participants maintained complete suppression of the virus for an average of 41.7 weeks following the bNAb transfusions.
The authors note that the bNAb combination was ineffective in suppressing HIV if participants harbored virus resistant to either or both experimental antibodies before receiving the infusions. The presence of pre-existing antibody-resistant HIV poses a major challenge going forward, according to the authors. No safety issues occurred in the study, and the infusions were well-tolerated.
The study authors conclude that the combination bNAb therapy can be highly effective in suppressing HIV in the absence of ART for extended periods, provided that antibody-resistant virus is not present at the time individuals begin antibody treatment. Larger studies are needed to confirm the findings, but as next-generation bNAbs with increased potency and durability become available, “there is reason to believe that infrequent administration (i.e., twice a year) of such antibodies, possibly along with a long-acting injectable antiretroviral drug, could lead to ART-free HIV suppression for extended periods (years) in infected individuals,” the authors wrote.
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Spreading cancer cells that escape a primary tumor site can seed in tissues distant from the tumor, but may take several years or decades to grow into full metastatic cancers. Understanding of tumor dormancy, the process by which this happens, was incomplete. Now, new laboratory research directed by investigators at the Johns Hopkins Kimmel Cancer Center and the Johns Hopkins Bloomberg School of Public Health finds that secreted age-induced changes in distant sites such as the lung can effectively reactivate dormant cells and cause them to grow.
The researchers found that age-related changes in the secreted factors from the lung fibroblasts, normal noncancer cells in the vicinity of the tumor, facilitated a pathway for growth of dormant melanoma cells. Age-related changes in the skin microenvironment suppressed the growth of melanoma cells but drove their dissemination, seeding the deadly spread of cancer to distant organs. The results of this multicenter study were published in the June 1 issue of Nature.
Aging can play a role in the development of cancer metastases, says senior study author Ashani Weeraratna, Ph.D., the E.V. McCollum Professor and chair of the Department of Biochemistry and Molecular Biology at the Bloomberg School of Public Health, a Bloomberg Distinguished Professor (cancer biology), a professor of oncology and co-leader of the cancer invasion and metastasis program at the Kimmel Cancer Center.
The study found that when melanoma cells were injected into the skin of young (8 weeks old, equivalent to young adult human) and older mice (18 months old, equivalent to humans age 55 to 65), they traveled to the lungs at similar rates initially, but in the aged lung, they grew rapidly and formed bigger tumors, whereas in the younger lung, they tended to remain as small, single-cell or double-cell colonies.
The researchers grew melanoma cells together with human skin or lung fibroblasts — common cells that help maintain the structure of tissue and repair injury — from young (under age 35) or older (above age 55) healthy donors. Melanoma cells in the aged lung fibroblast environment dramatically increased in proliferation compared to those in a young lung fibroblast environment. Conversely, melanoma cells in an aged skin fibroblast microenvironment proliferated more slowly when compared with young skin fibroblasts. Laboratory studies of melanoma cells suggested that changes in factors secreted by the fibroblasts were key to promoting these differences.
Next, the study team performed proteomic analysis (a study of proteins) on factors secreted by healthy human young and aged lung fibroblasts. The team identified changes in the WNT signaling pathway, specifically in secreted frizzled related proteins (SFRPs) that regulated WNT5A, a protein involved in various processes including melanoma metastasis. The researchers found WNT5A to be a master regulator in activating melanoma cell dormancy in the lung, enabling efficient dissemination, seeding and survival of melanoma cells in metastatic niches, but suppressing their outgrowth.
“These changes were very consistent with a phenomenon in melanoma we call phenotype switching, in which melanoma exists either in a state of growing or invading,” Weeraratna says. “What our data showed is that these cells use different arms of the WNT pathway to switch back and forth between these two states,” she adds. “When the WNT5A signaling pathway is activated, the cells are highly invasive but not very proliferative and don’t grow fast. By contrast, when the WNT5A signaling pathway is suppressed, the cells grow much faster.”
Age-induced re-programming of the lung fibroblasts increases the secretion of the protein sFRP1, which inhibits WNT5A and enables metastatic outgrowth. The team also identified the tyrosine kinase receptors AXL and MER — which play a role in normal cell proliferation — as helpers promoting the process from dormancy to reactivation.
“Our data revealed an unexpected complexity in the role of WNT signaling and other downstream pathways in melanoma cell dormancy and metastasis initiation that is regulated by aging,” says lead study author Mitchell Fane, Ph.D., a postdoctoral fellow in Weeraratna’s laboratory. “WNT5A promotes the initial dissemination of the tumor cells but then acts to maintain them in a dormant state to allow survival and adaptation in the lungs. This state is maintained until age-related changes in the distal site induce an emergence from tumor dormancy. Then, sFRP1 is secreted at higher levels by aged lung fibroblasts and decreases WNT5A expression to allow the reactivation from dormancy in the aged lung. We also defined an axis where AXL-MER converge downstream of WNT5A that helps reactivate the dormant cells.”
