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A Compound That Reverses Gut Inflammation Developed
Summary: Researchers have developed a new compound, dubbed FexD, that can prevent and reverse inflammation in mouse models of inflammatory bowel disease.
Source: Salk Institute
A drug developed by Salk Institute researchers acts like a master reset switch in the intestines. The compound, called FexD, has previously been found to lower cholesterol, burn fat, and ward off colorectal cancer in mice.
Now, the team reports in Proceedings of the National Academy of Sciences on December 12, 2022, that FexD can also prevent and reverse intestinal inflammation in mouse models of inflammatory bowel disease.
“The Salk-developed drug FexD provides a new way to restore balance to the digestive system and treat inflammatory diseases that are currently very difficult to manage,” says senior author and Salk Professor Ronald Evans, director of Salk’s Gene Expression Laboratory and March of Dimes Chair in Molecular and Developmental Biology.
Inflammatory bowel disease (IBD), which includes both Crohn’s disease and ulcerative colitis, is characterized by an excess of immune cells and inflammatory signaling molecules known as cytokines in the gut.
Existing treatments, which mostly work by either suppressing the entire immune system or by targeting individual cytokines, are only effective for some patients and carry a host of side effects.
For more than two decades, Evans’ lab has studied Farnesoid X receptor (FXR), a master regulator protein that senses the bile acids delivered to the digestive system to help digest food and absorb nutrients.
When FXR detects a shift in bile acids at the beginning of a meal, it prepares the body for an influx of food by flipping on and off dozens of cellular programs related to digestion, blood sugar, and fat metabolism.
In 2015, Evans and his colleagues developed a pill called fexaramine that activates FXR in the gut. The pill, they initially showed, can stop weight gain and control blood sugar in mice.
In 2019, they showed that FexD—an updated version of fexaramine—also prevented cancer-associated changes to stem cells in the gut. Their work suggested that FXR also played a role in regulating inflammation.
“Every time you eat, you’re causing small amounts of inflammation in your gut as your intestinal cells encounter new molecules. FXR makes sure inflammation stays under control during normal feeding,” says Senior Staff Scientist Michael Downes, co-corresponding author of the new paper.
In the new work, Evans’ group discovered that activating FXR can be used to ease symptoms in inflammation-driven diseases. When the researchers gave mice with IBD a daily dose of oral FexD, either before or after the onset of intestinal inflammation, the drug prevented or treated the inflammation.
By activating FXR, FexD reduced the infiltration of a class of highly inflammatory immune cells called innate lymphoid cells. In turn, levels of cytokines already implicated in IBD decreased to levels normally seen in healthy mice.
See also
“When we activate FXR, we restore appropriate signaling pathways in the gut, bringing things back to a homeostatic level,” says Senior Research Scientist Annette Atkins, co-author of the study.
Since FXR acts more like a reset button than an off switch for the immune system, cytokines are not completely blocked by FexD. This means that the immune system continues functioning in a normal way after a dose of FexD.
The compound still must be optimized for use in humans and tested in clinical trials, but the researchers say their findings provide important information about the complex links between gut health and inflammation and could eventually lead to an IBD therapeutic.
“In people with IBD, our strategy could potentially be very effective at preventing flare-ups and as a long-term maintenance drug,” says first author Ting Fu, previously a postdoctoral fellow at Salk and now an assistant professor at the University of Wisconsin-Madison.
Other authors of the paper include Yuwenbin Li, Tae Gyu Oh, Fritz Cayabyab, Nanhai He, Qin Tang, Morgan Truitt, Paul Medina, Mingxiao He, Ruth T. Yu, and Ye Zheng of Salk; and Sally Coulter and Christopher Liddle of the University of Sydney.
About this IBD and inflammation research news
Author: Press Office
Source: Salk Institute
Contact: Press Office – Salk Institute
Image: The image is in the public domain
Original Research: The findings will appear in PNAS
Report: Trey Lance avoided compound fracture of ankle
Sunday was a rough day for 49ers quarterback Trey Lance as he suffered a season-ending ankle injury in the first quarter of their 27-7 win over the Seahawks.
