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Latest Research on Lupus Treatment

Lupus happens because of an immune system misfire. Your immune cells mistakenly attack your organs and tissues, causing damage and inflammation. The main lupus treatments today – immunosuppressants and corticosteroids – work by lowering your immune response and bringing down inflammation.

Managing this autoimmune disease is tricky because lupus affects so many organs – joints, skin, kidneys, heart, brain, and lungs. If you've tried a few treatments without success, help could be on the way.

The search is on for new and more effective lupus treatments. Many of them work by calming the overactive immune response.

Here are just a few of the latest treatment approaches that have been recently approved or are working their way through clinical trials.

B-Cell Therapies

B cells are part of your immune system. They're like little soldiers in your body's army against germs. When they spot a foreign invader like bacteria or a virus, B cells release proteins called antibodies to stop it.

When you have lupus, your B cells turn against you. They make autoantibodies that attack your own organs. B cells also make chemicals that trigger more inflammation . A few new medicines kill or block B cells to treat lupus. Some of these drugs are monoclonal antibodies, which are lab-made proteins that act like the antibodies your immune system makes.

Obinutuzumab ( Gazyva ) is a monoclonal antibody that destroys B cells. It's already a treatment for blood cancers like chronic lymphocytic leukemia (CLL) and follicular lymphoma. Now researchers are looking at whether it might treat lupus, too. So far, results have been promising.

Rituximab ( Rituxan ) was first approved to treat lymphoma. Today it's also a treatment for rheumatoid arthritis. For many years, researchers have been trying to find out whether rituximab might treat lupus, too. Studies so far haven't shown much success, but rituximab might still work for more severe forms of lupus, or for lupus nephritis – kidney inflammation that lupus sometimes causes.

A few other medications block B cells instead of killing them. In studies, obexelimab improved lupus symptoms and prevented flares in some people who used it

Other lupus treatments in development work on BAFF, a protein that sends out signals to activate B cells. Blisibimod and TACI-Ig ( Atacicept ) block these signals. In one study, blisibimod helped people with lupus lower their steroid dose.

T-Cell Therapies

T cells are another type of immune cell that seeks out and kills germs. When you have lupus, your T cells make chemicals that increase inflammation. T cells also direct your B cells to make more autoantibodies.

In 2021, voclosporin ( Lupkynis ) was approved by the FDA to treat lupus nephritis . It blocks T cells from triggering an immune response in the kidneys. Tacrolimus ( Prograf ) interferes with T-cell function and is already approved to prevent rejection after an organ transplant. Research shows it might help with lupus, too.

Plasma Cell Treatments

Plasma cells are immune cells that release autoantibodies in lupus. These cells don't respond well to current lupus treatments that suppress the immune system.

The cancer drug daratumumab ( Darzalex ) destroys plasma cells directly. In one very small study, daratumumab led to a big improvement in lupus symptoms. Researchers need to do more studies to learn whether this drug might be useful for treating lupus.

Targeting Interferon

Interferons are part of your body's immune defenses. In people with lupus, immune cells called plasmacytoid dendritic cells release too much interferon, which produces a lot of inflammation. A couple of new treatments in studies either kill dendritic cells or reduce the amount of interferons these cells release.

Disease-Modifying Drugs

Leflunomide ( Arava ) stops the excess production of immune cells to reduce inflammation in the joints. It's already approved to treat rheumatoid arthritis. Small studies have shown that it also helps to relieve lupus joint symptoms. More research is needed to confirm whether leflunomide might be an effective lupus treatment.

Lupus Kidney Disease

Lupus can damage the kidneys to the point where these organs can't filter your blood. Lupus nephritis is the name for lupus kidney disease.

As mentioned above, voclosporin (Lupkynis) targets T cells to reduce inflammation in the kidneys. Another way to reduce kidney damage is to diagnose and treat lupus nephritis early. Researchers have found more than 230 different proteins in the urine, called biomarkers, that might one day help doctors find and treat lupus nephritis more easily.

Stem Cell Transplant

There are many new medicines to treat lupus, but they don't work for everyone. Sometimes lupus progresses to the point where it damages organs. Studies are under way to see whether stem cell transplant might be an option for people with severe lupus that hasn't improved with other treatments.

Stem cells are the very early cells that grow into other cell types, including immune cells. A stem cell transplant replaces your damaged immune cells with healthy ones from your own body or from a donor.

Some studies are looking at transplants of mesenchymal stem cells. These are a special kind of stem cell that may prevent your immune system from turning against your own body.

These are just some of the new lupus treatments researchers are studying. If you're interested in learning more about them, you might join a clinical trial . One of these studies could give you access to a new medicine before it's approved. Ask the doctor who treats your lupus if any studies might be a good fit for you.

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March 1, 2024

11 min read

These Cancers Were Beyond Treatment—But Might Not Be Anymore

New drugs called antibody-drug conjugates help patients with cancers that used to be beyond treatment

By Jyoti Madhusoodanan

Keith Negley

I n the long and often dispiriting quest to cure cancer, the 1998 approval of the drug Herceptin was a tremendously hopeful moment. This drug for breast cancer was the first to use a tumor-specific protein as a homing beacon to find and kill cancer cells. And it worked. Herceptin has benefited nearly three million people since that time, dramatically increasing the 10-year survival rate—and the cancer-free rate—for what was once one of the worst medical diagnoses. “Honestly, it was sort of earth-shattering,” says oncologist Sara M. Tolaney of the Dana-Farber Cancer Institute in Boston.

But the drug has a major limitation. Herceptin's beacon is a protein called HER2, and it works best for people whose tumors are spurred to grow by the HER2 signal—yet that's only about one fifth of breast cancer patients. For the other 80 percent of the approximately 250,000 people diagnosed with the disease every year in the U.S., Herceptin offers no benefits.

The hunt for better treatments led researchers to reimagine targeted therapies. By 2022 they had developed one that linked Herceptin to another cancer-killing drug. This therapy, for the first time, could damage tumors that had vanishingly low levels of HER2. The drug, named Enhertu, extended the lives of people with breast cancer by several months, sometimes longer. And it did so with fewer severe side effects than standard chemotherapies. The U.S. Food and Drug Administration approved its use in that year.

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The news got even better in 2023. Researchers reported that Enhertu appeared to work even on tumors with seemingly no HER2 at all. (It's possible the cancers did have the protein but at very low levels that escaped standard detection methods.) “Exciting!” says oncologist Shanu Modi of Memorial Sloan Kettering (MSK) Cancer Center in New York City, who helped to run the study that led to Enhertu's approval. “They did this provocative test and saw this almost 30 percent response rate” in tumors apparently lacking the cancer protein, she notes.

Enhertu belongs to an ingenious and growing class of targeted cancer drugs called antibody-drug conjugates, or ADCs. The compounds are built around a particular antibody, an immune system protein that homes in on molecules that are abundant on cancer cells. The antibody is linked to a toxic payload, a drug that kills those cells. An ADC's affinity for cancer means it spares healthy cells, avoiding many of the side effects of traditional chemotherapy. And each antibody can be paired with several different drugs. This Lego-like assembly opens up a world of mix-and-match possibilities. Researchers can use the same drug to treat many cancers by switching up the antibody, or they can attack one type of tumor with many different ADCs that target several cancer biomarkers on the cells. This ability “changes the way we think about drug development,” Tolaney says.

The idea for ADCs is not entirely new—the first one was cleared for patient use in 2000—but recently scientists have learned intricate chemical construction techniques that make the compounds much more effective, and they have identified new cancer-specific targets. These advances have driven a wave of new development. Fourteen ADCs have been approved for breast, bladder, ovarian, blood, and other cancers. Approximately 100 others are in the preclinical pipeline. One ADC for breast cancer, known as T-DM1, proved much more effective than Herceptin and has now become the standard of care for early stages of disease. “It is pretty cool to see how things have changed so quickly,” Tolaney says. Buoyed by the successes, researchers and pharmaceutical companies are pouring resources into developing more powerful ADCs—perhaps even ones that can work across a wide range of cancer types. Pharma giants such as Gilead, Roche and BioNTech have invested heavily in their ADC programs; in October 2023, for example, Merck put $4 billion into a partnership with Daiichi Sankyo, the biotechnology firm that partnered with AstraZeneca to produce Enhertu.

But the new drugs are still beset by some mysterious problems. Some ADCs have side effects similar to those caused by traditional chemotherapies—which shouldn't happen, because the drugs are supposed to target cancer cells alone. On patient forums, people describe needing to reduce their doses because of intolerable nausea or fatigue. These drawbacks limit ADCs' use, so scientists and pharma companies are urgently trying to figure out what is causing them.

In the clinical trial that led to Enhertu's approval, patients typically had already received different kinds of chemotherapy drugs, such as medications that stop cells from multiplying. But these drugs—and other forms of chemotherapy—do not distinguish between a cancer cell and a healthy one. Any cell trying to make DNA or multiply is vulnerable, and normal tissue as well as tumors can be attacked. Fully 64 percent of people on standard chemotherapy experience nausea, diarrhea, fatigue, and other negative side effects. For many, these can be as debilitating as cancer itself. Such effects limit the dose people can take and the length of treatment, leaving windows of opportunity for tumors to grow resistant and rebound.

For many years researchers have sought less toxic alternatives, envisioning precision drugs that target cancers and spare healthy cells. The idea of ADCs sprang from the exquisite specificity of antibodies. If highly toxic forms of chemotherapy could be strapped onto antibodies, the toxins would reach only the cancer cells and no others. Although the concept was straightforward, attempts at making ADCs faltered for decades.

Some of the earliest attempts used drugs that just weren't strong enough. In the 1950s, for instance, researchers linked a drug named methotrexate to an antibody that targets carcinoembryonic antigen, a common tumor marker, and tested whether the construct could treat advanced colorectal and ovarian cancers in people. The drug bound to its target but had little therapeutic effect. Researchers then swung too far to the other end of the spectrum and tried using much more toxic drugs instead. But these drugs triggered serious side effects.

Credit: Jen Christiansen; Graphics consultant: Greg Thurber/University of Michigan

Greg Thurber, a chemical engineer at the University of Michigan, looked into this conundrum. He began working on ADCs when studying how antibodies spread through the body to bind to their targets. After ADCs infiltrate a tumor through its network of blood vessels, the compounds slip out of these vessels and into cancer cells to kill them, Thurber says. But the ADCs that existed at the time never got past the cells just outside the blood vessels. They bound too tightly. The key to improved effects, it turned out, was tailoring the antibody parts so they zeroed in on cancer cells but had a loose enough grip for some to slip into the interior of the tumor. “A lot of people in the field had a very simple concept—we put a chemotherapy drug on an antibody, it targets it to the cancer cell, and it will avoid healthy tissue,” Thurber says. “That's not at all how they work in reality.”

Tinkering with the drug component of ADCs, as well as the antibody, eventually led to a cancer-killing sweet spot. In 2013 the fda greenlit T-DM1 for breast cancer. Its antibody is trastuzumab (the “T” in T-DM1), the same antibody used in Herceptin. The drug attached to this antibody is notable because it's too dangerous to be used on its own. Known as emtansine, it was initially discovered in the 1970s but shelved because it was too toxic to too many cells. Tethered together as T-DM1, however, the drug and antibody generally stayed away from healthy cells and proved to be a potent and precise combination.

In the early 2000s Modi helped to conduct a trial of T-DM1—branded Kadcyla by its maker, Genentech—in people who had an especially difficult disease: advanced HER2-positive breast cancer that had spread throughout the body. Only those who had run out of other treatment options were enrolled. “We were taking people who in some cases were really looking to go to hospice,” Modi says. Yet “almost every patient who was enrolled on that drug had benefits. It was really so satisfying.”

In another trial of about 1,500 people with early breast cancer, an interim data analysis, published in 2019, estimated that 88 percent of those who received T-DM1 would be cancer-free three years later, compared with just 77 percent of those who received Herceptin alone. The drug has proved “more active than most of the therapies we were giving to patients, and it was associated with a better safety profile,” Modi says.

Kadcyla's success against difficult-to-treat cancers didn't just transform some patients' lives. It pumped enthusiasm—and, perhaps more important, pharmaceutical industry dollars—into the idea of ADCs. Researchers now knew that when pieced together correctly, it was possible to load an antibody with drugs too toxic to be used otherwise and still produce a medicine that worked better than traditional chemotherapy.

Several similarly designed ADCs have been approved for a range of different cancer types. Many of these carry drugs that inhibit the enzyme topoisomerase 1, which is essential for DNA replication. Like emtansine, the drug used in Kadcyla, newer topoisomerase inhibitors are too toxic to be used as freestanding drugs but are much less harmful when they're largely restricted to tumor cells. And Kadcyla itself, after being shown to slow or stall late-stage breast cancer, is being tested on patients with very early-stage disease to see whether treatment at that point can not only slow cancer down but actually cure it. Its success “was sort of the catalyst for continued exploration,” Modi says. “Can we build on this? Can we do even better?”

D oing better, it turns out, involves designing good linker molecules that tie the antibody to the drug. These tiny structures act like chemical triggers. They must remain perfectly stable until they reach their target, then unclip from the antibody to discharge their payload at the tumor. Some of the earliest attempts at making ADCs failed not because of their antibodies or drugs but as a result of unstable linkers.

Modern ADCs rely on two types of linkers. One kind remains unbroken even when the ADC reaches its target. The other kind, known as cleavable linkers, are chemicals that break in response to very specific cues, such as enzymes that are abundant in tumors, in the spaces between individual cancer cells. Once an ADC is within the tumor's boundaries, these enzymes cleave the linker and release the drug payload.

