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“Following a thorough review of today’s mission, we look forward to flying our next crewed flight soon,” launch commentator Erika Wagner said as she wrapped up Blue Origin’s streaming-video coverage.

Her fellow commentator, Eddie Seyffert, said everything looked good during the 10-minute-long flight. “I would call this the best day at work for me,” he said.

The flight from Blue Origin’s Launch Site One in West Texas followed the profile that the New Shepard program has used for 23 previous missions over the past nine years — including six crewed flights. Liftoff came at 10:42 a.m. CT (8:42 a.m. PT), and the rocket booster sent the capsule toward the 100-kilometer (62-mile) line that marks the internationally accepted space boundary.

Capsule separation took place a little more than two minutes after launch. The reusable booster landed itself on a pad not far from where it was launched. Meanwhile, New Shepard’s capsule rose to a height of 65.8 miles (106 kilometers) above ground level, and then descended to its own parachute-assisted landing in the Texas desert.

This mission, known as NS24, carried 33 science payloads in the crew capsule, providing a few minutes of zero gravity to study the effects on samples and hardware. It was essentially a do-over for a flight in September 2022 that ended prematurely due to a malfunction of the New Shepard booster’s hydrogen-fueled rocket engine.

As was the case today, no crew members were aboard New Shepard for that NS23 mission. No injuries were reported on the ground, and New Shepard’s escape system worked as designed to push the capsule away from the booster for a safe landing. Nevertheless, the anomaly led to the suspension of Blue Origin launches and a yearlong investigation overseen by the Federal Aviation Administration.

This September, the FAA closed the investigation and required Blue Origin to take 21 corrective actions — including a redesign of the booster’s engine and nozzle as well as changes in procedures. Blue Origin began making the fixes even before the FAA issued the investigation’s findings, setting the stage for NS24.

An initial launch attempt on Monday was scrubbed due to a ground system issue that needed troubleshooting. In contrast, no major issues were reported today — although a couple of holds added a few minutes to the countdown.

More than half of the science payloads that flew on NS24 were developed with support from NASA. Others were built by schools, universities and other education-oriented organizations. Among the reflown NS23 payloads were an experiment from Honeybee Robotics, a subsidiary of Blue Origin, which studied the strength of planetary soils under different gravity conditions; and a fuel cell that’s being tested by Infinity Fuel Cells for space power applications.

The New Shepard capsule also carried 38,000 postcards that have been submitted — on paper and online — by students through a program organized by the Club for the Future, Blue Origin’s educational nonprofit group.

“A special thank you to all of our customers who flew important science today and the students who contributed postcards to advance our future of living and working in space for the benefit of Earth,” Phil Joyce, senior vice president for New Shepard, said in a news release. “Demand for New Shepard flights continues to grow and we’re looking forward to increasing our flight cadence in 2024.”

Blue Origin didn’t immediately announce a schedule for future crewed flights, but the company has been making extensive preparations to resume flying people — and it’s seeking to attract new customers. For example, an elevator was recently added to New Shepard’s launch tower, supplementing seven flights of stairs.

“We added the elevator to make New Shepard more accessible to people with disabilities, and more people in general,” Blue Origin’s Wagner explained. Seyffert said the change was the result of discussions conducted with New Hawking, a business resource group that deals with disability issues (and apparently takes its name from Stephen Hawking, the wheelchair-using physicist who died in 2018).

Since mid-2021, 31 people — including notables such as Star Trek actor William Shatner and Jeff Bezos himself — have taken suborbital space trips without incident. Bezos’ fiancée, Lauren Sanchez, has said that she hopes to lead an all-woman space mission early next year.

New Shepard’s return to flight comes amid an organizational handoff at Blue Origin, with veteran aerospace executive Bob Smith passing the CEO reins to former Amazon executive Dave Limp. Bezos has said Limp will help him accelerate Blue Origin’s progress in the year ahead — especially on development of the company’s orbital-class New Glenn rocket.

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Jimi Olaghere used to end up in the emergency room so often that the hospital reserved a bed for him. Sickle cell disease dominated his life. A genetic defect he was born with meant that instead of having flexible, round red blood cells like most people do, his were sticky and crescent-shaped. The cells clumped together, blocking blood flow and unleashing excruciating bouts of pain. He took painkillers to manage the episodes, but the drugs didn’t always help.

“It was a circus, bouncing from specialist to specialist and constantly desecrating my body with endless amounts of prescription pills, all in the hopes of finding a sliver of what it feels like to be alive,” Olaghere told an advisory committee to the US Food and Drug Administration in October.

When the opportunity came to participate in a clinical trial that would use Crispr gene editing in an attempt to permanently fix his disease, he didn’t hesitate. Now, more than three years after getting the one-time treatment, Olaghere is virtually pain-free. “My quality of life has soared to new heights,” he said during his testimony.

The therapy Olaghere received was approved in the UK on November 16, in the US on December 8, and in Europe on December 15 under the brand name Casgevy. It is the first publicly available medical treatment in the world to use Crispr technology. More are in the pipeline. The technology is poised to radically change the lives of patients with sickle cell—and eventually, many others.

“It’s the start of the era of Crispr medicine,” says Jennifer Doudna, a biochemist at the University of California, Berkeley, who shared the Nobel Prize in Chemistry in 2020 for her role in the development of the gene-editing technique. “I think it suggests that we’re on the edge of real transformation in medicine,” she says of Casgevy’s approval.

Doudna, along with Emmanuelle Charpentier, now of the Max Planck Unit for the Science of Pathogens in Germany, first described Crispr as a genome-editing system in the journal Science in June 2012. They extracted and simplified Crispr from the immune system of bacteria, which fight off attacking viruses by cutting up the invaders’ DNA.

The discovery changed science forever. Genome-editing tools such as zinc finger nucleases and TALENs (transcription activator-like effector nucleases) already existed, but Crispr proved to be far more efficient, not to mention easier and cheaper to use. Crispr can be used to knock out genes to investigate their function, but its real power lies in being able to change an organism’s DNA. Scientists have long imagined being able to correct defective genes to treat diseases at their source. Crispr offers a way to do that.

It took just over 11 years—lightning fast for drug-development timelines—for Crispr to move from a tool used in laboratories to a real therapy that could be prescribed to patients. “I’m very excited. I think this is an important milestone for the whole field,” says Feng Zhang, a biochemist at the Broad Institute of MIT and Harvard who, in January 2013, showed that it was possible to use Crispr to edit mouse and human cells in a dish.