49ers head coach Kyle Shanahan announced that Lance would miss the rest of the year after breaking his ankle on a running play. The injury was reminiscent of the one that Cowboys quarterback Dak Prescott suffered in the 2020 season, but Lance avoided one aspect of Prescott’s injury.
Tom Pelissero of NFL Media reports that Lance did not suffer a compound fracture on Sunday. That doesn’t change his outlook in terms of returning this season, but it should allow him to avoid some potential complications during his recovery.
That recovery will begin in earnest after Monday’s surgery on the ankle. Jimmy Garoppolo will be quarterbacking the 49ers now that Lance is out of commission.
Sea Corals Found To Be a Source of an Elusive “Anti-Cancer” Compound
Researchers proved that sea corals are a source of eleutherobin, a chemical with anti-cancer properties.
Researchers find that sea corals are a source of a sought-after “anti-cancer” compound
The ocean floor is riddled with mysteries, but scientists have just discovered one of its best-kept secrets. For the last 25 years, researchers have been looking for the source of a natural chemical that has shown promise in preliminary studies for treating cancer. Now, researchers at the University of Utah Health report that easy-to-find soft corals—flexible corals that resemble underwater plants—make the elusive compound.
Eric W. Schmidt, Ph.D., Professor, Medicinal Chemistry, University of Utah. Credit: Kristan Jacobsen for University of Utah Health
After determining the source, the researchers went on to discover the animal’s
A second research group led by Bradley Moore, Ph.D., from Scripps Institution of Oceanography at the University of California San Diego, independently showed that corals make related molecules. Both studies were recently published in the journal Nature Chemical Biology.
A World of Possibilities
Soft corals contain thousands of drug-like compounds that may be used as anti-inflammatory drugs, antibiotics, and other medicines. However, acquiring enough of these compounds has been a big obstacle to turning them into clinically useful medications. According to Schmidt, these other compounds should now be accessible using this new method.
Soft corals are thought to make thousands of drug-like compounds that could work as anti-inflammatory agents, antibiotics, anti-cancer therapeutics, and other drug leads. Credit: Bailey Miller.
Corals aren’t the only animals that harbor potential therapeutics. Nature is crawling with snakes, spiders, and other animals known to carry chemicals with healing properties. Yet that compounds from soft corals offer distinct advantages for drug development, Schmidt says.
Unlike venomous chemicals that are injected into prey, corals use their chemicals to ward off predators that try to eat them. Since they are made to be eaten, the soft coral chemicals are easily digestible. Similarly, drugs derived from these types of compounds should be able to be given as pills with a glass of water, rather than taken by injection or other more invasive means. “These compounds are harder to find but they’re easier to make in the lab and easier to take as medicine,” says Schmidt.
These possibilities had been just out of reach for decades. Getting to this point took the right know-how and a little luck.
Hunting for the Source
Scesa found the long-sought-after compound in a common species of soft coral living off the Florida coast—just a mile from his brother’s apartment. In the 1990s, marine scientists reported that a rare coral near Australia carried a chemical, eleutherobin, with anti-cancer properties. The chemical disrupts the cytoskeleton, a key scaffold in cells, and soft corals use it as a defense against predators. But laboratory studies showed that the compound was also a potent inhibitor of cancer cell growth.
In the decades after, scientists searched but could not find the fabled “holy grail” chemical in the quantities needed for drug development and couldn’t remedy the problem without understanding how the chemical was made. Dogma had it that, similar to other kinds of marine life, the chemical was synthesized by symbiotic organisms that lived inside the animals.
“It didn’t make sense,” Scesa says. “We knew that corals must make eleutherobin.” After all, he and Schmidt reasoned, some soft coral species don’t have symbiotic organisms and yet their bodies contain the same class of chemicals.