Cleavable linkers are showing impressive advantages, and more than 80 percent of currently approved ADCs now use them. An ADC with a noncleavable linker will kill only the cell it attaches to, but one that splits up could place drug molecules near neighboring tumor cells and destroy them as well. This so-called bystander effect can make the drugs much more effective, Thurber says.

Enhertu, for instance, uses the same antibody as Kadcyla but with a cleavable linker (Kadcyla uses a noncleavable version) and a different drug. Each Enhertu antibody carries approximately eight drug molecules, compared with about three per antibody in Kadcyla. In one recent study, researchers compared the effects of these two drugs in people with HER2-positive breast cancers. Enhertu was the clear winner. It stopped tumor growth for more than two years on average, whereas Kadcyla did so for just six months. “It was a landslide in terms of how much better it was,” Tolaney says. “It's a really nice example of how ADC technology leads to dramatic differences in outcomes.”

The bystander effect also explains, in part, why Enhertu is effective against tumors that have barely any HER2: once the ADC enters a tumor and the drug molecules detach, they can kill neighboring tumor cells even if those bystanders don't carry much HER2 on their surface. This action, along with the use of a diagnostic test that can miss extremely low HER2 levels, could explain the results from the trial where the drug seemed to work on tumors with no HER2. That trial employed an assay known as an IHC test. It is generally used to categorize cancers as HER2 positive or negative, not to measure the amount of the protein present. A negative result typically means 10 percent or fewer of the tumor's cells have HER2 on their surfaces. Yet 10 percent may be enough to attract a few Enhertu particles, and the bystander effect might be sufficient to destroy tumor cells, Modi says.

Enhertu is not the only ADC that appears to work this way. In a 2022 study, researchers found that Trodelvy, an ADC that targets a surface protein known as TROP2, seemed to be more effective than standard chemotherapy for people with metastatic triple-negative breast cancer, a particularly hard-to-treat disease. Trodelvy was better irrespective of how much or how little TROP2 was detected on tumors. “That, to me, is wild,” Tolaney says. “We're excited about it because these cancers are having benefits [apparently] without the target.”

This new generation of ADCs is making a difference in other types of cancers previously thought to be intractable, such as metastatic bladder cancer. In 2021 the fda approved Trodelvy and another ADC named Padcev to treat this illness. For 30 years the standard of care for this type of bladder cancer was chemotherapy alone, says oncologist David J. Benjamin, who treats genitourinary cancers at Hoag Family Cancer Institute in southern California. “Now we have multiple new treatments, and two of them happen to be antibody-drug conjugates,” Benjamin says. In clinical trials for patients with advanced bladder cancer, Padcev combined with a drug that stimulates the immune system shrank tumors or stalled their growth in more than 60 percent of people. In a whopping 30 percent of those who received the two-drug combination, their cancer completely disappeared—an unprecedented success.

But even newer ADCs aren't without problems. The bystander effect, which makes them so effective, can spread far enough from the tumor to affect healthy cells, causing hair loss, nausea, diarrhea, fatigue, and other side effects that are disturbingly similar to the fallout of old-school chemo. ADCs also have been linked to a variety of eye problems ranging from conjunctivitis to severe vision loss.

Another explanation for these nasty effects is that there are no protein targets that are exclusive to cancer cells. These proteins, also known as antigens, are more abundant in cancers but may appear in normal cells. That makes some binding of ADCs to healthy cells unavoidable. “I can't think of any examples of true tumor-specific antigens,” says Matthew Vander Heiden, a molecular biologist at the Koch Institute at the Massachusetts Institute of Techonology. Further, ADCs, like any other medicine or antibody, are eventually ingested and metabolized by noncancerous cells. This process fragments them into smaller pieces, releasing payload drugs from their linkers and triggering reactions.

Still, the ability to take ADCs apart and tweak their components—something that isn't possible with traditional treatments—offers researchers the chance to find versions with fewer side effects and more advantages. At present, most ADCs are used at the maximum dose a person can tolerate. That might not be true with future versions. When developing a medication, whether it's a simple painkiller, a chemotherapy or an ADC, researchers begin by figuring out the lowest dose at which the drug is effective. Then they work out the highest dose that people can receive safely. The space between those two doses, known as a therapeutic window, is usually small. But the ability to swap components offers ADC researchers many routes to widening it. Eventually drugmakers might create ADCs so effective that patients never need to take the highest tolerable dose—a much lower one would eliminate tumors without creating unintended consequences such as nausea or hair loss.

Shifting away from toxic chemotherapy-based drugs as payloads could also reduce side effects. Some recently approved ADCs, for instance, link antibodies to drugs that can activate the body's own immune system to attack cancer cells rather than relying on cell-poisoning chemicals. In addition, scientists are exploring ways to deliver radiation therapy directly to tumors by tethering antibodies to radioisotopes. Joshua Z. Drago, an oncologist at MSK Cancer Center, says that with the right kind of linkers, ADCs “could theoretically deliver any kind of small-molecule medication.”

Ultimately, recombined and improved components could lead to the type of swap that cancer patients really care about: exchanging their disease for a cure.

Jyoti Madhusoodanan  is a health and science journalist based in Portland, Ore. She has a Ph.D. in microbiology.

Psychology’s Replication Crisis Is Running Out of Excuses

Another big project has found that only half of studies can be repeated. And this time, the usual explanations fall flat.

Over the past few years, an international team of almost 200 psychologists has been trying to repeat a set of previously published experiments from its field, to see if it can get the same results. Despite its best efforts, the project, called Many Labs 2 , has only succeeded in 14 out of 28 cases. Six years ago, that might have been shocking. Now it comes as expected (if still somewhat disturbing) news.

In recent years, it has become painfully clear that psychology is facing a “ reproducibility crisis ,” in which even famous, long-established phenomena—the stuff of textbooks and TED Talks—might not be real. There’s social priming , where subliminal exposures can influence our behavior. And ego depletion , the idea that we have a limited supply of willpower that can be exhausted. And the facial-feedback hypothesis , which simply says that smiling makes us feel happier.

One by one, researchers have tried to repeat the classic experiments behind these well-known effects—and failed. And whenever psychologists undertake large projects , like Many Labs 2, in which they replicate past experiments en masse , they typically succeed, on average, half of the time.

Read: A worrying trend for psychology’s “simple little tricks”

Ironically enough, it seems that one of the most reliable findings in psychology is that only half of psychological studies can be successfully repeated.

That failure rate is especially galling, says Simine Vazire from the University of California at Davis, because the Many Labs 2 teams tried to replicate studies that had made a big splash and been highly cited. Psychologists “should admit we haven’t been producing results that are as robust as we’d hoped, or as we’d been advertising them to be in the media or to policy makers,” she says. “That might risk undermining our credibility in the short run, but denying this problem in the face of such strong evidence will do more damage in the long run.”

Many psychologists have blamed these replication failures on sloppy practices. Their peers, they say, are too willing to run small and statistically weak studies that throw up misleading fluke results, to futz around with the data until they get something interesting, or to only publish positive results while hiding negative ones in their file drawers.

But skeptics have argued that the misleadingly named “crisis” has more mundane explanations . First, the replication attempts themselves might be too small. Second, the researchers involved might be incompetent, or lack the know-how to properly pull off the original experiments. Third, people vary, and two groups of scientists might end up with very different results if they do the same experiment on two different groups of volunteers.

The Many Labs 2 project was specifically designed to address these criticisms. With 15,305 participants in total, the new experiments had, on average, 60 times as many volunteers as the studies they were attempting to replicate. The researchers involved worked with the scientists behind the original studies to vet and check every detail of the experiments beforehand. And they repeated those experiments many times over, with volunteers from 36 different countries, to see if the studies would replicate in some cultures and contexts but not others. “It’s been the biggest bear of a project,” says Brian Nosek from the Center for Open Science, who helped to coordinate it. “It’s 28 papers’ worth of stuff in one.”

Despite the large sample sizes and the blessings of the original teams, the team failed to replicate half of the studies it focused on. It couldn’t, for example, show that people subconsciously exposed to the concept of heat were more likely to believe in global warming , or that moral transgressions create a need for physical cleanliness in the style of Lady Macbeth , or that people who grow up with more siblings are more altruistic. And as in previous big projects , online bettors were surprisingly good at predicting beforehand which studies would ultimately replicate. Somehow, they could intuit which studies were reliable.

Read: Online bettors can sniff out weak psychology studies.

But other intuitions were less accurate. In 12 cases, the scientists behind the original studies suggested traits that the replicators should account for. They might, for example, only find the same results in women rather than men, or in people with certain personality traits. In almost every case, those suggested traits proved to be irrelevant. The results just weren’t that fickle.

Likewise, Many Labs 2 “was explicitly designed to examine how much effects varied from place to place, from culture to culture,” says Katie Corker from Grand Valley State University, who chairs the Society for the Improvement of Psychological Science. “And here’s the surprising result: The results do not show much variability at all.” If one of the participating teams successfully replicated a study, others did, too. If a study failed to replicate, it tended to fail everywhere.

It’s worth dwelling on this because it’s a serious blow to one of the most frequently cited criticisms of the “reproducibility crisis” rhetoric. Surely, skeptics argue, it’s a fantasy to expect studies to replicate everywhere. “There’s a massive deference to the sample,” Nosek says. “Your replication attempt failed? It must be because you did it in Ohio and I did it in Virginia, and people are different. But these results suggest that we can’t just wave those failures away very easily.”

This doesn’t mean that cultural differences in behavior are irrelevant. As Yuri Miyamoto from the University of Wisconsin at Madison notes in an accompanying commentary, “In the age of globalization, psychology has remained largely European [and] American.” Many researchers have noted that volunteers from Western, educated, industrialized, rich, and democratic countries— WEIRD nations —are an unusual slice of humanity who think differently than those from other parts of the world.

In the majority of the Many Labs 2 experiments, the team found very few differences between WEIRD volunteers and those from other countries. But Miyamoto notes that its analysis was a little crude—in considering “non- WEIRD countries” together, it’s lumping together people from cultures as diverse as Mexico, Japan, and South Africa. “Cross-cultural research,” she writes, “must be informed with thorough analyses of each and all of the cultural contexts involved.”

Read: Psychology’s replication crisis has a silver lining.

Nosek agrees. He’d love to see big replication projects that include more volunteers from non-Western societies, or that try to check phenomena that you’d expect to vary considerably outside the WEIRD bubble. “Do we need to assume that WEirD ness matters as much as we think it does?” he asks. “We don’t have a good evidence base for that.”

Sanjay Srivastava from the University of Oregon says the lack of variation in Many Labs 2 is actually a positive thing. Sure, it suggests that the large number of failed replications really might be due to sloppy science. But it also hints that the fundamental business of psychology—creating careful lab experiments to study the tricky, slippery, complicated world of the human mind—works pretty well. “Outside the lab, real-world phenomena can and probably do vary by context,” he says. “But within our carefully designed studies and experiments, the results are not chaotic or unpredictable. That means we can do valid social-science research.”

The alternative would be much worse. If it turned out that people were so variable that even very close replications threw up entirely different results, “it would mean that we could not interpret our experiments, including the positive results, and could not count on them happening again,” Srivastava says. “That might allow us to dismiss failed replications, but it would require us to dismiss original studies, too. In the long run, Many Labs 2 is a much more hopeful and optimistic result.”

* A mention of the marshmallow test was removed from an early paragraph, since the circumstances there differ from those of other failed replications.

R21 anti-malaria vaccine is a game changer: scientist who helped design it reflects on 30 years of research, and what it promises

Director of the Jenner Institute, University of Oxford

Disclosure statement

Adrian Hill receives funding from government and charitable funders of malaria vaccine development. He has received funding awarded to the University of Oxford from the Serum Institute of India to support clinical trials of the R21/Matrix-M vaccine. He may benefit for a share of any royalty stream to Oxford University from the vaccine.

University of Oxford provides funding as a member of The Conversation UK.

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Until three years ago nobody had developed a vaccine against any parasitic disease. Now there are two against malaria: the RTS,S and the R21 vaccines.

Adrian Hill , director of the Jenner Institute at the University of Oxford and chief investigator for the R21 vaccine, tells Nadine Dreyer why he thinks this is a great era for malaria control.

What makes malaria such a difficult disease to beat?

Malaria has been around for 30 million years . Human beings have not.

Our hominoid predecessors were being infected by malaria parasites tens of millions of years ago, so these parasites had a lot of practice at clever tricks to escape immune systems long before we came along. Homo sapiens first evolved in Africa about 315,000 years ago.

Malaria is not a virus and nor is it a bacterium. It’s a protozoan parasite, thousands of times larger than a typical virus. A good comparison is how many genes it has. COVID-19 has about a dozen, malaria has about 5,000.

Additionally, the malaria parasite goes through four life cycle stages. This is as complex as it gets with infectious pathogens.

Medical researchers have been trying to make malaria vaccines for over 100 years. In Oxford it’s taken us 30 years of research.

How does the R21/Matrix-M vaccine work?

The four malaria life cycles are all hugely different, with different antigens expressed. An antigen is any substance that causes the body to make an immune response against that substance.

We targeted the sporozoites , which is the form that the mosquito inoculates into your skin. We were working to trap them before they could get to the liver and then carry on their life cycle by multiplying furiously.

Each mosquito injects a small number of sporozoites, perhaps 20, into the skin. If you clear those 20, you’ve won. If one gets through, you’ve lost. The bad news is you’ve only got minutes.

So you need extraordinarily high levels of antibodies that the parasite hasn’t seen before and hasn’t learnt to evolve against. Technologically it’s like having to design a car that’s 10 times faster than anything else on the road.

Luckily, there are no symptoms of malaria at that stage.

Read more: Two new malaria vaccines are being rolled out across Africa: how they work and what they promise

A child dies every minute from malaria in Africa. Why are children more susceptible than adults?