Casgevy’s approval is proof that editing the code of life is not only possible, but also able to bring life-changing results for patients. But Crispr’s high sticker price and the complexities around administering it may limit its use for the foreseeable future. Casgevy will cost $2.2 million per patient in the US, and the therapy requires a lengthy hospital stay.

A Debilitating Disease

Sickle cell disease has been well understood for decades, making it a fitting first target for Crispr. Its cause, abnormal hemoglobin, was discovered in 1949 by chemist Linus Pauling. Hemoglobin is the protein in red blood cells that carries oxygen throughout the body. Pauling showed that hemoglobin has an altered chemical structure in people with sickle cell disease. It was the first time a disease was characterized at a molecular level.

In 1956, Vernon Ingram discovered that a single mutation in the HBB gene produces the abnormal hemoglobin. Everyone gets two copies of this gene, one from each parent. To have sickle cell disease, a person must inherit the mutated gene from both parents.

Abnormal hemoglobin alters the shape of red blood cells, turning them from discs to sickles. The misshapen cells stick together in vessels and cut off blood flow and oxygen, causing extreme pain. Sickled cells are also brittle and die more quickly than normal cells.

“The pain is far and away the worst part for patients,” says Alexis Thompson, a sickle cell expert and chief of the Division of Hematology at Children’s Hospital of Philadelphia. “They suffer from really debilitating pain.”

Over time, sickle cell damages organs and leads to early death. On average, patients with sickle cell disease in the US live to 52.6 years—more than two decades shorter than the rest of the population.

The first drug for sickle cell, hydroxyurea, wasn’t approved until 1998, and it was the only one on the market until 2017. Three more drugs have since become available to reduce pain crises, but they don’t help all patients.

The disease can be cured with a bone marrow transplant, which involves replacing a patient’s stem cells with healthy ones from a donor so that the patient can make normal red blood cells. But few get transplants, because they require a closely related donor and come with serious risks. After the procedure, the donor stem cells may attack the recipient’s body or fail to take over the role of producing new blood cells.

A Transformative Therapy

Casgevy, made by Crispr Therapeutics of Switzerland and Vertex Pharmaceuticals of Boston, doesn’t require a donor. It involves extracting a patient’s own stem cells from their bone marrow and editing them in a lab. The edited cells are then injected back into the patient. They travel to the bone marrow, where they take up residence and start producing healthy red blood cells.

Scientists don’t use Crispr to fix the mutated HBB gene directly. For all Crispr’s hype, it’s not good at replacing genes. But it is good at making targeted cuts in the genome. Casgevy targets a gene called BCL11A, which typically prevents the body from making a fetal version of hemoglobin. In the first several months of life, levels of fetal hemoglobin taper down and the body starts making adult hemoglobin instead. Making a cut in the gene releases the brakes, allowing cells to make the fetal type and override the abnormal adult kind.

In 1948, pediatrician Janet Watson noticed that children with sickle cell disease had normal blood cells as infants, but that the cells became sickled around six months. Scientists speculated that a fetal form of hemoglobin blocks the sickling process, but is turned off shortly after birth. They thought if they could figure out a way to switch on the production of fetal hemoglobin, they could override the mutation that causes sickle cell. The search took decades.

In the mid-2000s, research by Stuart Orkin’s lab at Boston Children’s Hospital found that switch: BCL11A. They first showed they could correct sickle cell disease in mice by knocking out the gene entirely. Then the group identified just a portion of the gene that could be inactivated and still turn on fetal hemoglobin—a safer approach, since genes often have many functions. In 2015, they showed that this stretch of DNA could be edited out with Crispr to boost fetal hemoglobin in mice and human cells.

Some people have a genetic condition in which they make fetal hemoglobin past infancy and are completely healthy. Crispr Therapeutics and Vertex used this insight to develop Casgevy. The companies launched a clinical trial in 2018. Of 31 patients who had multiple pain crises a year, 29 had none in the 12 months following treatment. “It is not an overstatement to say that gene therapy for this condition is transformational,” Thompson says.

For Olaghere, the treatment has given him the freedom to be a present father. And he’s now able to make long-term plans with his family, no longer worried about whether he’ll be stricken with another pain crisis. “Gene therapy has given me the ability to take full control of my life,” he told the FDA committee.

Who Will Get It?

Just how many patients will benefit from Casgevy remains to be seen. Sickle cell disease affects more than 100,000 people in the US, most of them of African and Caribbean descent. Adults and children 12 and older who experience recurrent pain crises are eligible to receive the therapy. Vertex says around 16,000 patients in the US and 2,000 patients in the UK may qualify.

But at $2.2 million, Casgevy is now one of the most expensive medicines in the world, and insurers have not yet said whether they’ll cover the cost of treatment. The Institute for Clinical and Economic Review, an independent nonprofit research institute in Boston, found that a price point of up to $2 million would be cost-effective considering the high lifetime costs of treating patients with severe sickle cell disease. In an email to WIRED, Heather Nichols, a spokesperson for Vertex, said the company launched a patient assistance program that connects patients and their caregivers to a care manager.

So far, only nine centers across the US are currently offering Casgevy, which may limit who gets access to it. Vertex says the number of participating sites will grow in the coming weeks and months.

And despite the promise of a pain-free future, the grueling process of getting Casgevy may be a deterrent for some.

Collecting stem cells from the blood can take hours, and multiple sessions may be needed to get enough cells to edit. After that is a harsh conditioning regimen. Patients must undergo chemotherapy to kill any lingering diseased cells and make room in the bone marrow for the newly edited ones. Chemotherapy can cause mouth sores, fatigue, hair loss, nausea, and other unpleasant side effects. It can also result in infertility. Vertex also plans to offer fertility support to commercially insured patients, but the benefit won’t extend to Medicaid recipients. In the US, freezing eggs and sperm can cost thousands of dollars, not to mention the cost of IVF.

Patients also need to be hospitalized for weeks while the edited cells make their way to the bone marrow and start making new blood cells. Olaghere spent a total of 17 weeks in the hospital to get Casgevy.

“I know there are going to be many patients who don’t go down this road because of fertility issues and the need to be in the hospital for a while,” says Sharl Azar, medical director of the Comprehensive Sickle Cell Disease Treatment Center at Massachusetts General Hospital, one of the initial centers to offer Casgevy. For those that do, he says resources such as housing, childcare, and food will be needed to help patients and their families. Nichols, the Vertex spokesperson, says the company will assist with travel and lodging and may help cover certain expenses such as hotels, transportation, and meals.