Paul Scesa, Ph.D., dives for soft corals off the Florida coast. He studies the potential of soft coral chemicals as drug leads. Credit: Paul Scesa
Solving the mystery seemed a job made for Scesa. As a boy growing up in Florida, the ocean was his playground, and he spent countless hours exploring its depths and wildlife. In graduate school, he developed a penchant for organic chemistry and combined the two interests to better understand the chemical diversity of the seas.
Later, he joined the lab of natural products scientist Schmidt with a mission to track down the source of the drug lead. Scesa suspected coral species familiar to him might have the answer and brought small live samples from Florida to Utah, and the real hunt began.
Decoding the Recipe
The next step was to find out whether the coral’s genetic code carried instructions for making the compound. Advances in DNA technology had recently made it possible to rapidly piece together the code of any species. The difficulty was that the scientists didn’t know what the instructions for making the chemical should look like. Imagine searching a cookbook for a certain recipe, only you don’t know what any of the words inside the book mean.
Eric Schmidt, Ph.D., and Paul Scesa, Ph.D., working through the steps to make the potential anti-cancer compound, eleutherobin. Credit: Kristan Jacobsen for University of Utah Health
“It’s like going into the dark and looking for an answer where you don’t know the question,” remarks Schmidt.
They addressed the problem by finding regions of coral DNA that resembled genetic instructions for similar types of compounds from other species. After programming bacteria grown in the lab to follow coral DNA instructions specific to the soft coral, the microorganisms were able to replicate the first steps of making the potential cancer therapeutic.
This proved that soft corals are the source of eleutherobin. It also demonstrated that it should be possible to manufacture the compound in the lab. Their work is now focusing on filling in the missing steps of the compound’s recipe and determining the best way to produce large amounts of the potential drug.
Paul Scesa uses a bioreactor to produce large amounts of chemicals that are found in small amounts in nature. Credit: Kristan Jacobsen for University of Utah Health
“My hope is to one day hand these to a doctor,” says Scesa. “I think of it as going from the bottom of the ocean to bench to bedside.”
The research was supported by the National Institutes of Health and the ALSAM Foundation.
Reference: “Ancient defensive terpene biosynthetic gene clusters in the soft corals” by Paul D. Scesa, Zhenjian Lin and Eric W. Schmidt, 23 May 2022, Nature Chemical Biology.
DOI: 10.1038/s41589-022-01027-1
An Entirely New Kind of Highly Reactive Chemicals Has Been Found in The Atmosphere
Every lungful of air we suck down is mostly made up of nitrogen, with a generous helping of oxygen, and a dash of carbon dioxide.
But dusting this atmospheric soup is a whole encyclopedia of different compounds and elements, some of which we can only speculate about.
One of those mysteries just came into focus, however. Chemists have shown that a reactive class of compounds called organic hydrotrioxides exists in the atmosphere, and while these chemicals last only briefly, they could have effects we don’t know about.
In fact, by the researchers’ calculations, you just sucked up a few billion molecules of them while reading this.
Exactly what this means for your health, not to mention the health of our planet, is literally and figuratively up in the air. But given that we’ve just discovered this new ingredient in Earth’s atmosphere, it’s well worth looking into.
“These compounds have always been around – we just didn’t know about them,” says chemist Henrik Grum Kjærgaard from the University of Copenhagen in Denmark.
“But the fact that we now have evidence that the compounds are formed and live for a certain amount of time means that it is possible to study their effect … and respond if they turn out to be dangerous.”
Quite often in chemistry, the addition of just a single new component can radically change how a material behaves.
Take water, for example. Thanks to the way its pair of hydrogens and single oxygen interact, organic chemistry can mix and swirl into an evolving phenomenon we call life.
Add just one more oxygen, though, and we get hydrogen peroxide – a far more reactive compound that can tear living chemistry apart.
Stick one more oxygen onto this angry little molecule, and the result is hydrotrioxide. To make it you just need the right kind of lab equipment, some saturated organic compounds, and some dry ice.
It’s not exactly the kind of party trick you’d use to spice up a margarita, but chemists have used their manufacture in the generation of a specific flavor of molecular oxygen as a step in producing various other substances.
Being highly reactive, there’s been an open question as to whether hydrotrioxides can easily form stable structures in the atmosphere.