Children under five years old account for about 80% of all malaria deaths in Africa. The age you’re most likely to die of malaria in Africa is when you are one year old.

For the first six months you are protected largely by your mother’s immunity and the antibodies she transfers during pregnancy.

If you survive to age two or three, and you’ve had a few episodes of malaria and you are still alive, you’ve got a bit of immunity. This improves over time.

Some children get up to eight episodes in three or four months. They get quite unwell with the first, and three weeks later they’re having a second bout and so on.

Natural immunity doesn’t work until you’ve had a lot of different infections and that’s why adults are generally protected against malaria and don’t become very unwell.

Without malaria, children would be healthier in general — the disease makes you susceptible to other infections.

What about the pace of vaccine rollouts?

We’ve been disappointed that it’s taken more than six months to roll out the R21 vaccine since it was approved in October last year. There are millions of doses of R21 sitting in a fridge in India.

There are a lot of organisations and processes involved in standard deployment that don’t seem necessary.

Compare that to a COVID-19 vaccine from Oxford and AstraZeneca that was approved on New Year’s Eve 2020 and rolled out in several countries the very next week.

In the same year malaria killed more people in Africa than COVID-19 did.

The first malaria vaccine, the RTS,S , has already been given to millions of children in a large safety trial and the uptake has been really high, so large coverage can be achieved in Africa.

How big a role will vaccines have in the fight to eradicate malaria?

We really think we have an opportunity now to make a big impact.

Nobody is quite sure how many of the older tools such as insecticides and bed nets we need to carry on with. The advice is to keep them all.

But mosquitoes are building resistance to insecticides . Anti-malaria medication only lasts for days and parasites are building up resistance against these drugs as well.

There are about 40 million children born every year in malaria areas in Africa who would benefit from a vaccine. The R21/Matrix-M has been designed to be manufactured at scale. The Serum Institute of India, our manufacturing and commercial partner, can produce hundreds of millions of doses each year.

Another real advantage is its low cost. At US$3.90 a dose the R21/Matrix-M appears to be the most effective single intervention we can deploy against malaria

Worldwide there is US$5 billion currently allocated to fight malaria each year.

We’re optimistic that if this money is spent sensibly we can make a big difference. Buying 200 million doses of the R21/Matrix-M vaccine would cost US$800 million.

Being in the field I’m aware of other vaccines coming along. Some are targeting the blood stage and others the mosquito stage of malaria, which is very exciting. This looks like a great era for malaria control.

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Then the endgame will be malaria eradication worldwide, which really should happen in the 2030s.

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• CAREER FEATURE
• 25 June 2024

How researchers navigate a PhD later in life

• Elizabeth Landau 0

Elizabeth Landau is a science writer based in Washington DC.

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On a roll: Krista Bresock celebrates in her local skate park after graduating with a PhD in mathematics from West Virginia University, Morgantown, aged 41. Credit: Michael Germana

Krista Bresock sat crying in her professor’s office. She had to discuss one of five questions with her professor, in person. It was the concluding step of her final exam in functional analysis, the last course that she needed to complete for her PhD in mathematics. He’d shuffled a set of five cards, and she’d picked Card Number Two — corresponding to the one problem that she had not fully studied.

Unlike her fellow students studying intractable maths problems, Bresock was in her late thirties redoing coursework that she had failed years earlier. As a full-time maths teacher at West Virginia University (WVU) in Morgantown, she could find time to study only during nights and weekends.

“Problem Number Two was just collateral damage to being able to maintain this life of work full-time and be in grad school full-time,” Bresock remembers. She “fell to her knees” in relief when, a week later, she learnt she’d still got an A- in the course.

Many think of doctoral degrees as the domain of people in their twenties. Yet according to the US National Science Foundation, 17% of people who gained a PhD in science or engineering in the United States in 2022, the most recent year for which figures are available, were aged 36 or older . In some countries, including Colombia, Mexico, Portugal, South Korea, Iceland, Greece and Israel, the median age for entering a doctoral programme is 32 or higher, according to 2017 data from the OECD in Paris 1 .

Resources for mid-career scientists

A PhD requires a vast commitment of time and energy, often lasting five or more years. Stipends, when available, are often lower than salaries for other full-time jobs or professions. What’s more, students might have to move to another city, or even a different country, to attend their chosen course. Although difficult for any age group, those constraints can create different challenges for prospective students in their thirties, forties and beyond than for their younger colleagues.

At the same time, age often brings wisdom and self-confidence, qualities that can help older students to cope with a strenuous academic life. “The extra ten years that I was out doing other things gave me a lot of perspective and maturity to the way in which I think and live, and I think that was a big reason why I’ve succeeded,” says Peter Swanton, a 36-year-old graduate student working towards a doctoral degree in astrophysics at the Australian National University in Canberra.

Motivation is key

For Bresock, a doctoral degree represented “unfinished business”. She had struggled with alcohol and drug addiction from the age of 16, but hit a dangerous low point in early 2013, when she was a graduate student at WVU the first time round. She dropped out and checked herself into an in-patient programme, but still drank heavily afterwards. With the support of friends, family and Alcoholics Anonymous, she became sober in July 2013.

Bresock then taught maths at WVU, first as an adjunct and then as a full-time instructor, but she didn’t forget her incomplete doctorate. Finally, at the age of 37, she re-enrolled. “This little voice was like, ‘You have more to say. You have more to do. You have this thing sitting on the back burner that is kind of eating away at you,’” she says.

Despite her drive to finish the degree, motivating herself was “really hard sometimes”, she says, “because if I didn’t finish, no one would care: I would just not finish and still have this job and be fine.” One of her top tips for others looking to pursue a doctorate in mid-life is to fully understand and reflect on their motivations. If the goal is “more money”, that might not be enough, she says.

Before returning to his studies, Swanton held a variety of jobs, including hauling sugar cane, working in nightclub security and tutoring in secondary schools. He has this advice for anyone who’s considering a doctorate: make sure you’re “doing it because you love it”. For him, that has meant finding ways to combine telescopic investigations of cosmic objects, such as active galactic nuclei, with preserving folklore about the cosmos from the Gamilaraay, the people of his Aboriginal culture.

Peter Swanton, a 36-year-old graduate student in cultural astronomy at the Australian National University in Canberra, says that his previous work experience has given him the maturity to cope with the strains of academic life. Credit: Lannon Harley/ANU

Swanton’s heritage influences both his academic interests and the way in which he wants to communicate them. For example, the Gamilaraay language was originally a purely oral one. So, rather than just writing “a big block of text” for his dissertation, Swanton says that he would like to include elders and community members telling their own stories, and to bridge their knowledge with the Western understanding of the universe.

“My success has come down to finding something I am passionate about, and not concerning myself with future employability, which was the focus of my earlier attempts at academia and ultimately the reason why I didn’t succeed” at the time, he says.

Finding mentors

María Teresa Martínez Trujillo arrived at the Paris Institute of Political Studies to embark on a graduate programme in political science at the age of 32. Having spent her whole life up to that point in Mexico, she felt isolated from her classmates because of linguistic and cultural barriers, in addition to being the oldest student in her cohort. Martínez Trujillo had already had a career in the Mexican government, including working as an adviser to the secretary of the interior, yet she felt “less brave” than younger students, and had many more questions about reading materials.

She also felt ashamed about her lack of fluency in French. Over time, with the help of a therapist, she learnt to be less judgemental of herself and to overcome her impostor syndrome. Classmates helped her to proofread some of her assignments and she focused on improving her language skills.

Cultural and linguistic barriers left María Teresa Martínez Trujillo feeling isolated from her peers when she arrived from Mexico, aged 32, to embark on a graduate programme at the Paris Institute of Political Studies. Credit: Hiram Romero

Martínez Trujillo’s advisers — Hélène Combes and Gilles Favarel-Garrigues — were key for her as she dived into reading and fieldwork on the relationship between drug trafficking and the business world in Morelia, Mexico, for her master’s project. “They let me go to the ‘forest’ and spend time and lose myself,” she says, adding that when she felt lost or stuck, her advisers helped her to find her way.

Time and money

Finances often pose a problem for graduate students who don’t already have savings and support, including those who have worked previously. Even with tuition covered, and a stipend to help towards living expenses, making ends meet can be challenging, especially for students who have other financial responsibilities, such as providing for family members or maintaining a home.

Martínez Trujillo received a stipend, but she spent almost all of it on rent and didn’t want to ask her family for money. She worked as a nanny, consulted for a Mexican think tank and spent summers working in Mexico on friends’ projects. “I’d never have free days,” she says.

Bresock wishes she could have spent more time away from both work and studies. “I did a terrible job of that. Make sure you make time for yourself. That dissertation will still be there, if you go take a walk, or if you go swim or whatever, for an hour out of your life.”

Training: Data Analysis: Planning and Preparing

Like Bresock, Marc Gentile kept a full-time job while doing his PhD in astrophysics at the Swiss Federal Institute of Technology in Lausanne in his mid-to-late-fortiess. He needed to earn enough to support both himself and his wife, and to address other financial responsibilities.

“The top advice would be establishing effective work and study habits right from the start,” he says. “In my case, time was the most precious resource, and I had to be very well organized to make the most of it.”

Gentile would work on his doctoral assignments from 5 a.m. to 6 a.m. each weekday, before leaving for his day job. He would then read articles while commuting by train, and tackle more PhD tasks or further reading in the evenings. “I was told that I was, on average, more productive and better organized than most other, younger students, because you develop such skills when you work professionally,” he said.

Family matters

When Wendy Bohon walked across the stage to receive her doctorate in geology, she was nearly 38 years old and pregnant with twins. She wound up at Arizona State University in Tempe after beginning her career as an actor, and then becoming fascinated with earthquakes after one shook her apartment in 1999.

For her dissertation, Bohon conducted fieldwork in India on two large fault systems, focusing on how fast they had been moving, their intersections and their frequency of earthquakes — as well as the growth of mountains around them — over the past 34 million years. Today, she heads the Seismic Hazards and Earthquake Engineering branch of the California Geological Survey in Sacramento.

Wendy Bohon was nearly 38, and pregnant with twins, when she graduated from Arizona State University in Tempe with a PhD in geology. Credit: Linda Bohon

As a student, her desire to expand her family had put her in a different life stage from younger peers. She had met her husband, who already had a young daughter, while in her graduate programme. And whereas her classmates had wanted to avoid pregnancy, she had struggled to conceive. “That emotional disconnect and the difference in their reality and my reality — it was really tough,” she says. Ultimately, she and her husband chose to try the intensive process of in vitro fertilization, which Bohon mostly kept secret. At the same time, she was helping to co-parent her husband’s daughter, and the couple were given full custody of the girl when she was seven.

Bohon coped with parenting and finishing graduate school with the help of “a built-in village of people around who could step in to help us”. Other graduate students would play the card game UNO with the girl, or colour pictures with her. And Bohon’s mentor, along with the mentor’s husband, became the child’s godparents.

“In a lot of ways, it was easier to parent during my PhD, because my schedule was relatively flexible, so I could stay home with her when she was sick, or attend school functions,” Bohon says. What’s more, she adds, “having a kiddo that needed me helped me to set and keep healthier boundaries than I think I would have otherwise”.

Charlotte Olsen, a postdoctoral researcher in astrophysics at the New York City College of Technology, earned a PhD at the age of 42 and now investigates the factors that influence star formation and galaxy evolution. Olsen says that working on her doctorate presented challenges for her marriage. “I’m not gonna lie: grad school is really rough on a relationship,” she says — adding that, especially at the beginning, “it’s an incredibly stressful time”.

Among the responsibilities that older students might have is taking care of ageing parents. Olsen recalls that during her qualifying exams, she hadn’t heard from her mother, who was 76 years old at the time, for a while. She assumed that her mother wanted to give her space during that stressful time. Later, she found out that her mother’s appendix had ruptured, necessitating surgery and a stay in a hospital’s intensive-care unit.

Through it all, Olsen’s spouse was an invaluable source of emotional support. “Having somebody who is there with you along the way” helps a lot, she says.

What happens next?

Not everyone who gets a PhD stays in their field. Gentile, now 60, works as a data scientist for a Swiss television station. He had a postdoctoral research position for five years after graduation — but for several reasons, including financial ones, he could not find an academic job afterwards. “If I had really wanted to continue in astrophysics, then I would have had to move abroad; it’s difficult now,” he says.

Still, Gentile found the PhD experience rewarding and worthwhile. As well as acquiring problem-solving techniques, he learnt coding and data-science skills, such as machine learning and statistical methods. And he has used all of these in subsequent jobs, including his current one.

His graduate work also remains relevant. Some of the algorithms and software that he worked on during his PhD helped to inform the tools that scientists will use to analyse data from the European Space Agency’s Euclid observatory, which aims to explore dark energy and dark matter.

Bresock received a promotion at West Virginia University after earning her PhD in maths in December 2022, aged 41. Her dissertation examined how students understand the definite integral, a fundamental concept in calculus, when solving different kinds of problem.

Today, she has greater empathy for her own students because of her own struggles as a graduate student. Finishing her doctorate remains one of her most satisfying accomplishments, she says. “When people ask me what’s the biggest thing I’ve ever done in my life, it’s: get sober, and then, finish my PhD. That’s a close second.”

doi: https://doi.org/10.1038/d41586-024-02109-x

Organisation for Economic Co-operation and Development. Education at a Glance 2019: OECD Indicators (OECD, 2019).

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New Experimental HIV Vaccine Shows Promise in Early Human Trials

An HIV vaccine candidate is showing positive early results, prompting a critical component of the human immune response in 97 percent of vaccine recipients.

It was a small, phase 1 trial testing a vaccine that was made out of an engineered version of a protein that exists on the HIV virus . This particle was designed to get the body ready to generate broadly neutralizing antibodies , which are thought to be critical to create immunity against HIV.