Much research is still needed to better understand the microenvironment at distant sites, including the brain, where melanoma also can metastasize, says Weeraratna.Study co-authors are Mitchell Fane, Yash Chhabra, Gretchen Alicea, Devon Maranto, Stephen Douglass, Vito Rebecca, Gloria Marino, Daniel Zabransky, Laura Hüser and Elizabeth Jaffee of Johns Hopkins; Marie Webster of the Lankenau Institute for Medical Research, Wynnewood, Pa.; Filipe Almeida, Brett Ecker, Thomas Beer, Hsin-Yao Tang, Andrew Kossenkov, Meenhard Herlyn and David Speicher of the Wistar Institute in Philadelphia; Wei Xu and Xiowei Xu of the Abramson Cancer Center at the University of Pennsylvania; and Julio Aguirre-Ghiso of the Cancer Dormancy and Tumor Microenvironment Institute, Albert Einstein College of Medicine, New York City.
The work was supported in part by the National Institutes of Health (grants RO1CA174746, RO1CA207935, P01CA11046, U01CA227550, R01CA232256), a Team Science Award from the Melanoma Research Alliance and the Wistar Science Discovery Fund. Weeraratna also is supported by a Bloomberg Distinguished Professorship and the E.V. McCollum Endowed Chair.
Weeraratna is on the board of Regain Therapeutics. The terms of this arrangement are managed by The Johns Hopkins University in accordance with its conflict of interest policies.

Turns out you’re not the only one who needs a good night’s rest to function well the next day.
Researchers with the University of Cincinnati found that mosquitoes whose slumber is disrupted are more interested in catching up on their sleep than looking for food the next day. The research demonstrates how vital this biological function is even among insects.
“It was a bit surprising. Sleep deprived or not, a blood meal should appeal to them,” UC doctoral student and study lead author Oluwaseun Ajayi said.
The study was published online on May 3 and in print on June 1 in the Journal of Experimental Biology.
The phenomenon of catching up on missed sleep, called sleep rebound, has been observed in other animals such as honeybees, fruit flies and people.
Biologists in UC’s College of Arts and Sciences and Virginia Tech’s Department of Biochemistry spent more than a year developing protocols to study mosquito sleep. While observations can affect the outcome of virtually any experiment — a phenomenon called the observer effect — UC biologist Joshua Benoit said this was especially true when studying mosquito sleep.

When your brain needs you to pay attention to something important, one way it can do that is to send out a burst of noradrenaline, according to a new MIT study.
This neuromodulator, produced by a structure deep in the brain called the locus coeruleus, can have widespread effects throughout the brain. In a study of mice, the MIT team found that one key role of noradrenaline, also known as norepinephrine, is to help the brain learn from surprising outcomes.
“What this work shows is that the locus coeruleus encodes unexpected events, and paying attention to those surprising events is crucial for the brain to take stock of its environment,” says Mriganka Sur, the Newton Professor of Neuroscience in MIT’s Department of Brain and Cognitive Sciences, a member of MIT’s Picower Institute for Learning and Memory, and director of the Simons Center for the Social Brain.
In addition to its role in signaling surprise, the researchers also discovered that noradrenaline helps to stimulate behavior that leads to a reward, particularly in situations where there is uncertainty over whether a reward will be offered.
Sur is the senior author of the new study, which appears today in Nature. Vincent Breton-Provencher, a former MIT postdoc who is now an assistant professor at Laval University, and Gabrielle Drummond, an MIT graduate student, are the lead authors of the paper.
Modulating behavior
Noradrenaline is one of several neuromodulators that influence the brain, along with dopamine, serotonin, and acetylcholine. Unlike neurotransmitters, which enable cell-to-cell communication, neuromodulators are released over large swathes of the brain, allowing them to exert more general effects.

New research has uncovered how genetic mutations hijack the production of blood cells in different periods of life. Scientists at the Wellcome Sanger Institute, the Cambridge Stem Cell Institute, EMBL’s European Bioinformatics Institute (EMBL-EBI) and collaborators show how these changes relate to ageing and the development of age-related diseases, including blood cancer.
The new study, published today (1 June) in Nature, represents the first time that the lifelong impact of genetic mutations on cell growth dynamics has been explored.