It’s not just an academic point of speculation, either. So much of the way our atmosphere operates, from the intricate ways it influences personal health to the massive scale of global climate, emerges from the way trace materials in it interact.
“Most human activity leads to emission of chemical substances into the atmosphere. So, knowledge of the reactions that determine atmospheric chemistry is important if we are to be able to predict how our actions will affect the atmosphere in the future,” says Kristan H. Møller, also a chemist from the University of Copenhagen.
The team’s investigations now provide the first direct observations of hydrotrioxide forming under atmospheric conditions from several substances known to be present in our air.
This allowed them to study the way the compound is likely to be synthesized, how long it sticks around for, and how it degrades.
One such emission, called isoprene, can react in the atmosphere to generate around 10 million metric tons of hydrotrioxide each year.
That’s just one potential source, though. Based on the team’s calculations, just about any compound could in theory play a role in the atmospheric formation of hydrotrioxides, which remain intact for anywhere between a few minutes to a few hours.
In that time, they can participate in a slew of other reactions as a powerful oxidant, some of which could be sheltered inside microscopic solids drifting on the winds.
“It is easy to imagine that new substances are formed in the aerosols that are harmful if inhaled. But further investigation is required to address these potential health effects,” says Kjærgaard.
Since aerosols also affect the way our planet reflects sunlight, knowing how their internal chemistry causes them to grow or degrade could change how we model our climate.
Further investigations will no doubt begin to unravel the role hydrotrioxides play in our planet’s atmospheric cocktail. As University of Copenhagen researcher Jing Chen notes, it really is just the start.
“Indeed, the air surrounding us is a huge tangle of complex chemical reactions,” says Chen.
“As researchers, we need to keep an open mind if we want to get better at finding solutions.”
This research is published in Science.
‘Magic mushroom’ compound creates a hyper-connected brain to treat depression
Psilocybin, the hallucinogenic compound found in “magic mushrooms,” could treat depression by creating a hyper-connected brain.
By boosting connectivity between different areas of the brain, the psychedelic may help people with depression break out of rigid, negative patterns of thinking, a new study suggests.
Recent clinical trials have suggested that psilocybin may be an effective treatment for depression, when carefully administered under the supervision of mental health professionals. In the new study, published Monday (April 11) in the journal Nature Medicine (opens in new tab), researchers probed exactly how the psychedelic works to improve peoples’ depressive symptoms. To do so, the team collected brain scans from about 60 patients who had participated in clinical trials for psilocybin therapy; these brain scans revealed distinct changes in the patients’ brain wiring that emerged after they took the drug.
If you or someone you know needs help, contact the National Suicide Prevention Lifeline at 1-800-273-TALK (8255).
“We see connectivity between various brain systems increasing dramatically,” first author Richard Daws, who was a doctoral student at Imperial College London at the time of the study, told Live Science. Healthy individuals with high levels of well-being and cognitive function tend to have highly connected brains, studies suggest, but in people with depression, “we sort of see the opposite of that — a brain characterized by segregation,” said Daws, now a postdoctoral research associate at King’s College London. This sort of organization undermines the brain’s ability to dynamically switch between different mental states and patterns of thinking, he said.
The study supports the idea that psilocybin relieves depressive symptoms, at least in part, by boosting connectivity between different brain networks, said Dr. Hewa Artin, the chief resident of outpatient psychiatry at the UC San Diego School of Medicine, who was not involved in the study. That said, “additional studies will be needed to replicate results and validate findings,” Artin told Live Science in an email.
Related: FDA calls psychedelic psilocybin a ‘breakthrough therapy’ for severe depression
Promising results
The new study included 59 people, 16 of whom participated in one clinical trial for psilocybin and 43 who participated in another.
The first trial included people with treatment-resistant depression, meaning the participants had tried various antidepressants in the past without experiencing improvement. In the trial, these patients initially received a 10-milligram dose of psilocybin, and then seven days later, they received an additional 25-milligram dose. The participants were carefully monitored during each treatment session and spoke with psychotherapists afterward, to reflect on their experiences.