Broadly neutralizing antibodies would recognize a large swath of HIV subtypes, which is necessary to provide immunity because the HIV virus mutates frequently.

Forty-eight participants either received the vaccine candidate or a placebo , and 35 out of 36 of those dosed with the vaccine candidate showed activation of broadly neutralizing antibody precursor B cells that could produce the first step on the way to immunity.

The crux of this technique is essentially to train the immune system to recognize a wide array of naturally occurring HIV subtypes, according to William Schief, one of the authors of the study. Schief is a professor in the department of immunology and microbiology at Scripps Research.

"There's only a few patches on the surface of the HIV spike that remain the same or relatively the same across different isolates. And we're trying to elicit very specific antibodies that have very specific properties that allow them to bind to those exact patches," Schief said.

In the phase 1 study, no one reported serious side effects, and other side effects like pain at the injection site or headaches were mild to moderate, and they resolved in one to two days.

These results, published in the academic journal Science on December 1st, 2022, which was World AIDS Day, were first announced in 2021 at the virtual conference hosted by the International AIDS Society HIV Research for Prevention. The trial was co-run by the International AIDS Vaccine Initiative and Scripps Research.

Researchers have been trying to create an HIV vaccine for nearly 40 years

HIV is notoriously difficult to vaccinate against. Part of this is because of HIV's tendency to mutate . By evolving and changing quickly, it can avoid the immune system by making itself harder to recognize.

Additionally, virtually no one, short of a few high-profile cases , has been cured of an HIV infection. That means we don't know what sorts of immune cells in the body can actually protect against infection.

Theoretically, this vaccine will be the first in a series of multiple shots, each using a different HIV particle to train the immune system. As the shots progress, the molecules get closer and closer to that of the actual HIV viruses , until antibodies produced can bind to many different kinds of HIV.

"That's sort of a whole new way of thinking about how to make a vaccine," Schief said.

Moderna is developing its HIV vaccine based on similar research

According to Schief, his team is currently working with biotech giant Moderna to develop and test a vaccine to deliver the immune-training HIV particles via mRNA, instead of the protein-based model this most recent study used. One phase 1 study is currently testing the same particle, as well as another engineered particle, with an mRNA delivery system. Another study is testing the same particle in a clinical trial in Africa.

It will take time before phase 2 trials can begin, according to Schief, and there's no guarantee that the vaccine will ultimately work.

But if it does, this technique could be used to make other vaccines, he said, like a universal coronavirus or flu vaccine.

"We're optimistic that there's some chances that this approach may be helpful for more than just HIV," said Schief, "even though if it only helps HIV that would be enormous."

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Neuroscientists find a way to make object-recognition models perform better

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Computer vision models known as convolutional neural networks can be trained to recognize objects nearly as accurately as humans do. However, these models have one significant flaw: Very small changes to an image, which would be nearly imperceptible to a human viewer, can trick them into making egregious errors such as classifying a cat as a tree.

A team of neuroscientists from MIT, Harvard University, and IBM have developed a way to alleviate this vulnerability, by adding to these models a new layer that is designed to mimic the earliest stage of the brain’s visual processing system. In a new study, they showed that this layer greatly improved the models’ robustness against this type of mistake.

“Just by making the models more similar to the brain’s primary visual cortex, in this single stage of processing, we see quite significant improvements in robustness across many different types of perturbations and corruptions,” says Tiago Marques, an MIT postdoc and one of the lead authors of the study.

Convolutional neural networks are often used in artificial intelligence applications such as self-driving cars, automated assembly lines, and medical diagnostics. Harvard graduate student Joel Dapello, who is also a lead author of the study, adds that “implementing our new approach could potentially make these systems less prone to error and more aligned with human vision.”

“Good scientific hypotheses of how the brain’s visual system works should, by definition, match the brain in both its internal neural patterns and its remarkable robustness. This study shows that achieving those scientific gains directly leads to engineering and application gains,” says James DiCarlo, the head of MIT’s Department of Brain and Cognitive Sciences, an investigator in the Center for Brains, Minds, and Machines and the McGovern Institute for Brain Research, and the senior author of the study.

The study, which is being presented at the NeurIPS conference this month, is also co-authored by MIT graduate student Martin Schrimpf, MIT visiting student Franziska Geiger, and MIT-IBM Watson AI Lab Co-director David Cox.

Mimicking the brain

Recognizing objects is one of the visual system’s primary functions. In just a small fraction of a second, visual information flows through the ventral visual stream to the brain’s inferior temporal cortex, where neurons contain information needed to classify objects. At each stage in the ventral stream, the brain performs different types of processing. The very first stage in the ventral stream, V1, is one of the most well-characterized parts of the brain and contains neurons that respond to simple visual features such as edges.

“It’s thought that V1 detects local edges or contours of objects, and textures, and does some type of segmentation of the images at a very small scale. Then that information is later used to identify the shape and texture of objects downstream,” Marques says. “The visual system is built in this hierarchical way, where in early stages neurons respond to local features such as small, elongated edges.”

For many years, researchers have been trying to build computer models that can identify objects as well as the human visual system. Today’s leading computer vision systems are already loosely guided by our current knowledge of the brain’s visual processing. However, neuroscientists still don’t know enough about how the entire ventral visual stream is connected to build a model that precisely mimics it, so they borrow techniques from the field of machine learning to train convolutional neural networks on a specific set of tasks. Using this process, a model can learn to identify objects after being trained on millions of images.

Many of these convolutional networks perform very well , but in most cases, researchers don’t know exactly how the network is solving the object-recognition task. In 2013, researchers from DiCarlo’s lab showed that some of these neural networks could not only accurately identify objects, but they could also predict how neurons in the primate brain would respond to the same objects much better than existing alternative models. However, these neural networks are still not able to perfectly predict responses along the ventral visual stream, particularly at the earliest stages of object recognition, such as V1.

These models are also vulnerable to so-called “adversarial attacks.” This means that small changes to an image, such as changing the colors of a few pixels, can lead the model to completely confuse an object for something different — a type of mistake that a human viewer would not make.

As a first step in their study, the researchers analyzed the performance of 30 of these models and found that models whose internal responses better matched the brain’s V1 responses were also less vulnerable to adversarial attacks. That is, having a more brain-like V1 seemed to make the model more robust. To further test and take advantage of that idea, the researchers decided to create their own model of V1, based on existing neuroscientific models, and place it at the front of convolutional neural networks that had already been developed to perform object recognition.

When the researchers added their V1 layer, which is also implemented as a convolutional neural network, to three of these models, they found that these models became about four times more resistant to making mistakes on images perturbed by adversarial attacks. The models were also less vulnerable to misidentifying objects that were blurred or distorted due to other corruptions.

“Adversarial attacks are a big, open problem for the practical deployment of deep neural networks. The fact that adding neuroscience-inspired elements can improve robustness substantially suggests that there is still a lot that AI can learn from neuroscience, and vice versa,” Cox says.

Better defense

Currently, the best defense against adversarial attacks is a computationally expensive process of training models to recognize the altered images. One advantage of the new V1-based model is that it doesn’t require any additional training. It is also better able to handle a wide range of distortions, beyond adversarial attacks.

The researchers are now trying to identify the key features of their V1 model that allows it to do a better job resisting adversarial attacks, which could help them to make future models even more robust. It could also help them learn more about how the human brain is able to recognize objects.

“One big advantage of the model is that we can map components of the model to particular neuronal populations in the brain,” Dapello says. “We can use this as a tool for novel neuroscientific discoveries, and also continue developing this model to improve its performance under this challenging task.”

The research was funded by the PhRMA Foundation Postdoctoral Fellowship in Informatics, the Semiconductor Research Corporation, DARPA, the MIT Shoemaker Fellowship, the U.S. Office of Naval Research, the Simons Foundation, and the MIT-IBM Watson AI Lab.

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How is crispr revolutionizing cancer research.

Despite the advances in health and medicine over the past few decades, the search for a cure for cancer continues.

According to the National Cancer Institute, cancer is one of the leading causes of death worldwide. Back in 2020, it was predicted that an estimated 1,806,590 new cases of cancer would be diagnosed in the U.S. alone, and about 606,520 people would succumb to the disease that year. Researchers have been trying to cure cancer with various methods from cell therapy to immunotherapy, but there still isn’t a reliable remedy for the disease. However, one of the more promising areas of research is the CRISPR (clustered regularly interspaced short palindromic repeats) method, which allows scientists to further understand how cancer cells work.

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What is CRISPR?

CRISPR technology is currently used to study and edit genomes. Researchers are aiming to use CRISPR to modify gene function, which includes stopping the growth of cancer cells and preventing their spread. Though the technique is still in its early stages of research, CRISPR has already shown some promising results in lab tests. Dr. Monte Winslow, an Associate Professor of Genetics and Pathology at the School of Medicine, is one such researcher who is making headway in CRISPR studies.

Putting CRISPR to good use

In his webinar, entitled “How CRISPR is revolutionizing cancer research,” Winslow discusses the many ways that genome editing can identify and target mutations that may drive cancer development. Winslow’s presentation gives a broad introduction to how CRISPR is being used to understand cancer better, as well as an overview of general cancer genetics and genome editing.

According to Winslow, the reason CRISPR is so exciting is because genomic change can essentially inactivate the gene that causes cells to multiply uncontrollably. By targeting certain genes and knowing exactly which ones cause cancer, genome editing can remove the offending cancer-causing genes.

These genetic alterations can result from specific mutations, structural alterations, or a combination of abnormalities in the DNA. Depending on each individual instance, this can lead to a loss of activity, gain in activity, or even a general change in activity of the cell. Using the CRISPR technique, with the help of a Cas9 protein and a guide RNA, scientists now have the ability to create a double-strand break anywhere in the genome and inactivate certain genes.

However, Winslow warns, it’s much easier to do in theory than in practice. Due to the complexity of genomic alterations, no two patients are the same. This means that each individual will have to go through different procedures and studies, especially because there's no one-size-fits-all solution for all patients.

CRISPR studies in the lab

In his lab, Winslow studies the results of genome editing by experimenting on mice. He and his lab cohort use the CRISPR method to analyze genes that can be used to create or suppress tumors.

“What if we made a pool of these lentiviral vectors, and in each one we put a guide RNA targeting a different tumor suppressor?” Winslow asks. “Then if we deliver it to mice, we can actually develop, in this case, eleven different [types] of tumors. We call them genotypes, because they have different genes mutated. Then we can, from one experiment, assess how all eleven of these genes might function.”

With the results of these tests, Winslow is able to start narrowing down how genetic editing can affect an organism. Through his lab’s findings, he hopes to help accelerate the investigation of carcinogenesis, increase the general understanding of cancer cell functionality, and work toward an eventual cure for all types of cancer.

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Fact check: The vaccine for COVID-19 has been nearly 20 years in the making

The claim: the covid-19 vaccine was developed in less than a year, but there are no vaccines against viruses and diseases that have existed for far longer .

It is approaching a year since the World Health Organization declared COVID-19 a pandemic , and on Dec. 8, Britain was the first Western country to begin vaccination against the virus. The rollout was followed by the U.S. Food and Drug Administration's emergency authorization of Pfizer-BioNTech's COVID-19 vaccine on Dec. 11 and Moderna's on Dec. 18 .

Given the quick scientific response to the newly emerging virus, one Instagram post is calling foul, questioning why vaccines for equally debilitating diseases, predating the pandemic, have not yet been developed. 

The Nov. 30 Instagram post  from author Boyce Watkins shares a screenshot of a Facebook comment alleging countless years of research effort have yielded no vaccine.

"40 years worth of research...no vaccine for HIV (sic) At least 100 years research...no vaccine for cancer (sic) Ongoing research...no vaccine for the common cold (sic) Less than a year for a covid (sic) vaccine? Thanks but a hard pass on that shot..." claims "Lee Morin" in the comment.

"This does make you wonder: How did you come up with this so fast, but you can't vaccinate against viruses that have been harming people for centuries?" asks Watkins. The post has received over 13,800 likes and comments agreeing with Watkins' charge. 

"Come on. You have 7 BILLION customers. No other virus/cancer/ailment has that many customer. Follow the money," writes Instagram user borzirtc.

Other social media users have posted the same or a similar claim, as recently as Jan. 13 .

USA TODAY has reached out to those who posted the claim for further comment.  

More: Fact check: COVID-19 outbreak at NY nursing home started before vaccinations

It began with chickens

Operation Warp Speed, the private-public partnership initiated by the White House during the pandemic , may give the impression the COVID-19 vaccine developed overnight, but in actuality, it depends on research dating back nearly 100 years. 

Coronaviruses were first encountered in April 1930, when a strange respiratory disease ravaged poultry farms across North Dakota and Minnesota, killing tens of thousands of baby birds, The Scientist reports . Unsure of what exactly this illness was, veterinarians Arthur Schalk and Merle Hawn of North Dakota Agricultural College, now North Dakota State University, called it "infectious bronchitis of baby chicks," the viral agent later named infectious bronchitis virus.

Further scientific research into IBV and recognition that it was not like influenza A, a flu virus known to cause bronchitis, would transpire over the next 30 years. In November 1968, a group of scientists wrote to the journal Nature asking for IBV, and viruses resembling it like mouse hepatitis virus discovered in 1947 , to be classified as coronaviruses, a name derived from its appearance – the spike proteins casting a halo around the surface, much like the sun's corona – on electron microscope imaging.

More: Fact check: Pregnant women do receive vaccines, but more study needed on COVID-19 shot

SARS was the first attempt at a human coronavirus vaccine

While coronaviruses could cause a variety of fatal diseases in animals, the two known to infect humans were not a grave concern, as they only caused the common cold . This belief was challenged in November 2002 with the emergence of a new respiratory illness in Guandong Province, China, that would infect over 8,000 people worldwide and claim 774 lives.