Sickle Cell and Beyond

Sickle cell may be the first disease to be treated with Crispr, but it won’t be the last. Researchers are setting the gene-editing tool against cancer, HIV, and other genetic diseases. But it can’t yet address every ailment.

For one, getting the Crispr system to the cells or organs you want to edit is still a challenge. By taking cells out of the body and editing them in the lab, Casgevy avoids this issue. But the approach is expensive, complex, and has limited uses. Another method uses an IV infusion to deliver Crispr in tiny bubbles called lipid nanoparticles that are taken up by the liver. But only some diseases can be treated this way. Ideally, Crispr would be given as an injection or even as a pill instead of a complicated cell transplant.

Newer forms of Crispr, including base editing, also promise to make more precise edits. With base editing, scientists can simply swap one DNA letter for another in order to correct a mutation or disable a gene. The first trial of a base-editing treatment is showing early hints that it may lower high cholesterol.

And Zhang, of the Broad Institute, recently used a search algorithm to discover hundreds of new Crispr systems hiding out in bacteria taken from breweries, Antarctic lakes, and even dog saliva. These new systems could be harnessed to edit human cells with even more accuracy.

Still, the long-term effects of Crispr remain unknown. Scientists hope gene editing is permanent, a one-and-done treatment. But they’ll have to follow patients for years to know for sure.

It’s why Azar is hesitant to call Crispr a cure. “We don't know what the long-term impacts are going to be,” he says. “We don't know what complication rates are going to look like, or whether this is going to have a mortality benefit or if this is going to truly stave off the life-threatening complications.”

Doudna is more optimistic. “I feel very excited about it. I think we have to be cautious, because it’s still the early days of Crispr, “ she told an audience at LiveWIRED in December. “But so far, it looks like people that receive this one-and-done treatment truly are cured of the effects of their disease.”

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You booked this doctor’s appointment weeks in advance. You took off work, endured the trip here, filled out paperwork while a cooking show blared from a TV on the wall, and now you’re finally in the inner sanctum, awkwardly perched on an exam table and staring at a jar of tongue depressors. Your doctor comes in, listens as you describe what’s been bothering you. She nods, a wrinkle of concern crossing her forehead. She asks a few follow-up questions. Then she says, “I’m going to prescribe you something that isn’t designed to treat these symptoms but may help you feel better. It’s a placebo.”

No doubt you’re confused. Placebos famously rely on deception: You, the patient, receive an inert substance that you believe to be active and are fooled into feeling better. The word placebo comes from the Latin placere, “to please” (as in “more to please than benefit the patient,” according to one 19th-century medical dictionary). How does your doctor expect you to be pleased, much less relieved of your symptoms, by a prescription for sugar pills? Is she a quack?

Fortunately, the answer is probably not. Many doctors—perhaps as many as 97 percent, according to a 2018 survey—prescribe placebos at some point in their careers. The American Medical Association green-lights placebo use as long as the patient is informed and consents; they need not be aware of when they’re getting a placebo, only that it may be among the treatments. (The Hippocratic oath says, “Do no harm” not “Tell the whole truth.”) A typical doctor might prescribe antibiotics even though the patient has a viral infection, or vitamin supplements even though there’s no deficiency. What’s different about your doctor is that she’s letting you in on the secret. She’s prescribing a so-called open-label placebo.

OLPs have become a source of fascination, and some consternation, in the medical community in recent years. They seem to work in some cases, but no one can explain why. A 2021 paper in Scientific Reports found that “OLPs appear to be a promising treatment in different conditions,” including menopausal hot flashes, seasonal allergies, attention deficit hyperactivity disorder, and major depression. Then again, a 2023 paper in the same journal concluded that “the overall quality of the evidence was rated low to very low.” As researchers work out what exactly OLPs are—silver bullets, codswallop, or something in between—it’s worth examining what their increasing appearance in research labs says about contemporary life. In a deepfake world where AIs masquerade as people, where marketing calls itself wellness, where politicians tell lies so brazen as to be self-debunking, and where you can be red-pilled, blue-pilled, black-pilled, and clear-pilled without ever being sure you’re seeing reality, there's perhaps nothing so refreshing as a tiny step in the opposite direction: prescribing a pill of nothing and calling it out as such.

While the idea of the placebo response goes back as far as the ancient Greeks, the open-label placebo has a more recent history. In the summer of 1963, in a psychiatric clinic in Baltimore, a group of researchers set out to test the assumption that placebos required deception to work. They explained to a group of 15 “admitted neurotics” that some patients with similar conditions had found relief from a sugar pill, a “pill with no medicine in it at all.” Then they prescribed it to the patients.

The resulting study, published in 1965 in The Archives of General Psychiatry, has its limitations: The sample size was woefully small, and the study had no control group. (Not to mention the term “neurotic” was dropped by the Diagnostic and Statistical Manual in 1994.) Yet it makes for fascinating reading. Most patients reported an improvement in their symptoms. At least five wanted the treatment to continue. Some were convinced the placebo did contain an active ingredient, and one man speculated that doctors had deceived him to make him “think that he was helping himself.” Many patients who believed the truth—that the pills were inert—still attributed their improvement to them. One described the sugar pill as “a symbol or something of someone caring about you, thinking about you three or four times a day.”

These patients were intuiting a field of research that essentially had yet to be invented. In more rigorous clinical trials over the past few decades, researchers have floated a number of hypotheses for why OLPs work. Maybe it’s because doing something rather than nothing can make us feel better. (Psychologists call this “action bias.”) Maybe it’s because people living in well-off countries with huge industrial-pharmaceutical complexes have been conditioned to expect the pills their doctors give them to work. Maybe the act of taking an OLP—twisting off the bottle cap, swallowing the pill—triggers some biomedically useful pathways, just as bloodcurdling movies can curdle (or coagulate) the blood even though the viewer knows everything in the film is fake. Or maybe the OLP begins to take effect before it’s even ingested, during the set of rituals, the enveloping theater, of the “therapeutic encounter.” Most clinical trials involving OLPs begin with a conversation between researcher and patient that lasts 15 to 20 minutes, about the length of a typical doctor’s visit in the US. The researcher’s bedside manner is crucial, one 2017 paper says; they are to be “warm, empathic, natural, and truthful about the design and methods of the study with all patients.” Maybe we start to feel better when someone listens to us, shows respect for our views, and makes common cause with us against our ailments.