To see how the patients’ brains changed after treatment, the researchers used a technique called functional magnetic resonance imaging (fMRI), which measures changes in blood flow to different parts of the brain. The movement of oxygenated blood through the brain reflects which regions of the organ are active through time. The participants underwent fMRI scans prior to the start of therapy and then one day after their 25-milligram dose; and their depressive symptoms were also assessed before and after treatment.
The fMRI scans showed that the patients’ brain networks became less siloed and more integrated with one another following the treatment, as evidenced by the dynamic flow of blood between them. These changes correlated with long-term improvements in the patients’ depressive symptoms.
The second trial differed from the first in that it was a “randomized controlled trial,” considered the gold-standard form of clinical trial. The participants were randomly assigned to receive either psilocybin or the conventional antidepressant escitalopram (Lexapro); neither the participants nor researchers knew which medication was given to which participant.
Related: The trippy reason ‘magic’ mushrooms evolved to get you high
The psilocybin group received two 25-milligram doses of the psychedelic, spaced three weeks apart, and also took sugar pills throughout the trial. The escitalopram group received two 1-milligram doses of psilocybin, also spaced three weeks apart, and took daily escitalopram pills throughout the trial.
The 1-milligram doses of psilocybin would not be expected to have any appreciable psychedelic effect, so they served as a placebo, senior author Robin Carhart-Harris, who was the head of the Centre for Psychedelic Research at Imperial College London at the time of the study, told Live Science. It would usually take a dose three to five times that amount to generate an effect, said Carhart-Harris, who is now director of the Psychedelics Division within Neuroscape, the University of California, San Francisco’s translational neuroscience center.
The escitalopram group showed no significant changes in brain connectivity after treatment, but as in the first trial, those who took psilocybin showed marked increases in brain network integration. And notably, patients in the psilocybin group experienced “significantly greater” improvements in their depressive symptoms than those who took escitalopram.
“That’s very important, because it sort of suggests that psilocybin’s antidepressant effect works via a different mechanism to the way that sort of conventional antidepressants work,” Daws said.
What is that mechanism? It likely involves a structure on brain cells known as a serotonin 2A receptor, Carhart-Harris said.
Like LSD and other psychedelics, psilocybin plugs into serotonin 2A receptors in the brain and activates them. These receptors appear in particularly high quantities in specific regions of the wrinkled cerebral cortex that are involved in high-level cognitive functions like introspection and executive functioning, Carhart-Harris said. After exposure to psilocybin, these receptors undergo a kind of “reset” that brings their activity back in line with what’s typical in a healthy brain, he theorizes.
“Action at the [serotonin] 2A receptor seems to be part of the picture of psilocybin’s mechanism of action,” although more research is needed to fully understand how the receptors and their associated brain regions change following exposure to the drug, Artin said.
In the meantime, to move psilocybin therapy for depression toward Food and Drug Administration (FDA) approval, large-scale clinical trials with hundreds of patients will need to be conducted, Daws said. (The largest trial to date included 233 patients.)
Carhart-Harris is also involved with ongoing research at Imperial College London to see if psilocybin therapy could benefit patients with other conditions, such as anorexia. In addition, at UCSF, Carhart-Harris is studying how the benefits of the psychedelic vary when the drug is paired with different forms of psychotherapy, or a lack thereof.
“I’m of the opinion that, really, the safety and efficacy rests on the drug being used with psychotherapy,” Carhart-Harris said. Assuming psilocybin therapy for depression is eventually approved, Carhart-Harris said that he might expect patients with treatment-resistant depression to have three to four dosing sessions in a year, in conjunction with psychotherapy similar to what they employed in their clinical trials.
Originally published on Live Science.
Chemical Compound Promotes Healthy Aging – Add Muscle, Strength and Energy While Losing Fat
The study was conducted on mice, and more research will be needed to determine BAM15’s effectiveness for people. However, the findings have important implications for improving the quality of life for older adults, especially for the rapidly growing number of people with obesity.