In less than a month, researchers decoded the enormous genome of the new virus, which caused a disease called severe acute respiratory syndrome. Researchers concluded it was a coronavirus, likely to have jumped from animals to humans because it was only somewhat related to other known coronaviruses . (It took over 15 years of search to identify bats as the potential animal source.) By July 2003, thanks to isolating and quarantining patients, the World Health Organization declared SARS officially contained .

Nevertheless, fears of future seasonal SARS outbreaks called for a vaccine. SARS-CoV's spike protein was an obvious choice for a target. Prior research found the spike protein was critical  in determining which species a coronavirus infected, where it preferred to hunker down – called organ or cell tropism – and disease severity. The spike protein had even been proposed as a vaccine target for canine coronavirus in 1991 .

More: Fact check: Vaccination helped eradicate smallpox

A number of vaccines targeting the spike protein were designed, tested in animal models and found to be quite promising against SARS and other coronavirus illnesses like Middle East respiratory syndrome,  which appeared in 2012 . But further testing reached an impasse when funding declined steadily in the years following the 2003 outbreak, said Dr. Peter Hotez , a vaccine scientist and dean of the National School of Tropical Medicine at Baylor College of Medicine in Houston, whose team collaborated with Galveston National Laboratory to create a SARS vaccine  in 2016.

"We manufactured a really great SARS 1 vaccine in the lab. We actually had a manufacturer at Walter Reed, but then we couldn't raise the money to do all the clinical testing," he told USA TODAY.

Funding was not the only issue. Testing whether a vaccine can prevent disease requires the disease to still be around . Since there have been no major outbreaks of SARS since 2003, testing vaccine efficacy was difficult. But more instrumental is interest: Few SARS or MERS cases meant pharmaceutical companies were less inclined to invest in a likely rarely used vaccine.

More: Fact check: Doctors say Hilary Duff likely didn't contract pink eye from COVID-19 tests

Laying the groundwork

Typically, the road to creating new vaccines is long, with many steps : Finding and developing a vaccine target (exploratory), testing it in tissue or cell cultures and animal models (preclinical) followed by three phases of clinical trials with human volunteers.

If a vaccine proves its mettle, its developers have to seek and gain approval from the FDA before manufacturing. Lastly, in phase four, quality control monitors for any possible vaccine side effects.  

For vaccines to be effective, a specific target is needed. This vaccine target, also called an antigen, is typically a fragment of the disease-causing agent that instructs the immune system on how to recognize and destroy it upon contact. Searching for a suitable antigen can be an arduous process but prior coronavirus research made it all easier.     

"When the Chinese put up the COVID-19 sequence on bioRxiv in January, our community of scientists looked at it and said, 'Yeah, we got this because we know how to do it.' It was all about plug and play based on all that experience," said Hotez.

Having a running start does not mean the testing process was accelerated, however. Hotez, whose recombinant protein subunit COVID-19 vaccine is undergoing clinical trials in India , stated the vaccine still underwent testing among a large group of human volunteers, even more than a typical trial with over 30,000 to 60,000 people. 

What accelerated the vaccine process was manufacturing.   

"The two accelerants are doing the manufacturing of risk (scaling up manufacturing based on the assumption the vaccine will work, also called at-risk manufacturing) and manufacturing the vaccine in parallel with clinical trials. That's new because we usually wait for the phase three results," he said.

More: Fact check: The US saw more deaths in 2020 than in 2019, driven by the COVID-19 pandemic

So why is there no vaccine for HIV, cancer, or the common cold?

Human immunodeficiency virus , the culprit behind acquired immunodeficiency syndrome, commonly known as AIDS, is a tricky virus. Much like the novel coronavirus, HIV binds to a protein on the surface of T cells, a type of white blood cell, to enter. Once inside, HIV integrates its genetic material with its host cell's DNA, using the host's DNA replication machinery to create new viruses, which blast off to infect and kill other T cells.

Finding a specific and effective vaccine target is therefore difficult, especially since HIV mutates frequently in order to mask itself from the immune system. According to the National Institute of Allergy and Infectious Disease , common vaccine approaches using inactivated or live HIV forms have either not been "effective in eliciting immune responses in clinical trials" or are too dangerous to use.

The same goes for the common cold , which is caused by a smorgasbord of viruses including over 150 different types of rhinovirus, a common troublemaker. 

"It's hard to create a vaccine when you have so many different viruses causing similar symptoms. To make a universal vaccine against all of them is probably pretty daunting, it might be doable, but it's daunting," explained Hotez.

More: Fact check: Biden said he plans to increase COVID-19 small business relief to people of color and women

Cancer, abnormal growth of the body's own cells due to unchecked genetic mutations , is no virus, but the struggle in finding a suitable vaccine target is not any easier. 

"The challenge is getting antigen targets and also access because a lot of the antigens, or cancer proteins, are first inside the cell. They may not be presented to the immune system so these are much more complicated targets," said Hotez. 

Advances in messenger RNA-based vaccine technology in recent years may help fast-track some cancer vaccines, he acknowledged. The platform, which provides the body the equivalent of a genetic assembly instruction booklet for manufacturing target-specific antibodies, has been used for rabies , influenza and Zika and is considered an attractive approach for its low cost, speed of manufacturing, potency and versatility, Nature reported .

Many cancer vaccines using mRNA are in the works, like Moderna's personalized cancer vaccine , mRNA-4157, which is being tested in patients with metastatic common epithelial cancer. The Boston-based pharmaceutical company also announced on Jan. 11 it was working on an mRNA HIV vaccine with phase I clinical trials expected sometime in 2021 .

Our ruling: Missing context

We rate this claim MISSING CONTEXT because without additional context it might be misleading. Vaccines require specific targets against which they train the immune system. COVID-19's spike protein was identified nearly 20 years ago as a potential vaccine target during the development of the SARS vaccine, following the 2003 SARS outbreak. This has helped expedite the vaccine process, given that vaccine platform technologies have advanced in recent years, as well. Another accelerant was the commercial-scale production of COVID-19 vaccine doses prior to FDA clearance, called at-risk manufacturing, when early results appeared promising. Finding suitable vaccine targets for HIV, cancer and the common cold has been more difficult in comparison as these diseases have either elusive or highly variable targets. 

Our fact-check sources:

• World Health Organization, March 11, 2020, " WHO Director-General's opening remarks at the media briefing on COVID-19 - 11 March 2020 "
• USA TODAY, Dec. 8, 2020, " 'V-Day': A year after COVID-19 pandemic began in China, UK is first in West to start vaccinations "
• U.S. Food & Drug Administration, Jan. 12, " Pfizer-BioNTech COVID-19 Vaccine "
• U.S. Food & Drug Administration, Jan. 12, " Moderna COVID-19 Vaccine " 
• U.S. Department of Health and Human Services, Dec. 21, " Fact Sheet: Explaining Operation Warp Speed " 
• The Scientist, Sept. 1, 2020, " Coronavirus Closeup, 1964 "
• Prairie Public News, Dec. 16, 2020, " A Coronavirus in 1930 "
• Nature, Nov. 16, 1968, " Virology: Coronaviruses " 
• Laboratory Animals, Dec. 13, 1996, " Enterotropic mouse hepatitis virus " 
• Medical Microbiology, accessed Jan. 14, " Chapter 60 Coronaviruses "
• Centers for Disease Control and Prevention, April, 26, 2013, " CDC SARS Response Timeline "
• Nature Reviews Microbiology, Dec. 1, 2003, " SARS - beginning to understand a new virus " 
• Science, May 30, 2003, " The Genome Sequence of the SARS-Associated Coronavirus "
• Nature, Dec. 1, 2017, " Bat cave solves mystery of deadly SARS virus — and suggest new outbreak could occur " 
• World Health Organization, July 5, 2003, " SARS outbreak contained worldwide " 
• The National Academies Learning from SARS: Preparing for the Next Disease Outbreak, accessed Jan. 14, " Coronavirus Research: Keys to Diagnosis, Treatment, and Prevention of SARS " 
• Virology, Oct. 12, 2000, " Coronavirus Spike Proteins in Viral Entry and Pathogenesis " 
• Nature Reviews Microbiology, Feb. 9, 2009, " The spike protein of SARS-CoV — a target for vaccine and therapeutic development "
• Google Patents, April 25, 1991, " DNA encoding the Canine coronavirus spike protein "
• Journal of Biomedical Science, Dec. 20, 2020, " Coronavirus vaccine development: from SARS and MERS to COVID-19 "
• Centers for Disease Control and Prevention, Aug. 2, 2019, " Middle East Respiratory Syndrome (MERS) " 
• NBC News, March 5, 2020, " Scientists were close to a coronavirus vaccine years ago. Then the money dried up. "
• Medscape, May 28, 2020, " COVID-19 Data Dives: Why Don't We Have a Vaccine for SARS or MERS? "
• Infectious Diseases and Therapy, April 23, 2020, " Vaccines for SARS-CoV-2: Lessons from Other Coronavirus Strains "
• George Washington Online Public Health, March 6, 2019, " Producing Prevention: The Complex Development of Vaccines "
• Baylor College of Medicine News, Nov. 16, 2020, " Biological E. Limited and Baylor COVID-19 vaccine begins clinical trial in India "
• Transfusion Medicine and Hemotherapy, May 9, 2016, " Human Immunodeficiency Virus (HIV) "
• National Institute of Allergy and Infectious Disease, May 17, 2018, " Infographic — Progress Toward an HIV Vaccine " 
• Mayo Clinic, April 20, 2019, " Common cold "
• National Institute of Health, Feb. 9, 2015, " What is Cancer? "
• Lancet, July 25, 2017, " Safety and immunogenicity of an mRNA rabies vaccine in healthy adults: an open-label, non-randomised, prospective, first-in-human phase 1 clinical trial "
• Vaccine, May 31, 2019, " mRNA vaccines against H10N8 and H7N9 influenza viruses of pandemic potential are immunogenic and well-tolerated in healthy adults in phase 1 randomized clinical trials "
• Clinical Trials, Aug. 22, 2019, " Safety, Tolerability, and Immunogenicity of Zika Vaccine mRNA-1893 in Healthy Flavivirus Seropositive and Seronegative Adults "
• Nature, Oct. 16, 2019, " Unlocking the potential of vaccines built on messenger RNA "
• BioSpace, Nov. 11, 2020, " Moderna's Personalized Cancer Vaccine Shows Promise in Early-Stage Trial "
• Moderna, Jan. 11, " Moderna Provides Business Update and Announces Three New Development Programs in Infectious Disease Vaccines "

Thank you for supporting our journalism. You can subscribe to our print edition, ad-free app, or electronic newspaper replica here.

Our fact check work is supported in part by a grant from Facebook.

New Research

Scientists Replicated 100 Psychology Studies, and Fewer Than Half Got the Same Results

The massive project shows that reproducibility problems plague even top scientific journals

Brian Handwerk

Science Correspondent

Academic journals and the press regularly serve up fresh helpings of fascinating psychological research findings. But how many of those experiments would produce the same results a second time around?

According to work presented today in Science , fewer than half of 100 studies published in 2008 in three top psychology journals could be replicated successfully. The international effort included 270 scientists who re-ran other people's studies as part of The Reproducibility Project: Psychology , led by Brian Nosek of the University of Virginia .

The eye-opening results don't necessarily mean that those original findings were incorrect or that the scientific process is flawed. When one study finds an effect that a second study can't replicate, there are several possible reasons, says co-author Cody Christopherson of Southern Oregon University. Study A's result may be false, or Study B's results may be false—or there may be some subtle differences in the way the two studies were conducted that impacted the results.

“This project is not evidence that anything is broken. Rather, it's an example of science doing what science does,” says Christopherson. “It's impossible to be wrong in a final sense in science. You have to be temporarily wrong, perhaps many times, before you are ever right.”

Across the sciences, research is considered reproducible when an independent team can conduct a published experiment, following the original methods as closely as possible, and get the same results. It's one key part of the process for building evidence to support theories. Even today, 100 years after Albert Einstein presented his general theory of relativity, scientists regularly repeat tests of its predictions and look for cases where his famous description of gravity does not apply.

"Scientific evidence does not rely on trusting the authority of the person who made the discovery," team member Angela Attwood , a psychology professor at the University of Bristol, said in a statement "Rather, credibility accumulates through independent replication and elaboration of the ideas and evidence."

The Reproducibility Project, a community-based crowdsourcing effort, kicked off in 2011 to test how well this measure of credibility applies to recent research in psychology. Scientists, some recruited and some volunteers, reviewed a pool of studies and selected one for replication that matched their own interest and expertise. Their data and results were shared online and reviewed and analyzed by other participating scientists for inclusion in the large Science study.

To help improve future research, the project analysis attempted to determine which kinds of studies fared the best, and why. They found that surprising results were the hardest to reproduce, and that the experience or expertise of the scientists who conducted the original experiments had little to do with successful replication.

The findings also offered some support for the oft-criticized statistical tool known as the P value , which measures whether a result is significant or due to chance. A higher value means a result is most likely a fluke, while a lower value means the result is statistically significant.

The project analysis showed that a low P value was fairly predictive of which psychology studies could be replicated. Twenty of the 32 original studies with a P value of less than 0.001 could be replicated, for example, while just 2 of the 11 papers with a value greater than 0.04 were successfully replicated.

But Christopherson suspects that most of his co-authors would not want the study to be taken as a ringing endorsement of P values, because they recognize the tool's limitations. And at least one P value problem was highlighted in the research: The original studies had relatively little variability in P value, because most journals have established a cutoff of 0.05 for publication. The trouble is that value can be reached by being selective about data sets , which means scientists looking to replicate a result should also carefully consider the methods and the data used in the original study.