You might think that having a positive attitude about the nothing-pill is what transforms it into a something-pill. Perhaps OLPs are a sort of meta-placebo, a testament to how much we believe in our power of belief. But the real driving impulse for many patients who enroll in clinical trials isn’t positive expectation. It seems to be a more uncertain emotion: hope. As the 2017 study puts it, “Hope is a paradoxical combination of opposites, balancing despair and the counterfactual notion that things can improve—a kind of ‘tragic optimism.’” A patient who has suffered for years from some condition, taken drugs, undergone procedures, and gotten no relief may think: A sugar pill probably won’t help, but what the heck, let’s see what happens. As a 2016 paper in the journal Pain puts it, “Engendering hope when participants feel hopeless about their condition can be therapeutic.”

However a patient may find relief from an open-label placebo, this sugar pill that we know is a sugar pill gives us something that its deceptive counterpart doesn’t. It tells us we aren’t dupes who can be fooled by lab-coated experts into thinking our pain has improved or that our allergies have abated. It reminds us that the pharmacologically formulated active ingredient in any given drug is not the only thing that makes it work.

Photograph: Sahar Rana

When you venture outside the scientific literature into the world of contemporary consumer marketing, most of the placebos you’ll find are still the deceptive kind. You know how it works: People given samples of chocolate or wine rate the supposedly expensive ones as better even though the samples are identical. They like Coke or Pepsi more than anonymous colas that are actually Coke or Pepsi. They eagerly press the button at the crosswalk or adjust the thermostat in the office, never thinking that these are placebos placed there by traffic engineers and air-conditioning professionals to have no effect other than making people feel better. The same is true of “save” buttons on word-processing programs, which have been autosaving for decades, and progress wheels that gratifyingly make it seem like websites are toiling to serve you up some personalized experience when really they’re just stalling for time. These placebos grant us the sense of being in control even if it’s what psychologist Ellen Langer called the “illusion of control.”

Placebos also haunt what the political scientist Murray Edelman famously termed the “symbolic uses of politics.” In voters’ “anxious search for direction,” Edelman argued, they might be drawn to leaders who can “dramatize” confidence “in a world many of them find alien”—regardless of whether that performance achieves anything for the voter. “In place of impersonal threatening forces, followers are reassured by a dramaturgy of personal coping,” Edelman wrote. That was in the 1960s, but he could just as well have been describing any number of modern politicians.

Increasingly, though, cultural (as opposed to clinical) placebos are becoming open-label too. A whole slew of “meta-ads,” as The Atlantic called them, work on the idea that savvy consumers know they’re being sold to. Characters in Wayfair ads say things like: “Are we in a Wayfair commercial?” The narrator of a Liberty Mutual ad says, “Research shows that people remember ads with young people having a good time, so here’s a pool party.” Call it open-label marketing.

So why, when we know the sham treatment is a sham, does it work? My best bet is that whether we're in a medical setting or casting a vote, we want to feel like someone's taking care of us. In a cynical, despairing world, a sugar pill that calls itself a sugar pill might be the sweetest thing around.

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It’s always interesting to see how our fellow European neighbours are dealing with common issues and Denmark are yet again leading the way. In response to attempted suicides amongst schoolchildren going over 1000 in 2021, the Danish government started a 10-year action plan with the goals of (and I quote) “prioritising prevention, early detection, and equitable access to high-quality care, as well as improving the overall mental health and wellbeing of the population.” The Danish Liberal Party are the second largest in the current coalition government and have made it clear that education is a key priority; shown clearly in their pledge to treble operating grants for voluntary children’s and youth work.

The Young Liberals Conference will be held in February, and I plan to propose a policy regarding the funding for mental health services outside of schools. The Liberal Democrats have already set out a bold policy for tackling the mental health crisis through trebling the tax on social media companies to fund a mental health professional in school, a distinguishable and direct plan of action which will prove crucial as the general election draws closer. However, it’s of national importance to make sure that during periods of education young people are supported as much as possible. NHS Mental Health Services as well as CAMHS are going to exist whether the government chooses to truly support them not, so why not make our mental health services one of the prides of our nation.

As usual when it comes to the Conservative government, their priorities are firmly in the wrong places. Instead of investing into paying or recruiting teachers, Rishi Sunak has instead put his focus on making sure all students receive some form of maths education till 18. I would like to ask Mr Sunak if he can reach into his magic hat to find the teachers, because as of now I don’t see where they’re coming from.

When it comes to maths, Britain are sat in 12th place in the world in the latest PISA rankings, yet Rishi Sunak continues to preach that we have an anti-maths mindset despite being one of the world’s leading nations in the subject. As a student preparing to sit his GCSE exams in the summer, my peers and I have a very mixed view of the topic of mathematics however those with the ‘anti-maths mindset’ didn’t generate it from birth. Any young student who plans to enter unrelated professions or secure different post-16 qualifications aren’t interested in maths outside of securing a grade good enough to reach sixth-form or college. The argument that maths is essential for everyday life is valid, however, I recommend that people take a look at the latest AQA maths specification and try to figure out why the boy who wants to join the military should enjoy mathematics. Until we adapt our curriculum for the modern world students will continue to see school as a struggle rather than the learning period of their lives.

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More than a decade ago, in a Harvard Business Review article, Thomas Davenport declared data scientist to be the "sexiest job of the 21st century". Today, in an age of generative artifical intelligence (AI), is "prompt engineer" about to assume that title?

What's already certain is that it's one of the hottest jobs around. Prompt engineering involves getting the best and most relevant answers from generative AI tools, and is both conversational, "but also programmatic with prompts embedded in code," fellow ZDNET contributor David Gerwitz explains. 

Professional AI prompt-engineering job rates are hitting $175,000, but can be well over $300,000 per year, he notes, adding that "being a good AI prompt engineer involves more than being able to ask leading questions. You need to combine the disciplines of AI, programming, language, problem-solving, and even art to thrive on this career path."

With the world abuzz about generative AI, prompt engineers are in demand -- huge demand. The problem is that finding prompt-engineering skills is an intractable challenge. Recruiting prompt engineers is not for the faint-hearted. "I think that most people that are recruiting are stealing," quips Greg Beltzer, head of technology at RBC Wealth Management. 