All human cells acquire genetic changes in their DNA throughout life, known as somatic mutations, with a specific subset of mutations driving cells to multiply. This is common in professional blood making cells, known as blood stem cells, and results in the growth of populations of cells with identical mutations known as ‘clones’. This process, termed ‘clonal haematopoiesis’, becomes ubiquitous with age, and is a risk factor for developing blood cancer and other age-related conditions.
To understand how and when clonal haematopoiesis develops, how it is influenced by ageing, and how it relates to disease, the researchers tracked nearly 700 blood cell clones from 385 individuals aged over 55, who were part of the SardiNIA longitudinal study. Participants donated regular blood samples for up to 16 years.
DNA sequencing of blood samples showed that 92.4 per cent of clones expanded at a stable exponential rate over the period studied. The rate of growth was primarily influenced by the nature of the mutated gene in each clone.
After capturing the behaviour of clones in later life, the team used mathematical models to infer their growth patterns over the entire human lifespan. They uncovered that clone behaviour changed dramatically with age depending on the identity of the mutated gene.
First, clones driven by mutations in DNMT3A, expanded fast in young people and then deceleratedin old age. Second, clones driven by mutations in TET2 appeared and grew uniformly throughout life, such that they became more common than DNMT3A-mutant clones after the age of 75. Finally, clones with mutations in splicing genes, U2AF1 and SRSF2, only expanded exclusively later in life and exhibited some of the fastest growth.
These age-dependent clonal behaviours mirror the frequency of emergence of different types of blood cancers and reveal that mutations associated with fast clonal growth are more likely to lead to malignancy.
Dr Margarete Fabre, lead researcher on the study and PhD student at the Wellcome Sanger Institute and the University of Cambridge, said: “Our findings reveal how acquired genetic changes hijack blood formation during our lifetimes, with normal blood stem cells competing against cells with pre-leukemia mutations. Understanding why some mutations prevail in youth and others in old age could help us find ways to maintain the health and diversity of our blood cells.”
Dr Moritz Gerstung, co-senior author of the study, from EMBL’s European Bioinformatics Institute and the German Cancer Research Centre (DKFZ), said: “For the first time we have been able to use genomic analysis to understand the past, present and future of mutant clones in our blood. These data show that the dynamics of blood clones are surprisingly predictable over a period of years, but also highlight that they change over a lifetime in ways we don’t understand yet.”
Professor George Vassiliou, co-senior author of the study, formerly from the Wellcome Sanger Institute, and now Professor of Haematological Medicine at the Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, and Cambridge University Hospitals, said: “Collectively, our work reveals an astonishing interaction between advancing age and mutations in the DNA of our blood cells that is played out as the expansion of cells with different mutations at different ages. Remarkably, these changes lead to the emergence of different types of blood cancers at different ages, and with different risks of progression. With this new understanding, researchers can begin to develop approaches and treatments to stop the development of blood cancer in its tracks.”

New research has uncovered how genetic changes that accumulate slowly in blood stem cells throughout life are likely to be responsible for the dramatic change in blood production after the age of 70.
The study, by scientists at the Wellcome Sanger Institute, the Wellcome-MRC Cambridge Stem Cell Institute and collaborators, is published today (1 June) in the journal Nature, and suggests a new theory of ageing.
All human cells acquire genetic changes throughout life, known as somatic mutations. Ageing is likely to be caused by the accumulation of multiple types of damage to our cells over time, with one theory being that build-up of somatic mutations causes cells to progressively lose functional reserve. However, it is currently unclear how such gradual accumulation of molecular damage could translate into the abrupt deterioration in how our organs function after the age of 70 years.
To investigate this ageing process, the team from the Wellcome Sanger Institute, the Cambridge Stem Cell Institute and collaborators studied the production of blood cells from the bone marrow, analysing 10 individuals ranging in age from new-borns to the elderly. They sequenced the whole genomes of 3,579 blood stem cells, identifying all the somatic mutations contained in each cell. The team used this to reconstruct ‘family trees’ of each person’s blood stem cells, showing, for the first time, an unbiased view of the relationships among blood cells and how these relationships change across the human lifespan.
The researchers found that these ‘family trees’ changed dramatically after the age of 70 years. The production of blood cells in adults aged under 65 came from 20,000 to 200,000 stem cells, each of which contributed in roughly equal amounts. In contrast, blood production in individuals aged over 70 was very unequal. A reduced set of expanded stem cell clones — as few as 10 to 20 — contributed as much as half of all blood production in every elderly individual studied. These highly active stem cells had progressively expanded in numbers across that person’s life, caused by a rare subset of somatic mutations known as ‘driver mutations’.