It's also not yet clear whether psychology might be a particularly difficult field for reproducibility—a similar study is currently underway on cancer biology research. In the meantime, Christopherson hopes that the massive effort will spur more such double-checks and revisitations of past research to aid the scientific process.

“Getting it right means regularly revisiting past assumptions and past results and finding new ways to test them. The only way science is successful and credible is if it is self-critical,” he notes. 

Unfortunately there are disincentives to pursuing this kind of research, he says: “To get hired and promoted in academia, you must publish original research, so direct replications are rarer. I hope going forward that the universities and funding agencies responsible for incentivizing this research—and the media outlets covering them—will realize that they've been part of the problem, and that devaluing replication in this way has created a less stable literature than we'd like.”

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Brian Handwerk | READ MORE

Brian Handwerk is a science correspondent based in Amherst, New Hampshire.

• Future Perfect

Science has been in a “replication crisis” for a decade. Have we learned anything?

Bad papers are still published. But some other things might be getting better.

by Kelsey Piper

Much ink has been spilled over the “replication crisis” in the last decade and a half, including here at Vox . Researchers have discovered, over and over, that lots of findings in fields like psychology, sociology, medicine, and economics don’t hold up when other researchers try to replicate them.

This conversation was fueled in part by John Ioannidis’s 2005 article “ Why Most Published Research Findings Are False” and by the controversy around a 2011 paper that used then-standard statistical methods to find that people have precognition .But since then, many researchers have explored the replication crisis from different angles. Why are research findings so often unreliable? Is the problem just that we test for “statistical significance” — the likelihood that similarly strong results could have occurred by chance — in a nuance-free way? Is it that null results (that is, when a study finds no detectable effects) are ignored while positive ones make it into journals?

A recent write-up by Alvaro de Menard, a participant in the Defense Advanced Research Project’s Agency’s (DARPA) replication markets project (more on this below), makes the case for a more depressing view: The processes that lead to unreliable research findings are routine, well understood, predictable, and in principle pretty easy to avoid. And yet, he argues, we’re still not improving the quality and rigor of social science research.

While other researchersI spoke with pushed back on parts of Menard’s pessimistic take, they do agree on something: a decade of talking about the replication crisis hasn’t translated into a scientific process that’s much less vulnerable to it. Bad science is still frequently published, including in top journals — and that needs to change.

Most papers fail to replicate for totally predictable reasons

Let’s take a step back and explain what people mean when they refer to the “replication crisis” in scientific research.

When research papers are published, they describe their methodology, so other researchers can copy it (or vary it) and build on the original research. When another research team tries to conduct a study based on the original to see if they find the same result, that’s an attempted replication. (Often the focus is not just on doing the exact same thing, but approaching the same question with a larger sample and preregistered design.)If they find the same result, that’s a successful replication, and evidence that the original researchers were on to something. But when the attempted replication finds different or no results, that often suggests that the original research finding was spurious.

In an attempt to test just how rigorous scientific research is, some researchers have undertaken the task of replicating research that’s been published in a whole range of fields. And as more and more of those attempted replications have come back, the results have been striking — it is not uncommon to find that many, many published studies cannot be replicated.

One 2015 attempt to reproduce 100 psychology studies was able to replicate only 39 of them. A big international effort in 2018 to reproduce prominent studies found that 14 of the 28 replicated, and an attempt to replicate studies from top journals Nature and Science found that 13 of the 21 results looked at could be reproduced.

The replication crisis has led a few researchers to ask: Is there a way to guess if a paper will replicate? A growing body of research has found that guessing which papers will hold up and which won’t is often just a matter of looking at the same simple, straightforward factors.

A 2019paper by Adam Altmejd, Anna Dreber, and others identifies some simple factors that are highly predictive: Did the study have a reasonable sample size? Did the researchers squeeze out a result barely below the significance threshold of p = 0.05? (A paper can often claim a “significant” result if this “p”threshold is met, and many use various statistical tricks to push their paper across that line.) Did the study find an effect across the whole study population, or an “interaction effect” (such as an effect only in a smaller segment of the population) that is much less likely to replicate?

Menard argues that the problem is not so complicated.“Predicting replication is easy,” he said. “There’s no need for a deep dive into the statistical methodology or a rigorous examination of the data, no need to scrutinize esoteric theories for subtle errors — these papers have obvious, surface-level problems.”

A 2018 study published in Nature had scientists place bets on which of a pool of social science studies would replicate. They found that the predictions by scientists in this betting market were highly accurate at estimating which papers would replicate.

“These results suggest something systematic about papers that fail to replicate,” study co-author Anna Dreber argued after the study was released.

Additional research has established that you don’t even need to poll experts in a field to guess which of its studies will hold up to scrutiny. A study published in August had participants read psychology papers and predict whether they would replicate. “Laypeople without a professional background in the social sciences are able to predict the replicability of social-science studies with above-chance accuracy,” the study concluded, “on the basis of nothing more than simple verbal study descriptions.”

The laypeople were not as accurate in their predictions as the scientists in the Nature study, but the fact they were still able to predict many failed replications suggests that many of them have flaws that even a layperson can notice.

Bad science can still be published in prestigious journals and be widely cited

Publication of a peer-reviewed paper is not the final step of the scientific process. After a paper is published, other research might cite it — spreading any misconceptions or errors in the original paper. But research has established that scientists have good instincts for whether a paper will replicate or not. So, do scientists avoid citing papers that are unlikely to replicate?

This striking chart from a 2020 study by Yang Yang, Wu Youyou, and Brian Uzzi at Northwestern University illustrates their finding that actually, there is no correlation at all between whether a study will replicate and how often it is cited. “Failed papers circulate through the literature as quickly as replicating papers,” they argue.

Looking at a sample of studies from 2009 to 2017 that have since been subject to attempted replications, the researchers find that studies have about the same number of citations regardless of whether they replicated.

If scientists are pretty good at predicting whether a paper replicates, how can it be the case that they are as likely to cite a bad paper as a good one? Menard theorizes that many scientists don’t thoroughly check — or even read — papers once published, expecting that if they’re peer-reviewed, they’re fine. Bad papers are published by a peer-review process that is not adequate to catch them — and once they’re published, they are not penalized for being bad papers.

The debate over whether we’re making any progress

Here at Vox, we’ve written about how the replication crisis can guide us to do better science . And yet blatantly shoddy work is still being published in peer-reviewed journals despite errors that a layperson can see.

In many cases, journals effectively aren’t held accountable for bad papers — many, like The Lancet , have retained their prestige even after a long string of embarrassing public incidents where they published research that turned out fraudulent or nonsensical. (The Lancet said recently that, after a study on Covid-19 and hydroxychloroquine this spring was retracted after questions were raised about the data source, the journal would change its data-sharing practices. )

Even outright frauds often take a very long time to be repudiated, with some universities and journals dragging their feet and declining to investigate widespread misconduct .

That’s discouraging and infuriating. It suggests that the replication crisis isn’t one specific methodological reevaluation, but a symptom of a scientific system that needs rethinking on many levels. We can’t just teach scientists how to write better papers. We also need to change the fact that those better papers aren’t cited more often than bad papers; that bad papers are almost never retracted even when their errors are visible to lay readers; and that there are no consequences for bad research.

In some ways, the culture of academia actively selects for bad research. Pressure to publish lots of papers favors those who can put them together quickly — and one way to be quick is to be willing to cut corners. “Over time, the most successful people will be those who can best exploit the system,” Paul Smaldino, a cognitive science professor at the University of California Merced, told my colleague Brian Resnick.

So we have a system whose incentives keep pushing bad research even as we understand more about what makes for good research.

The world needs more wonder

The Unexplainable newsletter guides you through the most fascinating, unanswered questions in science — and the mind-bending ways scientists are trying to answer them. Sign up today .

Researchers working on the replication crisis are more divided, though, on the question of whether the last decade of work on the replication crisis has left us better equipped to fight these problems — or left us in the same place where we started.

“The future is bright,” concludes Altmejd and Dreber’s 2019 paper about how to predict replications. “There will be rapid accumulation of more replication data, more outlets for publishing replications, new statistical techniques, and—most importantly—enthusiasm for improving replicability among funding agencies, scientists, and journals. An exciting replicability ‘upgrade’ in science, while perhaps overdue, is taking place.”

Menard, by contrast, argues that this optimism has not been borne out — none of our improved understanding of the replication crisis leads to more papers being published that actually replicate. The project that he’s a part of — an effort to design a better model to predict which papers replicate run by DARPA in the Defense Department — has not seen papers grow any more likely to replicate over time .

“I frequently encounter the notion that after the replication crisis hit there was some sort of great improvement in the social sciences, that people wouldn’t even dream of publishing studies based on 23 undergraduates any more ... In reality there has been no discernible improvement,” he writes.

Researchers who are more optimistic point to other metrics of progress. It’s true that papers that fail replication are still extremely common, and that the peer-review process hasn’t improved in a way that catches these errors. But other elements of the error-correction process are getting better.

“Journals now retract about 1,500 articles annually — a nearly 40-fold increase over 2000, and a dramatic change even if you account for the roughly doubling or tripling of papers published per year,” Ivan Oransky at Retraction Watch argues. “Journals have improved,” reporting more details on retracted papers and improving their process for retractions.

Other changes in common scientific practices seem to be helping too. For example, preregistrations — announcing how you’ll conduct your analysis before you do the study — lead to more null results being published .

“I don’t think the influence [of public conversations about the replication crisis on scientific practice] has been zero,” statistician Andrew Gelman at Columbia University told me. “This crisis has influenced my own research practices, and I assume it’s influenced many others as well. And it’s my general impression that journals such as Psychological Science and PNAS don’t publish as much junk as they used to.”

There’s some reassurance in that. But until those improvements translate to a higher percentage of papers replicating and a difference in citations for good papers versus bad papers, it’s a small victory. And it’s a small victory that has been hard-won. After tons of resources spent demonstrating the scope of the problem, fighting for more retractions, teaching better statistical methods, and trying to drag fraud into the open, papers still don’t replicate asmuch as researcherswould hope,and bad papers are still widely cited — suggesting a big part of the problem still hasn’t been touched.

We need a more sophisticated understanding of the replication crisis, not as a moment of realization after which we were able to move forward with higher standards, but as an ongoing rot in the scientific process that a decade of work hasn’t quitefixed.

Our scientific institutions are valuable, as are the tools they’ve built to help us understand the world. There’s no cause for hopelessness here, even if some frustration is thoroughly justified. Science needs saving, sure — but science is very much worth saving.

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These chemists cracked the code to long-lasting roman concrete.

Calcium-rich rocks embedded in the material can heal cracks, experiments show

Built from concrete around 126 A.D., the Pantheon in Rome still stands, including its soaring dome (shown).

Stephen Knowles Photography/Moment/Getty Images Plus

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By Carolyn Gramling

January 17, 2023 at 9:00 am

MIT chemist Admir Masic really hoped his experiment wouldn’t explode.

Masic and his colleagues were trying to re-create an ancient Roman technique for making concrete, a mix of cement, gravel, sand and water. The researchers suspected that the key was a process called “hot mixing,” in which dry granules of calcium oxide, also called quicklime, are mixed with volcanic ash to make the cement. Then water is added.

Hot mixing, they thought, would ultimately produce a cement that wasn’t completely smooth and mixed, but instead contained small calcium-rich rocks. Those little rocks, ubiquitous in the walls of the Romans’ concrete buildings, might be the key to why those structures have withstood the ravages of time.

That’s not how modern cement is made. The reaction of quicklime with water is highly exothermic, meaning that it can produce a lot of heat — and possibly an explosion.

“Everyone would say, ‘You are crazy,’” Masic says.

But no big bang happened. Instead, the reaction produced only heat, a damp sigh of water vapor — and a Romans-like cement mixture bearing small white calcium-rich rocks.

Researchers have been trying for decades to re-create the Roman recipe for concrete longevity — but with little success. The idea that hot mixing was the key was an educated guess.

Masic and colleagues had pored over texts by Roman architect Vitruvius and historian Pliny, which offered some clues as to how to proceed. These texts cited, for example, strict specifications for the raw materials, such as that the limestone that is the source of the quicklime must be very pure, and that mixing quicklime with hot ash and then adding water could produce a lot of heat.

The rocks were not mentioned, but the team had a feeling they were important.

“In every sample we have seen of ancient Roman concrete, you can find these white inclusions,” bits of rock embedded in the walls. For many years, Masic says, the origin of those inclusions was unclear — researchers suspected incomplete mixing of the cement, perhaps. But these are the highly organized Romans we’re talking about. How likely is it that “every operator [was] not mixing properly and every single [building] has a flaw?”

What if, the team suggested, these inclusions in the cement were actually a feature, not a bug? The researchers’ chemical analyses of such rocks embedded in the walls at the archaeological site of Privernum in Italy indicated that the inclusions were very calcium-rich.

That suggested the tantalizing possibility that these rocks might be helping the buildings heal themselves from cracks due to weathering or even an earthquake. A ready supply of calcium was already on hand: It would dissolve, seep into the cracks and re-crystallize. Voila! Scar healed.

But could the team observe this in action? Step one was to re-create the rocks via hot mixing and hope nothing exploded. Step two: Test the Roman-inspired cement. The team created concrete with and without the hot mixing process and tested them side by side. Each block of concrete was broken in half, the pieces placed a small distance apart. Then water was trickled through the crack to see how long it took before the seepage stopped.

“The results were stunning,” Masic says. The blocks incorporating hot mixed cement healed within two to three weeks. The concrete produced without hot mixed cement never healed at all , the team reports January 6 in Science Advances .