I had a chance to sit down with Beltzer at the recent Salesforce conference in New York, where he talked about the challenges of skilling up in the age of AI. "A good prompt engineer is more expensive than a data scientist today," he observes. "Just outrageously difficult trying to find somebody who has experience. You're not going to find someone who has more than five years of experience. At the most you might get two or three years, but it's hard to find." 

Beltzer continues: "There is a dramatic need to get people up to speed on prompt engineering. But is it a science? Is it an art? Are we going to build more tools?" The good news is that once tooling is in place, it may be easier to train AI models with prompts conducted "systematically and programmatically", he says. 

Yet until robust and useful tools are available, prompt engineering will remain a challenge. Even with tools, Beltzer says it's important to note that this skillset goes beyond technical acumen. What's more, it's too early to identify exactly the requirements and background that are best suited for a prompt engineer. 

For instance, Beltzer doesn't think it would make sense to train a data scientist or another adjacent professional to adopt prompt-engineering skills: "A lot of it needs to be business contextual. You need to think like the user to help with that prompt engineering -- it's not just code. It's not just development. It's like a business technical skillset that's also creative."

Some of the people coming into the field, he observes, aren't necessarily technical at all: "They're writers," he observes. "They just know how to write. And that's a part of it." 

RBC keeps an eye on in its internal talent, with a focus on combined business and technical acumen, says Beltzer, "We're really looking for those folks that are most likely on the business side that has a technical bent. Personally, I don't want to make a bet until the tooling comes a little farther along."

The level of investment in AI and generative AI ventures during the past year, is "also going to shape what type of talent we're going to have,"

Beltzer says. "Until then, the talent market is going to be very lean. If you look at the turnover within these hot companies, they can name their price."

At RBC, which was once a highly conservative company, change has become the rule -- starting with its rising adoption of cloud-based capabilities and services, such as Salesforce. "Once we moved to the cloud, we've been doing 25 releases a year," says Beltzer. "Which for financial services is crazy -- the industry average was one release a year. We have a great team that is business and IT joined together, and we can iterate on the platform very, very quickly."

At the same time, Beltzer does not see his organization going all-in on AI anytime soon. While AI may help developers and business strategists with 80% of their tasks, the remaining 20% requires human involvement, he says: "I think AI is real. But I think we still have some work to do for the commercial viability in my industry."

For example, RBC employs generative AI to assist contact center engagements. "We have some pretty good use cases -- but it's cost mitigation, versus actual revenue generating," says Beltzer. "But it's a good start."

At a more general level, AI might never fully replace humans in the wealth management sector, he adds. "What we've seen in down markets is people don't want to talk to a machine telling them, 'It's going to be okay.' People want to hear, 'We built a portfolio that had this model for this type of scenario. You're still on track -- you're not retiring for another 20 years, you have plenty of time in the market, you continue to invest, it's going to be okay.' But you can't just have a bot telling you that."

AI capabilities are useful, however, in assisting employees as they talk directly to customers. "More and more people are using wealth management than ever before, because we have more assets," says Beltzer. "So, they're going to be able to service their clients with more technology -- making sure this box is checked, or that paperwork is done for them. That's where we need to scale. So, advisors can focus on the relationship with the client, and make sure what they invested in is going to meet their long-term goals."

As an IT manager, "our challenge is to make systems more scalable and more efficient," Beltzer says. "I need to make the human able to do what they love more and take away those baseline activities that don't add more value." 

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Officially, long COVID means persisting symptoms three months after infection with the SARS-CoV-2 virus. Worldwide, at least 10 percent of infected people are thought to suffer from the condition, with recently published research indicating higher rates in multiple countries.

Incidence rates in Africa, though, are well above any of these other estimates. Why that is the case is unclear. In low-income countries, estimates of the incidence of long COVID vary greatly, due to hidden infections and the difficulty of accessing tests.

Between African nations, for instance, previous estimates range from just 2 percent in Ghana to 86 percent in Egypt.

The fact that fewer than 51.8 percent of people in African nations are fully vaccinated could also be another factor at play. Yet specific data on vaccination status and COVID-19 outcomes in this part of the world are largely unknown.

What's more, a large percentage of the patients analyzed in the current review were hospitalized or admitted to the intensive care unit, indicating a bias toward the most severe cases.

The team behind the review, led by researchers from the University of Bari in Italy, wants more research to be done, so that experts can properly assess the impact of long COVID on the African continent and get treatment and support to those who need it.

"To our knowledge, this is the first meta-analysis exploring prevalence, risk factors and symptomatology of long COVID in Africa," write the researchers in their published paper.

"Nearly 50 percent of the people included in this meta-analysis exhibited long COVID symptoms. This finding reinforces the critical significance of this emerging condition."

Older people are more likely to experience long COVID, the review showed, which fits in with previous research. What didn't match the results of earlier studies was that there was no significant difference between men and women and long COVID risk.

Cognitive impairment was the most common neurologic symptom, with shortness of breath the most common respiratory symptom. Psychiatric conditions were common, with a quarter of those with long COVID reporting post-traumatic stress disorder (PTSD).

"This is concerning, because the additional burden in mental health disorder brought by the COVID-19 pandemic and its chronic consequences meets a health system which is largely unprepared to address mental health conditions," write the researchers.

While long COVID severity and symptoms can vary, it is a debilitating condition for many. Here, the team found that a quarter of people with long COVID said they had a poor quality of life as a result, with fatigue and loss of appetite often mentioned.

Right now, we don't have a cure for long COVID, though the symptoms can be treated to some extent in some cases. Research is continuing into how the condition affects the body, and how it might be combated.

As far as Africa is concerned, the researchers are calling for more data to be collected on long COVID across the continent, and for a raising awareness of how prevalent this condition might be – something that could ultimately help those affected.

"High-quality studies addressing this condition in African settings are urgently needed," write the researchers.

The research has been published in Scientific Reports.

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A new study conducted an analysis of exposure levels comparable to those found in firefighters and other people who come into regular contact with per- and poly-fluoroalkyl substances (PFAS).

Firefighters' blood levels of PFAS tend to be higher than the general population's because of their frequent exposure to firefighting foam, which contains PFAS chemicals for its flame retardant properties.

Firefighters are more likely than the general population to develop and die from a variety of cancers that include colorectal cancer. Environmental factors are believed to be related to about 80 percent of CRC cases.