These findings led the team to propose a model in which age-associated changes in blood production come from somatic mutations causing ‘selfish’ stem cells to dominate the bone marrow in the elderly. This model, with the steady introduction of driver mutations that cause the growth of functionally altered clones over decades, explains the dramatic and inevitable shift to reduced diversity of blood cell populations after the age of 70. Which clones become dominant varies from person to person, and so the model also explains the variation seen in disease risk and other characteristics in older adults. A second study, also published today in Nature, explores how different individual driver mutations affect cell growth rates over time.
Dr Emily Mitchell, Haematology Registrar at Addenbrooke’s Hospital, PhD Student at the Wellcome Sanger Institute, and lead researcher on the study, said: “Our findings show that the diversity of blood stem cells is lost in older age due to positive selection of faster growing clones with driver mutations. These clones ‘outcompete’ the slower growing ones. In many cases this increased fitness at the stem cell level likely comes at a cost — their ability to produce functional mature blood cells is impaired, so explaining the observed age-related loss of function in the blood system.”
Dr Elisa Laurenti, Assistant Professor and Wellcome Royal Society Sir Henry Dale Fellow at the Wellcome-MRC Cambridge Stem Cell Institute at the University of Cambridge, and joint senior researcher on this study, said: “Factors such as chronic inflammation, smoking, infection and chemotherapy cause earlier growth of clones with cancer-driving mutations. We predict that these factors also bring forward the decline in blood stem cell diversity associated with ageing. It is possible that there are factors that might slow this process down, too. We now have the exciting task of figuring out how these newly discovered mutations affect blood function in the elderly, so we can learn how to minimise disease risk and promote healthy ageing.”
Dr Peter Campbell, Head of the Cancer, Ageing and Somatic Mutation Programme at the Wellcome Sanger Institute, and senior researcher on the study, said: “We’ve shown, for the first time, how steadily accumulating mutations throughout life lead to a catastrophic and inevitable change in blood cell populations after the age of 70. What is super exciting about this model is that it may well apply in other organ systems too. We see these selfish clones with driver mutations expanding with age in many other tissues of the body — we know this can increase cancer risk, but it could also be contributing to other functional changes associated with ageing.”
This research was funded by Wellcome and the William B Harrison Foundation.

A remarkable discovery and collaborative effort have revealed a new type of triterpenes, a group of organic compounds which are an important source of many medicines. Until now, all triterpenes were believed to be derived from squalene, itself a type of triterpene. However, for the very first time, researchers witnessed biosynthesis, the formation of complex compounds from simple ones in living organisms, of triterpenes in fungi without the use of squalene. This important discovery opens up a whole new world of possibilities for pharmaceutical science.
Triterpenes are organic compounds which are abundantly found in animals, plants, microorganisms and even us. About 20,000 different triterpenes have been found and they are widely used in cosmetics, food supplements and, most importantly, medicine, thanks to their anti-inflammatory, anti-cancer, anti-diabetic and other valuable properties. Until now, all known triterpenes were thought to be generated from a common precursor or source, squalene.
However, as revealed in Nature, a collaborative effort among the University of Tokyo and KEK in Japan, Wuhan University in China and Bonn University in Germany, has found a new type of triterpenes that doesn’t require squalene.
“Nobody could have imagined this happening in nature. This is the discovery of a new biosynthetic machine,” explained Professor Ikuro Abe from the Graduate School of Pharmaceutical Sciences at the University of Tokyo.
Often, multiple enzyme reactions are needed to create complex molecular compounds, such as when our bodies use squalene to create hormones and bile acid. However, in just a single enzyme reaction, a simple molecule called a C5 isoprene unit, or building block, was the starter to construct a very complex triterpene molecular structure.
The discovery happened almost by accident by the team at Wuhan University, who were working on genome mining to find new natural products. They were not necessarily searching for triterpenes, but they found new genes widely distributed in fungi. “They didn’t know the genes’ function,” said Abe. “So they did a characterization of these news genes, and one of them happened to be triterpene synthesis.”
That is when they asked the other teams to get involved. According to Abe, the team at Bonn University are good at chemistry, so they worked on elucidating the detailed enzyme reaction mechanism, and researchers at the University of Tokyo and KEK applied their expertise in structural analysis. He said that once you understand the structure, you can modify it. “Change something here or there and see what happens. We can understand the structure-function relationship. It’s like a puzzle,” he explained.
“Chemistry in nature is more efficient than the chemical synthesis we use in industry. That is why we are interested in the biosynthetic processes done in nature,” Abe said. “Nature’s method is a better, cheaper and cleaner process. We are trying to better understand how processes take place in nature so that we can recreate or redesign it in the lab, to get more and more important and useful compounds.”
This new discovery is only the beginning. “Now that we have solved the protein structure, we are already manipulating the biosynthetic machinery to try to produce more useful molecules, for example, for drug development,” Abe said.
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