Cracking the recipe could be a boon to the planet. The Pantheon and its soaring, detailed concrete dome have stood nearly 2,000 years , for instance, while modern concrete structures have a lifespan of perhaps 150 years, and that’s a best case scenario ( SN: 2/10/12 ). And the Romans didn’t have steel reinforcement bars shoring up their structures.

More frequent replacements of concrete structures means more greenhouse gas emissions. Concrete manufacturing is a huge source of carbon dioxide to the atmosphere, so longer-lasting versions could reduce that carbon footprint. “We make 4 gigatons per year of this material,” Masic says. That manufacture produces as much as 1 metric ton of CO 2 per metric ton of produced concrete, currently amounting to about 8 percent of annual global CO 2 emissions.

Still, Masic says, the concrete industry is resistant to change. For one thing, there are concerns about introducing new chemistry into a tried-and-true mixture with well-known mechanical properties. But “the key bottleneck in the industry is the cost,” he says. Concrete is cheap, and companies don’t want to price themselves out of competition.

The researchers hope that reintroducing this technique that has stood the test of time, and that could involve little added cost to manufacture, could answer both these concerns. In fact, they’re banking on it: Masic and several of his colleagues have created a startup they call DMAT that is currently seeking seed money to begin to commercially produce the Roman-inspired hot-mixed concrete. “It’s very appealing simply because it’s a thousands-of-years-old material.”

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Science Is Full of Errors. Bounty Hunters Are Here to Find Them

In 2010, two famous economists, Carmen Reinhart and Kenneth Rogoff, released a paper confirming what many fiscally conservative politicians had long suspected: that a country’s economic growth tanks if public debt rises above a certain percentage of GDP. The paper fell on the receptive ears of the UK’s soon-to-be chancellor, George Osborne, who cited it multiple times in a speech setting out what would become the political playbook of the austerity era: slash public services in order to pay down the national debt.

There was just one problem with Reinhart and Rogoff’s paper. They’d inadvertently missed five countries out of their analysis: running the numbers on just 15 countries instead of the 20 they thought they’d selected in their spreadsheet. When some lesser-known economists adjusted for this error, and a few other irregularities, the most attention-grabbing part of the results disappeared. The relationship between debt and GDP was still there, but the effects of high debt were more subtle than the drastic cliff-edge alluded to in Osborne’s speech.

Scientists—like the rest of us—are not immune to errors. “It’s clear that errors are everywhere, and a small portion of these errors will change the conclusions of papers,” says Malte Elson, a professor at the University of Bern in Switzerland who studies, among other things, research methods. The issue is that there aren’t many people who are looking for these errors. Reinhart and Rogoff’s mistakes were only discovered in 2013 by an economics student whose professors had asked his class to try to replicate the findings in prominent economics papers.

With his fellow meta-science researchers Ruben Arslan and Ian Hussey, Elson has set up a way to systematically find errors in scientific research. The project—called ERROR —is modeled on bug bounties in the software industry, where hackers are rewarded for finding errors in code. In Elson’s project, researchers are paid to trawl papers for possible errors and awarded bonuses for every verified mistake they discover.

The idea came from a discussion between Elson and Arslan, who encourages scientists to find errors in his own work by offering to buy them a beer if they identify a typo (capped at three per paper) and €400 ($430) for an error that changes the paper’s main conclusion. “We were both aware of papers in our respective fields that were totally flawed because of provable errors, but it was extremely difficult to correct the record,” says Elson. All these public errors could pose a big problem, Elson reasoned. If a PhD researcher spent her degree pursuing a result that turned out to be an error, that could amount to tens of thousands of wasted dollars.

Error-checking isn’t a standard part of publishing scientific papers, says Hussey, a meta-science researcher at Elson’s lab in Bern. When a paper is accepted by a scientific journal—such as Nature or Science –it is sent to a few experts in the field who offer their opinions on whether the paper is high-quality, logically sound, and makes a valuable contribution to the field. These peer-reviewers, however, typically don’t check for errors and in most cases won’t have access to the raw data or code that they’d need to root out mistakes.

The end result is that published science is littered with all kinds of very human errors—like copying the wrong value into a form, failing to squash a coding bug, or missing rows in a spreadsheet. The ERROR project pairs authors of influential scientific papers with reviewers who go through their work looking for errors. Reviewers get paid up to 1,000 Swiss francs ($1,131) to review a paper and earn bonuses for identifying minor, moderate, and major errors. The original authors are also paid for submitting their paper. ERROR has 250,000 Swiss francs from the University of Bern to pay out over four years, which should be enough for about 100 papers.

Jan Wessel, a cognitive neuroscientist at the University of Iowa, was the first scientist to have his work checked by ERROR . Elson already knew Wessel, and asked the researcher whether he’d like to take part in the project. Wessel agreed, on the proviso that he submitted a paper where he was the lone author. If they found a major error, Wessel wanted it to be clear that it was his mistake alone, and not risk jeopardizing the career of a colleague or former student.

Wessel offered a paper he’d published in 2018 and was paired with Stanford neuroscientist Russ Poldrack, who checked the paper for errors. Wessel’s paper was about a common test used in neuroscience to test impulsivity and inhibition, and involved taking data from lots of other published studies to see how different versions of that test compare. In his review of Wessel’s study, Poldrack found that the neuroscientist had occasionally made mistakes when he extracted the data from those preexisting studies. The errors weren’t enough to skew the results of the paper, but Wessel was still surprised at just how many there were.

“I was shocked at the amount of errors that Russ found,” says Wessel. Poldrack only sampled a small subset of the 241 papers covered in Wessel’s paper, so the neuroscientist decided to go back and find the true error rate. Wessel asked his lab colleagues to go back through all the remaining papers and check for instances where the figure in an original paper didn’t match the one that Wessel had put in his work. They found that for one variable, Wessel had recorded the incorrect value about 9 percent of the time.

What was even more interesting were the mistakes that Wessel’s error-hunting researchers made. Even though they knew they were looking out for errors, Wessel’s colleagues made errors at an ever greater rate—nearly 13 percent of the time. Like Wessel, they copied down the wrong number or misread a value in a paper. Wessel was so intrigued by this that he ran an analysis to see how likely it was that two people would make the exact same mistake on any one of the papers they examined. He discovered there was a more than 50 percent chance that would happen at some point across the 241 papers.

For meta-science researchers, none of this is surprising. If you look hard enough, you’ll start to find errors everywhere. As more researchers have started to work with very large datasets and complex code, the potential for errors has increased, says Poldrack. One potential issue is that if a bug in some code leads to a particularly interesting scientific result—the kind that could turn into a great research paper—there is no real incentive for scientists to squash that bug. The only reward for their diligence would be scrapping the research. No bug, no paper.

Changing the culture around scientific error could make it less likely for mistakes to end up in published work. Surgeons dissect their mistakes in morbidity and mortality meetings, which are supposed to be a judgment-free space where doctors figure out how to stop the same situation happening again. The same is true of plane crash investigations. The Convention on International Civil Aviation states that the purpose of investigations is not to apportion blame, but to figure out how to prevent similar accidents in the future.

Error-checking needs to be rewarded, says Brian Nosek, executive director of the nonprofit Center for Open Science (COS) and a member of the ERROR advisory board. “It could be something that is a career-enhancing prospect.” The COS is currently partnering with ERROR as part of a trial called Lifecycle Journals that is aimed at making scientific publishing more transparent and rigorous.

Even the most assiduous error-hunters are limited by their access to data. The errors in the Reinhart and Rogoff paper were discovered only after the economists shared their working spreadsheet with curious researchers. Elson is targeting authors of influential psychology papers, but they’re not obliged to take part. Only between a quarter and a third of researchers he emails actually reply, estimates Elson. It could be that scientists who suspect their work is full of errors simply choose not to expose themselves to that kind of scrutiny, skewing the results of the project.

Elson and Hussey know their project is open to these kinds of biases. They see it as more of a work-in-progress, an example of how error-correction might be incorporated into the scientific process. Elson says that the approach might be of interest to journals, universities, and particularly funders, who are keen to see that the work they’re paying for has the impact they hope.

“My hope for this is that it goes from something that was unimaginable until it happened, and then it was unthinkable not to do it,” says Hussey. “You have to give people the permission, and incentive, to think in the first place that errors might exist.”

Updated 6-21-2024 3:00 pm ET: The spelling of Ruben Arslan’s name was corrected.

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Global trends in climate change litigation: 2024 snapshot

This report provides a numerical analysis of how many climate change litigation cases were filed in 2023, where and by whom, and a qualitative assessment of trends and themes in the types of cases filed. It is the sixth report in the series, produced by the Grantham Research Institute in partnership with the Sabin Center for Climate Change Law and drawing on the Sabin Center’s Climate Change Litigation Databases . Each report provides a synthesis of the latest research and developments in the climate change litigation field.

Key messages

• At least 230 new climate cases were filed in 2023. Many of these are seeking to hold governments and companies accountable for climate action. However, the number of cases expanded less rapidly last year than previously, which may suggest a consolidation and concentration of strategic litigation efforts in areas anticipated to have high impact.
• Climate cases have continued to spread to new countries, with cases filed for the first time in Panama and Portugal in 2023.
• 2023 was an important year for international climate change litigation, with major international courts and tribunals being asked to rule and advise on climate change. Just 5% of climate cases have been brought before international courts, but many of these cases have significant potential to influence domestic proceedings.
• There were significant successes in ‘government framework’ cases in 2023; these challenge the ambition or implementation of a government’s overall climate policy response. The European Court of Human Rights’ decision in April 2024 in the case of KlimaSeniorinnen and ors. v. Switzerland is likely to lead to the filing of further cases.
• The number of cases concerning ‘climate-washing’ has grown in recent years. 47 such cases were filed in 2023, bringing the recorded total to more than 140. These cases have met with significant success, with more than 70% of completed cases decided in favour of the claimants.
• There were important developments in ‘polluter pays’ cases: more than 30 cases worldwide are currently seeking to hold companies accountable for climate-related harm allegedly caused by their contributions to greenhouse gas emissions.
• Litigants continue to file new ‘corporate framework’ cases, which seek to ensure companies align their group-level policies and governance processes with climate goals. The New Zealand Supreme Court allowed one such case to proceed, although cases filed elsewhere have been dismissed. The landmark case of Milieudefensie v. Shell is under appeal.
• In this year’s analysis a new category of ‘transition risk’ cases was introduced, which includes cases filed against corporate directors and officers for their management of climate risks. Shareholders of Enea approved a decision to bring such a case against former directors for planned investments in a new coal power plant in Poland.
• ESG backlash cases, which challenge the incorporation of climate risk into financial decision-making.
• Strategic litigation against public participation (SLAPP) suits against NGOs and shareholder activists that seek to deter them from pursuing climate agendas.
• Just transition cases, which challenge the distributional impacts of climate policy or the processes by which policies were developed, normally on human rights grounds.
• Green v. green cases, which concern potential trade-offs between climate and biodiversity or other environmental aims.

Recent previous reports in the series:

2023 snapshot

2022 snapshot

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Hidden Brain

Scientific findings often fail to be replicated, researchers say.

Shankar Vedantam

A massive effort to test the validity of 100 psychology experiments finds that more than 50 percent of the studies fail to replicate. This is based on a new study published in the journal "Science."

Copyright © 2015 NPR. All rights reserved. Visit our website terms of use and permissions pages at www.npr.org for further information.

NPR transcripts are created on a rush deadline by an NPR contractor. This text may not be in its final form and may be updated or revised in the future. Accuracy and availability may vary. The authoritative record of NPR’s programming is the audio record.

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Biden’s Family Tells Him to Keep Fighting as They Huddle at Camp David

President Biden is trying to figure out how to tamp down Democratic anxiety after last week’s disastrous debate performance.

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By Katie Rogers and Peter Baker

Katie Rogers and Peter Baker cover the White House.

President Biden’s family is urging him to stay in the race and keep fighting despite last week’s disastrous debate performance, even as some members of his clan privately expressed exasperation at how he was prepared for the event by his staff, people close to the situation said on Sunday.

Mr. Biden huddled with his wife, children and grandchildren at Camp David while he tried to figure out how to tamp down Democratic anxiety. While his relatives were acutely aware of how poorly he did against former President Donald J. Trump, they argued that he could still show the country that he remains capable of serving for another four years.

Mr. Biden has been soliciting ideas from advisers about how to proceed, and his staff has been discussing whether he should hold a news conference or sit for interviews to defend himself and change the narrative, but nothing has been decided yet. The campaign scheduled what could be a critical call with its national finance committee for Monday to calm nerves and take temperatures.

One of the strongest voices imploring Mr. Biden to resist pressure to drop out was his son Hunter Biden, whom the president has long leaned on for advice, said one of the people informed about the discussions, who, like others, spoke on condition of anonymity to share internal deliberations. Hunter Biden wants Americans to see the version of his father that he knows — scrappy and in command of the facts — rather than the stumbling, aging president Americans saw on Thursday night.

Other family members were trying to figure out how they could be helpful. At least one of the president’s grandchildren has expressed interest in getting more involved with the campaign, perhaps by talking with influencers on social media, according to the informed person.

One of the people informed about the situation said “the entire family is united” and added flatly that the president was not getting out of the race and had not discussed doing so. “You get up and keep fighting,” the person said.

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American Airlines Bets on Hydrogen-Electric Engines Despite Limits

Meghna Maharishi , Skift

July 2nd, 2024 at 12:45 PM EDT

Airlines have been making larger investments in hydrogen-electric startups as they look for ways to become more sustainable. But it’s unclear if such engines can be used on a wide scale.

Meghna Maharishi

American Airlines announced Tuesday that it entered a conditional purchase agreement for 100 hydrogen-electric engines with startup ZeroAvia to fuel its regional jets. 