In the new research, PFAS exposure in the lab induced CRC cells to migrate to new positions, implying a potential role in cancer spreading (metastasis) in living organisms.

"It doesn't prove it's metastasis, but they have increased motility, which is a feature of metastasis," says Yale University epidemiologist Caroline H. Johnson.

PFAS are human-made chemicals based on carbon-fluorine bonds, and as the nickname 'forever chemicals' suggests, these bonds are very strong and resistant to degradation, which makes PFAS popular for use in many kinds of products. Unfortunately, it also allows them to survive in the environment for years in ever-increasing concentrations.

"PFAS make up a prevalent class of persistent organic pollutants of increasing public concern worldwide," says co-first author and physiologist Jie Zheng from Yale University.

"They have been frequently detected in the environment, such as in drinking water, indoor dust, cleaning products, and coatings."

Many of these 'forever chemicals' are still present in everyday items, though the hazards of PFAS are largely unclear – partially because of the many different compounds involved.

Research has shown that these long-lasting chemicals spread throughout the environment, and exposure to high levels has been linked to harmful health effects in people and animals.

Perfluorooctanoic acid (PFOA), a widely used PFAS, was classified as carcinogenic to humans by the International Agency for Research on Cancer in November 2023, and perfluorooctanesulfonic acid (PFOS), another common PFAS, was classified as possibly carcinogenic to humans.

To study how they affect aggressive CRC, Zheng, Johnson, and colleagues used lab-grown CRC cells and metabolomics – a process that measures the levels of metabolites, thousands of small molecules like amino acids, lipids, and proteins.

"We look at patterns that occur within an exposed group of people or a diseased group of people, then try to generate a hypothesis as to why somebody may develop a disease or have progression of disease," Johnson says.

"Metabolomics is one of the only tools where you can measure environmental exposures in the same sample as the biological effect."

Two CRC cell types, formed into balls called spheroids, were used in the experiments. A wild-type KRAS gene was present in one type, while the other had a common mutation in the KRAS gene, which is linked to particularly aggressive CRC.

When exposed to PFOS and PFOA, the cells showed increased movement and a higher tendency of spreading. In a different test with CRC cells grown in a flat layer, a line was scratched down the middle to split them. When the chemicals were introduced, the cells grew and moved toward each other again.

To dig deeper, the researchers examined the chemicals' effects on the cell's metabolism. PFAS exposure altered various metabolites crucial for cell function, like amino acids and fatty acids, as well as signaling proteins associated with metastasis.

Substances that are usually anti-inflammatory and protective against cancer were reduced in the CRC cells after exposure, too. Some differences were more noticeable in the mutated cells, which could mean that cancers with this mutation may be more likely to spread with exposure to PFAS.

These results in the lab indicate that exposure to high levels of PFOS and PFOA could potentially increase the risk of CRC spreading in real-life conditions. This is crucial information for those in jobs with potential high exposure, the team says, and monitoring these chemicals is key to safeguarding their health, as are future clinical studies.

"Many in vitro studies can't be translated into humans," Johnson explains, "but I think understanding first the mechanisms of how they can actually affect cancer cell growth is important."

The study has been published in Environmental Science & Technology.

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Previous studies have linked changes in retinal nerves with altered brain structures, and from there to Autism Spectrum Disorder ( ASD). The evidence suggests the eye really is a window to the brain, via the interconnectedness of the central nervous system.

"Individuals with ASD have structural retinal changes that potentially reflect brain alterations, including visual pathway abnormalities through embryonic and anatomic connections," researchers write in their new paper.

"Whether deep learning algorithms can aid in objective screening for ASD and symptom severity using retinal photographs is unknown."

In this study, a team from the Yonsei University College of Medicine in the Republic of Korea wanted to see if AI could spot ASD in retinal patterns. First, the model was trained on images where the AI was told if the subject had autism or not.

Then, the AI was asked to analyze the retinas of 958 children and teenagers with an average age of 7.8 years overall, half of whom had been diagnosed with autism. It managed a perfect score in identifying those who had autism and those who didn't.

The AI wasn't quite as good at predicting symptom severity from the retina photos – it was only accurate between 48-66 percent of the time. Still, there's lots of potential here to help kids get a useful assessment at an earlier age, with a shorter wait.

In this case, the researchers limited the training data to children and adolescents between the ages of 4 and 18, but they think that it could work on even younger kids as well – that's something that future studies might be able to look into.

"This question remains unexplored because the youngest age group in our sample was four years," write the researchers. "Retinal alterations in individuals with ASD may manifest even before retinal maturation."

In a study published last year, researchers were able to link the retina's response to light to cases of Attention Deficit Hyperactivity Disorder ( ADHD) and ASD, another example of how the eyes can act as a kind of mirror to an individual's brain activity.

Around one in 36 people is thought to be autistic, based on prevalence among eight-year-olds – and being aware of that diagnosis as early as possible can make a huge difference in young people understanding themselves and making their way through the world.

"The findings of this study suggest that retinal photographs may serve as a viable candidate for an objective method to screen for autism and possibly for symptom severity," write the researchers.

The research has been published in JAMA Network Open.

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As Hurricane Larry curved north in the Atlantic in 2021, sparing the eastern seaboard of the United States, a special instrument was waiting for it on the coast of Newfoundland. Because hurricanes feed on warm ocean water, scientists wondered whether such a storm could pick up microplastics from the sea surface and deposit them when it made landfall. Larry was literally a perfect storm: Because it hadn’t touched land before reaching the island, anything it dropped would have been scavenged from the water or air, as opposed to, say, a highly populated city, where you’d expect to find lots of microplastics.

As Larry passed over Newfoundland, the instrument gobbled up what fell from the sky. That included rain, of course, but also gobs of microplastics, defined as bits smaller than 5 millimeters, or about the width of a pencil eraser. At its peak, Larry was depositing over 100,000 microplastics per square meter of land per day, the researchers found in a recent paper published in the journal Communications Earth and Environment. Add hurricanes, then, to the growing list of ways that tiny plastic particles are not only infiltrating every corner of the environment, but readily moving between land, sea, and air.

As humanity churns out exponentially more plastic in general, so does the environment get contaminated with exponentially more microplastics. The predominant thinking used to be that microplastics would flush into the ocean and stay there: Washing synthetic clothinglike polyester, for instance, releases millions of microfibres per load of laundry, which then flow out to sea in wastewater. But recent research has found that the seas are in fact burping the particles into the atmosphere to blow back onto land, both when waves break and when bubbles rise to the surface, flinging microplastics into sea breezes.