BAM15 helped geriatric mice with obesity add muscle, strength, and energy while losing fat.
A recently discovered chemical compound helped elderly mice with obesity lose weight, add muscle and strength, reduce age-related inflammation and increase physical activity, a new study shows.
The study, published in the Journal of Cachexia, Sarcopenia and Muscle, provides the first evidence that BAM15, a mitochondrial uncoupler, prevents sarcopenic obesity, or age-related muscle loss accompanied by an increase in fat tissue.
“Loss of muscle mass is typically not a concern in younger adults with obesity. However, as people age, that changes. Older adults with sarcopenic obesity suffer accelerated muscle loss. They become less active. As a result, they are at high risk for falls, stroke, heart disease, poorer quality of life, and premature death,” said Christopher Axelrod, MS, Director of Pennington Biomedical Research Center’s Integrated Physiology and Molecular Medicine Laboratory.
Mitochondrial uncoupling makes mitochondria, the power plants of the cell, less efficient. As a result, the mitochondria burn more energy. Elderly mice given BAM15 lost fat, gained muscle and strength, and increased physical activity. Credit: Pennington Biomedical Research Center
The weakness and frailty common to sarcopenic obesity are offset in older mice – the equivalent of aged 60-65 in human years – given BAM15. The mice, all of whom had obesity, were fed high-fat diets. Despite that, the mice given BAM15 lost weight and got stronger and more active.
“These data highlight that mitochondrial uncouplers may play an important role in improving health span – the time a person enjoys good health – in advanced age.” — John Kirwan, Ph.D.
“Typically, when you lose weight, you also lose muscle, and in some circumstances, you can lose a lot of it,” Axelrod said. “In this study, the aged mice increased their muscle mass by an average of 8 percent, their strength by 40 percent, while they lost more than 20 percent of their fat.”
BAM15 works by making the mitochondria, the power plants of the cell, less efficient. The result is that the mitochondria burn more energy. The researchers are reluctant to describe BAM15 as a miracle drug. More research will be needed to determine its effectiveness for people.
However, the findings about BAM15 have important implications for improving the quality of life for older adults, especially for the rapidly growing number of people with obesity. Preventing, delaying, or reversing the causes and consequences of sarcopenic obesity may allow people to live longer and healthier lives.
“These data highlight that mitochondrial uncouplers may play an important role in improving health span – the time a person enjoys good health – in advanced age,” said Pennington Biomedical Executive Director John Kirwan, Ph.D.
BAM15 improves many of the key determinants of health and aging, including:
- Removing damaged mitochondria, the power plants of the cell
- Making more healthy mitochondria, and
- Reducing “inflammaging,” or age-related inflammation, linked to muscle loss
“Extending health span is even more important than extending lifespan,” Kirwan said. “Suppose you could add 20 or 30 years to a person’s life. What would be the point if their quality of life was awful?”
Reference: “Mitochondrial uncoupling attenuates sarcopenic obesity by enhancing skeletal muscle mitophagy and quality control” by Wagner S. Dantas, Elizabeth R. M. Zunica, Elizabeth C. Heintz, Bolormaa Vandanmagsar, Z. Elizabeth Floyd, Yongmei Yu, Hisashi Fujioka, Charles L. Hoppel, Kathryn P. Belmont, Christopher L. Axelrod, John P. Kirwan, 19 March 2022, Journal of Cachexia, Sarcopenia and Muscle.
DOI: 10.1002/jcsm.12982
Axelrod and Kirwan are the study’s corresponding authors. Wagner Dantas, Ph.D., a Postdoctoral Researcher in Kirwan’s Integrated Physiology and Molecular Medicine Laboratory, is the lead author.
This work used core facilities that are supported in part by Pennington Biomedical’s Center for Biomedical Research Excellence through National Institutes of Health awards 5P30GM118430 and 1P20GM135002 and Nutrition Obesity Research Center through National Institutes of Health award P30DK072476. This research was supported in part by the National Institutes of Health award U54GM104940. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Open science, done wrong, will compound inequities
Ten years ago, as a new PhD graduate looking for my next position, I found myself in the academic cold. Nothing says “you are an outsider” more than a paywall asking US$38 for one article. That fuelled my advocacy of open science and, ultimately, drove me to research its implementation.