ZeroAvia has been developing hydrogen-electric engines for commercial aircraft that can emit close to zero emissions, another potential way the airline industry has been eyeing to become more sustainable. 

“This announcement will help accelerate the development of technologies needed to power our industry and uphold our commitment to make American a sustainable airline so we can continue to deliver for customers for decades to come,” American CEO Robert Isom said in a statement.  American is not the only airline to make an investment in hydrogen-electric engines. For example, United Airlines and Alaska Airlines invested $35 million in ZeroAvia in 2021.

Growing Appeal but Many Barriers to Sustainability

Many airlines have been interested in the possibility of using hydrogen engines to make flying more sustainable but there have been some caveats. 

Universal Hydrogen, another startup that had successfully flown a hydrogen-powered aircraft in 2024, folded just days ago after going through $100 million of investor capital. 

The startup was labeled by Fast Company as one of the “most innovative companies of 2024.” Universal Hydrogen CEO, Mark Cousin, wrote to the board that the company had failed to secure enough financing to move forward, according to a report from The Seattle Times . 

Another major issue with hydrogen-electric engines is that they can only power smaller aircraft. When Universal Hydrogen flew the first regional jetliner powered by hydrogen-electric engines, it could only use one such engine due to safety issues. 

Since the technology isn’t yet developed for hydrogen-electric engines to power larger planes, most of the investment has been limited to regional ones instead. But even with regional jets, hydrogen-electric engines tend to take up more space than jet fuel, potentially leaving less room for passengers. 

ZeroAvia founder and CEO Val Miftakhov said the startup was on the path to serving larger airlines when referring to the deal with American. 

“The solutions that can serve the largest airlines are within reach, and the clean future of flight is coming,” he said in a statement. 

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This smiling robot face made of living skin is absolute nightmare fuel

Giving robots a human-like exterior has been the standard for years — centuries even. But giving them actual, living skin that can be manipulated into horrifying, slimy expressions? That’s new.

The new work, published in the journal Cell Reports Physical Science , is very much just an experiment. This will not be the face of your next smart home hub or vacuum.

But it may well be that the ingenious machinery produced by billions of years of evolution may be better in some situations than artificial skin (also very much in development) or simpler surfaces. This brings up several questions — many, in fact, but only one is really the topic of the paper, as is proper in scientific inquiry.

To wit: How would such a living tissue surface, whatever its advantages and disadvantages, attach to the mechanical foundation of a robot’s limb or “face”?

In humans and other animals, there is a network of ligaments that anchors the skin to underlying muscle and tissue. This works pretty well, I’ve found. And the researchers at the University of Tokyo and Harvard wanted to test whether they could create a version of this that let living skin both cling closely to an artificial substrate, and also be manipulated in various directions without tearing or unintended distortion.

How did their “dermis equivalent” turn out? I’ll let you be the judge:

Ah, nightmare fuel. But you can’t accuse it of being anything less than well-moisturized.

Of course it’s horrifying now, but it’s not intended to be realistic or beautiful — just to illustrate a potential method for attachment of living tissue to robotic undercarriage.

Yes, that is in fact exactly what a Terminator T-100 model has, but let’s not get ahead of ourselves. Skin-covered robots could do all kinds of useful stuff in addition to infiltrating the past to destroy humanity’s future.

Cultured skin, as they put it, can heal itself, carry biological sensors like our own to provide sensitive touch, and could also have benefits in medical or human interaction contexts.

But only if it can stay alive on there and also be moved around in the same ways our own skin is during everyday use. That’s part of what the paper is intended to show: a working method for attachment and manipulation that conceivably could be used on — or as — a face.

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2024 Common Law Honours Society Inductees

By Common Law

Communication, Faculty of Law

• The Honourable Bernadette Clement, Senator LLB ’88, LLL ‘87
• Yves Le Bouthillier, LLB ’84
• The Honourable Maria Linhares de Sousa, LLB ’76

Bernadette Clement LLB ’88, LLL ‘87 is a legal aid lawyer and politician. She was the first woman to be elected as mayor of Cornwall, Ontario, and the first Black woman to serve as a mayor in Ontario. Prior to this, she served three terms as a city councillor.

She was appointed to the Senate on June 22, 2021, representing Ontario. She continues to live in Cornwall, where she remains connected with her community.  

Senator Clement is proud of her complex intersectional identity: her francophone mother grew up in Manitoba and her centenarian anglophone father grew up in Trinidad. As a bilingual Canadian, Senator Clement is a proud advocate for this country’s linguistic plurality – French, English, and Indigenous language rights and revitalization.

A passionate speaker, Bernadette intervenes in committee study and Senate debate most often in defense of marginalized groups. She is also eager to connect youth and other Canadians with the Senate through social media, community events, and speaking engagements.

Senator Clement joined the Independent Senators Group after her appointment, and since December 2022, has served as Chamber Coordinator – which combines her interests in rules and procedure with her love of politics.

Bernadette holds degrees in Civil Law and Common Law from the University of Ottawa. In 1991, after being called to the Bar of Ontario, she moved to Cornwall and started her legal career with the non-profit  Roy McMurtry Legal Clinic, where she still works part-time. She worked as a lawyer, before serving as Deputy Director for 16 years, and Executive Director for four years.

Senator Clement continues to practice law, focusing on representing injured workers. She is an ardent advocate for marginalized groups and, over the course of her career, has volunteered with Maison Baldwin House, Kinsmen Community Residence, Cornwall and District Immigrant Services Agency, and Inspire Community Support Services.

Bernadette also taught Ethics and Legalities to health care students at St. Lawrence College from 2001 to 2005. She is a member of the Association des juristes d’expression française de l’Ontario and the Stormont, Dundas & Glengarry Law Association. She is a recipient of a Cornwall District and Labour Council award for outstanding service to injured workers and a Legal Aid Ontario GEM award for outstanding achievement. 

Professor Yves Le Bouthillier LLB ’84 joined the French Common Law Program (FCLP) in 1987, a few years after it was established.  His longstanding major contributions to the program have made him part of the foundation on which it has been built and has developed its distinct identity.    

An expert in several areas of law, both international and public, Professor Le Bouthillier has taught 16 different courses during his career. Along with Professor Delphine Nakache, he has co-edited reference works on citizenship law. He has held many leadership positions, both within and outside the Faculty. He was vice-dean of the FCLP on three separate occasions, as well as co-director of the secretariat of the International Union for Conservation of Nature (IUCN) Academy of Environmental Law for many years, along with Professor Jamie Benidickson. He was president of the Law Commission of Canada, a member of the Board of Governors of the Law Commission of Ontario and vice-president of the Canadian Council on International Law.  

From August 2000 to June 2002, Professor Le Bouthillier was scholar-in-residence in the Economic, Oceans and Environmental Law Division of the Department of Foreign Affairs and International Trade. In 2001, he was part of the negotiating team that received the Head of the Public Service Award for its contribution to the development and adoption of the Stockholm Convention on Persistent Organic Pollutants. Prior to that, from 1999 to 2000, he was responsible for human rights projects at the Agence de la Francophonie in Paris.  

In 2008, the Association des juristes d'expression française de l'Ontario named him to its Order of Merit for his contribution to the promotion and improvement of legal services in French in Ontario.  

The Honourable Maria Linhares de Sousa LLB ’76 was born in Portugal and immigrated to Canada with her family in 1954.  She completed her primary and secondary education in Toronto and obtained a BA and MA from the University of Toronto in history.  In 1973, she moved to Ottawa to pursue her legal studies at the Common Law Section of the University of Ottawa.  

After graduating cum laude in 1976, she articled for Bell, Baker, Oyen and Webber. Immediately following her call to the Bar in 1978, she served for one year as law clerk to the Chief Justice of the Supreme Court of Ontario, the Honourable Gregory Evans.

In 1979, Maria was appointed as a Family Law Commissioner and Official Referee for the Supreme Court of Ontario. She presided over family law references and exercised dispute resolution in the family law matters before the Court.

In 1989, Maria was appointed to the criminal division of the Ontario Provincial Court where she presided, in both official languages, over criminal matters and eventually, family and child protection matters when the Ontario Court of Justice was created, known as the Justice Heidi Levenson Polowin Course in Child Protection.

In 1999, when the Family Division of the Superior Court of Justice was established in Ottawa, Maria was appointed to that Division, presiding primarily over all areas of family law and child protection as well as criminal and civil matters, until her retirement in November 2019.

During her judicial career, Maria took a particular interest in judicial education and participated in, and led, many judicial education programs, both nationally and internationally.

In 2011-2012, during a sabbatical, she created and taught the first complete stand-alone child protection course to be offered at the Common Law Section, which continues to be taught today.

Since her retirement and following the pandemic, Maria has been trying to put a dent in the long list of books she planned to read but couldn’t because of work demands.  She has also taken courses at the University of Ottawa and St. Paul’s University in areas of personal interest such as ethics, philosophy, and theology.    She has also been involved in some volunteer work, acting for that last four years as the Safe Environment Coordinator for Notre Dame Cathedral of the Archdiocese of Ottawa-Cornwall and fundraising for such worthy causes as the Ottawa Mission through The Coldest Night of the Year, a winter family-friendly walk in support of local charities serving people experiencing hurt, hunger, and homelessness.

Maria says that having the leisure and capacity to pursue these interests since her retirement has been a blessing. 

Thank you to the 2024 Honours Society Selection Committee:  

• Kristen Boon, Susan & Perry Dellelce Dean
• Katie Black LLB ’09, 2017 Honour Society Inductee
• Alan D’Silva LLB ’87, 2015 Honour Society Inductee
• Philippe David LLB ’85
• Josephine Palumbo LLB ’91
• Mark Power LLB ’02
• Karen Restoule JD ’12, 2014 Honour Society Inductee)

Inductees will be formally honoured at a special event in the Fall.  

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June 24, 2024

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New research shows why you don't need to be perfect to get the job done

by Howard Hughes Medical Institute

When neuroscientists think about the strategy an animal might use to carry out a task—like finding food, hunting prey, or navigating a maze—they often propose a single model that lays out the best way for the animal to accomplish the job.

But in the real world, animals—and humans—may not use the optimal way, which can be resource-intensive. Instead, they use a strategy that's good enough to do the job but takes a lot less brain power.

In new research appearing in Science Advances , Janelia scientists set out to better understand the possible ways an animal could successfully solve a problem, beyond just the best strategy.

The work shows there is a huge number of ways an animal can accomplish a simple foraging task . It also lays out a theoretical framework for understanding these different strategies, how they relate to each other, and how they solve the same problem differently.

Some of these less-than-perfect options for accomplishing a task work nearly as well as the optimal strategy but with a lot less effort, the researchers found, freeing up animals to use precious resources to handle multiple tasks.

"As soon as you release yourself from being perfect, you would be surprised just how many ways there are to solve a problem," says Tzuhsuan Ma, a postdoc in the Hermundstad Lab, who led the research.

The new framework could help researchers start examining these "good enough" strategies, including why different individuals might adapt different strategies, how these strategies might work together, and how generalizable the strategies are to other tasks. That could help explain how the brain enables behavior in the real world.

"Many of these strategies are ones we would have never dreamed up as possible ways of solving this task, but they do work well, so it's entirely possible that animals could also be using them," says Janelia Group Leader Ann Hermundstad. "They give us a new vocabulary for understanding behavior."

Looking beyond perfection

The research began three years ago when Ma started wondering about the different strategies an animal could possibly use to accomplish a simple but common task: choosing between two options where the chance of being rewarded changes over time.

The researchers were interested in examining a group of strategies that fall between optimal and completely random solutions: "small programs" that are resource-limited but still get the job done. Each program specifies a different algorithm for guiding an animal's actions based on past observations, allowing it to serve as a model of animal behavior.

As it turns out, there are many such programs—about a quarter of a million. To make sense of these strategies, the researchers first looked at a handful of the top-performing ones. Surprisingly, they found they were essentially doing the same thing as the optimal strategy, despite using fewer resources.

"We were a little disappointed," Ma says. "We spent all this time searching for these small programs, and they all follow the same computation that the field already knew how to mathematically derive without all this effort."

But the researchers were motivated to keep looking—they had a strong intuition that there had to be programs out there that were good but different from the optimal strategy. Once they looked beyond the very best programs, they found what they were looking for: about 4,000 programs that fall into this "good enough" category. And more importantly, more than 90% of them did something new.

They could have stopped there, but a question from a fellow Janelian spurred them on: How could they figure out which strategy an animal was using?

The question prompted the team to dive deep into the behavior of individual programs and develop a systematic approach to thinking about the entire collection of strategies. They first developed a mathematical way to describe the programs' relationships to each other through a network that connected the different programs. Next, they looked at the behavior described by the strategies, devising an algorithm to reveal how one of these "good enough" programs could evolve from another.

They found that small changes to the optimal program can lead to big changes in behavior while still preserving performance. If some of these new behaviors are also useful in other tasks, it suggests that the same program could be good enough for solving a range of different problems.

"If you are thinking about an animal not being a specialist who is optimized to solve just one problem, but rather a generalist who solves many problems, this really is a new way to study that," Ma says.

The new work provides a framework for researchers to start thinking beyond single, optimal programs for animal behavior. Now, the team is focused on examining how generalizable the small programs are to other tasks, and designing new experiments to determine which program an animal might be using to carry out a task in real time. They are also working with other researchers at Janelia to test their theoretical framework .

"Ultimately, getting a strong grasp on an animal's behavior is an essential prerequisite to understanding how the brain solves different types of problems, including some that our best artificial systems only solve inefficiently, if at all," Hermundstad says. "The key challenge is that animals might be using very different strategies than we might initially assume, and this work is helping us uncover that space of possibilities."

Journal information: Science Advances

Provided by Howard Hughes Medical Institute

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