The instrument in a clearing on Newfoundland was quite simple: a glass cylinder, holding a little bit of ultrapure water, securely attached to the ground with wooden stakes. Every six hours before, during, and after the hurricane, the researchers would come and empty out the water, which would have collected any particles falling—both with and without rain—on Newfoundland. “It’s just a place that experiences a lot of extreme weather events,” says Earth scientist Anna Ryan of Dalhousie University, lead author of the paper. “Also, it’s fairly remote, and it’s got a pretty low population density. So you don’t have a bunch of nearby sources of microplastics.”

The team found that even before and after Larry, tens of thousands of microplastics fell per square meter of land per day. But when the hurricane hit, that figure spiked up to 113,000. “We found a lot of microplastics deposited during the peak of the hurricane,” says Ryan, “but also, overall deposition was relatively high compared to previous studies.” These studies were done during normal conditions, but in more remote locations, she says.

The researchers also used a technique known as back trajectory modeling—basically simulating where the air that arrived at the instrument had been previously. That confirmed that Larry had picked up the microplastics at sea, lofted them into the air, and dumped them on Newfoundland. Indeed, previous research has estimatedthat somewhere between 12 and 21 million metric tons of microplastic swirl in just the top 200 meters of the Atlantic, and that was a significant underestimate because it didn’t count microfibres. The Newfoundland study notes that Larry happened to pass over the garbage patch of the North Atlantic Gyre, where currents accumulate floating plastic.

These new figures from Newfoundland are also likely to be significant underestimates—and necessarily so. It remains difficult and expensive to look for the smallest of plastic particles: This research searched for bits as small as 1.2 microns (1.2 millionths of a meter), but there were likely way, way more pieces of plastic smaller than that falling into the instrument. “From previous studies, we know that there’s an exponential curve for particle numbers as you go smaller,” says University of Birmingham microplastic researcher Steve Allen, coauthor of the new paper. “So we’ve been talking about 113,000 particles per square meter a day of big stuff. It just must be staggering, what is smaller.”

The researchers could also determine what kinds of plastic had fallen out of the sky. “We saw not an overwhelming amount of one certain polymer—there’s a real variety,” says Ryan. “In the ocean, there’s such a mix of particles that you have a little bit of everything. And also because the hurricane came from so far away: It formed off the west coast of Africa, and you could potentially have particles picked up from all the way back there.”

This echoes what other scientists have been finding with microplastics in the environment. Microplastic pollution comes from so many sources—our clothing, car tires, paint chips, broken-down bottles and bags—that it’s all mixed into a kind of multi-polymer soup out there. That’s true both in the oceans and in the sky: In remote stretches of the American West, microplastic-sampling instruments similar to the one in Newfoundland have been gathering huge numbers of particles falling as plastic rain. Microplastics haven’t just gone airborne, but have become a fundamental component of Earth’s atmosphere.

So microplastics don’t just flush into the sea and stay there—they blow into the atmosphere and back onto land, only to get picked back up again by winds and blown out to sea. Back and forth, back and forth. “It’s becoming quite clear that the ocean-to-atmosphere exchange is a very real thing,” says Allen. “And the numbers in this paper here are just staggering. It’s arriving in Newfoundland at just the time of year when all the biota—in the ponds and things—are all just trying to fatten up and breed for winter.”

Because microplastics travel so readily on winds and ocean currents, what were once considered pristine environments are now anything but. Scientists are racing to figure out how the particles are affecting the organisms there. Microplastics from Europe, for instance, have polluted the Arctic, in turn contaminating the algae Melosira arctica, which grows on the underside of sea ice. The algae are the very base of the Arctic food chain, meaning all sorts of organisms are consuming them plus their accumulated microplastic.

As if hurricanes couldn’t get any worse, they’re yet another way for plastic particles to spread where they don’t belong.

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“There’s no tech industry without semiconductors,” said Stacy Rasgon, senior semiconductor analyst at Bernstein Research.

Semiconductors represent a $574 billion industry globally and are on pace to cross the trillion-dollar mark by the end of the decade. The industry has been caught in the crosshairs between the U.S. and China, two of the world’s largest economies.

The U.S., which leads the world in global semiconductor market share, recently issued sweeping restrictions on the sale of advanced chips and chipmaking equipment to China, in an attempt to restrict Beijing’s access to critical technologies. The Biden administration has said the export controls are aimed in part at preventing the use of American-made chips in China’s military. China, meanwhile, has accused the U.S. of abusing export restrictions to impede the country’s technological advances.

“We cannot allow China to have our most sophisticated semiconductor chips for use in the Chinese military,” U.S. Secretary of Commerce Gina Raimondo said in an interview with CNBC on Oct. 30, 2023. “That’s where we’ve drawn the cut line.”

Watch the video above to find out more about how the semiconductor industry became the centerpiece of a technological tug-of-war between the U.S. and China, and what the potential implications are for companies caught in the middle of it all.

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In the first experiment of its kind in the South Asian country, planes equipped with cloud seeding equipment flew over 10 areas of the city, often ranked one of the worst places globally for air pollution.

The "gift" was provided by the United Arab Emirates, said caretaker chief minister of Punjab, Mohsin Naqvi.

"Teams from the UAE, along with two planes, arrived here about 10 to 12 days ago. They used 48 flares to create the rain," he told the media.

He said the team would know by Saturday night what effect the "artificial rain" had.

The UAE has increasingly used cloud seeding, sometimes referred to as artificial rain or “blueskying,” to create rain in the arid expanse of the country.

The weather modification involves releasing common salt — or a mixture of different salts — into clouds.

The crystals encourage condensation to form as rain.

It has been deployed in dozens of countries, including the United States, China and India.

Even very modest rain is effective in bringing down pollution, experts say.

Air pollution has worsened in Pakistan in recent years, as a mixture of low-grade diesel fumes, smoke from seasonal crop burn off and colder winter temperatures coalesce into stagnant clouds of smog.

Lahore suffers the most from the toxic smog, choking the lungs of more than 11 million residents in Lahore during the winter season.

Levels of PM2.5 pollutants — cancer-causing microparticles that enter the bloodstream through the lungs — were measured as hazardous in Lahore on Saturday at more than 66 times the World Health Organization's danger limits.