Now, open science is mainstream, increasingly embedded in policies and expected in practice. But the ways in which it is being implemented can have unintended consequences, and these must not be ignored.
Since 2019, I’ve led ON-MERRIT, a project funded by the European Commission that uses a mixture of computational and qualitative methods to investigate how open science affects the research system. Many in the movement declare equity as a goal, but reality is not always on track for that. Indeed, I fear that without more critical thought, open science could become just the extension of privilege. Our recommendations for what to consider are out this week (see go.nature.com/3kypbj8).
Open science is a vague mix of ideals. Overall, advocates aim to increase transparency, accountability, equity and collaboration in knowledge production by increasing access to research results, articles, methods and tools. This means that data and protocols should be freely shared in high-quality repositories and research articles should be available without subscriptions or reading fees.
Making all that happen is expensive. Wealthy institutions and regions can afford this better than can poorer ones. At my university, in a high-income nation, I know I am privileged. In a collaboration to introduce open science at Ukrainian universities (including those displaced by conflict post-2014), I’ve been privy to difficult conversations about how to pay publication fees that are three times a professor’s monthly salary, and how to meet data-sharing requirements to be eligible for funding when institutional support is lacking. And privilege comes in many forms. For instance, the fact that career-advancement criteria don’t reward open practices puts early-career adherents at a disadvantage.
Failing to address structural inequalities directly means that the advantages of those who are already privileged will grow, especially given that they have the most influence over how open science is implemented.
A particularly pressing issue is open access (OA) publication fees, in which the benefit of free readership is being offset by new barriers to authorship. To support OA publishing, journals commonly charge authors, and charges are rising as the practice expands. My group and others have found that article-processing charges are creating a two-tier system, in which richer research teams publish more OA articles in the most prestigious journals. One analysis of 37,000 articles in hybrid ‘parent’ journals and their fully OA ‘mirrors’ (with the same editorial board and acceptance standards) found that the geographic diversity of authors was much greater for non-OA articles than for OA articles (A. C. Smith et al. Quant. Sci. Stud. 2, 1123–1143; 2022). Another analysis found that authors of OA articles were more likely to be male, senior, federally funded and working at prestigious universities (A. J. Olejniczak and M. J. Wilson Quant. Sci. Stud. 1, 1429–1450; 2020). Worse still, citation advantages linked to OA mean that the academically rich will get even richer.
That open science can increase inequity should alarm science reformers. At the very least, they should commit to monitoring how researchers are affected.
To be sure, equity is not the sole priority for many advocates. When my team first announced its project, some critics objected. They argued that the key aims of open science are to improve research integrity by making processes and products more amenable to inspection, and boosting efficiency by making others’ work reusable. Still, as our work has shown, equity is often cited as a key aim (T. Ross-Hellauer et al. R. Soc. Open Sci. 9, 211032; 2022).
Even those rooting for equity often argue that we should first enable access and then consider unintended side effects, such as marginalization of authors from low-income countries. But how change is implemented will have long-lasting consequences. Once new forms of inequity are in place, it will be too late to fix the system efficiently.
How can we ensure that open knowledge creation becomes fairer than it is now? First, we need more shared understanding and global dialogue. Open science is an umbrella term for a coalition of diverse practices with sometimes conflicting aims of transparency, participation and equity. We desperately need to untangle these.
Second, reform should encompass the research system as a whole, rather than country- or region-based policies that target specific practices. The UNESCO Recommendation on Open Science is an example of how this can work. Our recommendations include more focus on shared infrastructure, as well as on who participates and how. That means discussing ways to have open access without publishing fees, plus making open practices easier, cheaper and more valued by promotion and grant evaluators.
I do think that open science can bring much good. Like many of its advocates, I aim to make research more accessible and collaborative and to establish a system that rewards current merit, not past success or current privilege. Any potential for open science to compound inequalities must be vigilantly monitored by the academic community — otherwise we idealists risk scoring an own goal.
Cannabis compound CBD stops coronavirus in test tube, but can it treat COVID?
Jan 25 (Reuters) – Early research suggesting that a popular non-psychoactive compound derived from marijuana might help prevent or treat COVID-19 warrants further investigation in rigorous clinical trials, researchers say.
Several recent laboratory studies of cannabidiol, or CBD, have shown promising results, attracting media attention.
However, many other potential COVID treatments that showed promise in test tubes, from hydroxychloroquine to various drugs used to treat cancer and other diseases, ultimately failed to show benefit for COVID-19 patients once studied in clinical trials.
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Marsha Rosner of the University of Chicago led a team that found CBD appeared to help curb SARS-CoV-2 in infected cells in laboratory experiments. “Our findings do not say this will work in patients. Our findings make a strong case for a clinical trial,” she said.
Using small doses of highly purified CBD that approximate what patients receive in an oral drug already approved for severe epilepsy, Rosner and colleagues found that CBD did not keep the coronavirus from infecting cells in test tubes.
Rather, it acted soon after the virus entered the cells, blocking it from making copies of itself in part via effects on the inflammatory protein interferon. They found similar effects in infected mice, according to a report in Science Advances.
When they looked at a group of adults with severe epilepsy, the researchers found those who were taking the approved CBD drug had lower rates of COVID-19. But a backward look at a small number of patients does not yield conclusive information. Only randomized clinical trials can do that, Rosner said.
“I know my message is not something people want to hear,” she said.
Small doses of tetrahydrocannabinol (THC) – the marijuana ingredient that causes the high – cannabidiolic acid (CBDA), cannabidivarin (CBDV), cannabichromene (CBC), and cannabigerol (CBG) did not keep the virus out of cells or prevent it from replicating, her team found.
“Not only did THC not work, but combining it with CBD prevented CBD from working,” Rosner said.
NO COVID CURES AT CBD DISPENSARY
A separate team reported recently in the Journal of Natural Products that high doses of CBG and CBDA do prevent the coronavirus from breaking into cells.
Richard van Breemen from Oregon State University told Reuters that the doses his team tested were non-toxic to cells. It is not clear yet that similarly high doses would be safe for humans, his team said.
“You want the lowest possible effective dose,” Rosner said, because of potential side effects as the drug is filtered through the liver.
The CBD her team tested was more than 98% pure, while purity in commercial products is far lower. “People should not run out and get CBD from their favorite dispensary,” she said.
CBD products have become widely available in many forms and have been touted – often without proof from clinical trials – as treatments for pain and other ailments.
Small CBD trials in humans with COVID-19 are underway.
In one completed study, researchers in Brazil randomly assigned 105 patients with mild or moderate COVID-19 to receive CBD or a placebo for 14 days along with standard care. The CBD had no apparent effect, according to an October report in Cannabis and Cannabinoid Research.
In a proof-of-concept study at Sheba Medical Center in Israel, researchers are randomly assigning patients with mild COVID to receive CBD or a placebo.
An early-stage trial at Rabin Medical Center, also in Israel, aims to test the effect of CBD in severely or critically ill patients. However, study leader Dr. Moshe Yeshurun told Reuters that accruing participants has been difficult because the current Omicron-driven coronavirus wave “consists mostly of patients with mild to moderate disease.”
Rosner’s team is exploring the possibility of a clinical trial that would likely focus on asymptomatic or mild cases of COVID. Meanwhile, she is concerned that media reports overstating the potential of cannabinoids will lead people to self-medicate with CBD, stop using masks and avoid vaccines.
“We would love to be able to say specifically” that a certain dose of cannabinoids is helpful, she said, but at this point, “vaccine-induced antibodies and antibody drugs are much more effective at blocking infection.”
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Reporting by Nancy Lapid; Editing by Michele Gershberg and Bill Berkrot
Our Standards: The Thomson Reuters Trust Principles.