Breathing the poisonous air has catastrophic health consequences.

Prolonged exposure can trigger strokes, heart disease, lung cancer and respiratory diseases, according to the WHO.

Successive governments have used various methods to reduce air pollution in Lahore, including spraying water on the roads, and weekend shutdowns of schools, factories and markets, with little or no success.

When asked about a long-term strategy to combat smog, the chief minister said the government needs studies to formulate a plan.

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Long before ChatGPT blasted onto the scene and sucked all the air out of the room, there was IBM Watson. Watson itself blasted to fame when, in 2011, it beat reigning champion Ken Jennings on the TV game show Jeopardy.

Fun fact: ZDNET's own Steven J. Vaughn-Nichols was once a clue on Jeopardy.

Anyway, back to our story. My point is that IBM has a long history with AI and has not been sitting still. Its generative AI solution is called Watsonx. It focuses on enabling businesses to deploy and manage both traditional machine learning and generative AI, tailored to their unique needs.

Also: AI in 2023: A year of breakthroughs that left no human thing unchanged

I'm telling you this because if any company has the cred to offer a credential on AI fundamentals, it's IBM.

IBM's AI Fundamentals program is built inside of its SkillsBuild learning portal. The credential takes about ten hours to complete, across six courses.

Because I have had a long interest in AI ethics (I did a thesis on AI ethics way back in the day), I took the AI ethics class. It was good.

It discussed the challenge of balancing technology with ethical responsibility. Key topics included the five pillars of AI ethics, the importance of fairness and avoiding bias, and the need for AI systems to be transparent, explainable, and robust against attacks. The session also emphasized governance, the protection of personal data, and the significance of privacy through data minimization and differential privacy.

I'll probably take the rest of the courses over the holiday break. 

To get started, create a free account on IBM's SkillsBuild learning portal. All of the following links to IBM's free AI courses require you to have created that account and logged in before you'll be able to use them. 

Artificial Intelligence Fundamentals Learning Plan: In this learning plan, you'll explore AI's history, and then see how it can change the world. Along the way, you'll deep dive into ways that AI makes predictions, understands language and images, and learns using circuits inspired by the human brain. After a hands-on simulation in which you build and test a machine-learning model, you'll finish with tips on how to find your career in AI.

Introduction to Artificial Intelligence (1 hour 15 mins): Less than a century old, AI has already undergone three waves of transformative development. Today it gives humanity the most powerful tools for analyzing complex data, not only to find meaning but also to learn without human intervention. In this course, you'll survey AI's history and explore ways that it can shed light on unstructured data.

Natural Language Processing and Computer Vision (1 hour 30 mins): You might already know that some AI systems can understand human language, identify visual images, and even create original art. But do you know how these systems do it? In this course, you'll explore the theory of natural language and vision processing and learn how these technologies drive real-world mechanisms such as chatbots and photo analysis.

Machine Learning and Deep Learning (2 hours): In this course, you'll see how machines can learn and make amazing, evidence-based predictions. Explore the logic behind computers' ability to learn, then investigate new ways that AI systems inspired by neurons in the human brain can solve difficult problems.

Run AI Models with IBM Watson Studio (1 hour and 45 mins): In this course, you'll practice creating an AI machine learning model in a series of simulations, using IBM Watson Studio. This is hands-on time that can help you do actual work with AI.

AI Ethics (1 hour and 45 mins): You might have heard about problems that arise when AI systems misinterpret data or propose solutions that reflect human prejudice. This is the course I talked about above. Through real-world examples you'll learn about AI ethics, how they are implemented, and why AI ethics are so important in building trustworthy AI systems.

Your Future in AI: The Job Landscape (1 hour): Are you considering a career in AI? In this course, learn about the AI job market's rapid growth and the skills needed for success in this exciting field. You'll hear how real professionals got their start, and find resources and learning opportunities that could help you work alongside them.

More resources

This is the third article in our series of free learning resources for those interested in exploring AI or building a career around this amazing technology. I also explored Amazon's free AI courses and free AI courses from OpenAI and DeepLearning. 

So there you go. Sign up now and use your holiday time to get a new credential. If you take any of these courses, please report back below in the comments and let us know what you think. And stay tuned. I expect to provide more resources early in 2024 for you to continue your free AI learning journey.

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This particular combo of 'why to reduce' and 'how to reduce' messaging can be useful for promoting good health in a population, the researchers found in a 2021 study.

Too much drinking doesn't just lead to cancer, of course. Overdoing it on the booze is associated with a whole range of problems, including premature death, heart disease, digestive issues, and an increased risk of dementia.

"We found that pairing information about alcohol and cancer with a particular practical action – counting their drinks – resulted in drinkers reducing the amount of alcohol they consumed," said economist and psychologist Simone Pettigrew from The George Institute for Global Health when the findings were announced.

For the study, three surveys were filled out: 7,995 people completed the first, 4,588 of those people completed the second three weeks later, and 2,687 people finished the final survey three weeks after that. The participants were split up into different groups and shown different advertisements and messages about drinking.

One combination stood out, compared to a control group: A TV ad linking booze and cancer, together with a suggestion to keep count of your drinks, was one of the most effective at getting people to try and cut down on alcohol intake.

It was also the only combination where people actually did significantly reduce their alcohol consumption over the six weeks.

Other approaches – like encouraging people to decide on a number of drinks and then stick to it – did prompt some of the volunteers to try and cut down, but there was a clear winner based on the people taking part in this research.

"Many people don't know that alcohol is a carcinogen," said Pettigrew. "It's important information that drinkers should have access to. But telling people alcohol causes cancer is just part of the solution – we also need to give them ways to take action to reduce their risk."

Alcohol consumption can be attributed to as many as 7 percent of premature deaths worldwide, according to the World Health Organization, and making drinkers more aware of the health risks is one way of tackling that problem.

While health agencies have also looked at ways of making booze less readily available and more expensive, ultimately, personal choices will determine whether or not behavior around alcohol will shift in the long term.

In this particular study, the participants were chosen to be "broadly demographically representative of the Australian drinking public", so it's not an approach that will necessarily work elsewhere – but it seems that counting your drinks could be one option to try if you want to cut down.

"There are limited resources available for alcohol harm-reduction campaigns, so it's important to find out which messages resonate best to ensure they have the best chance of working," said Pettigrew.

The research was published in Addictive Behaviors.

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Sunday, 17 December

• Who: Orienspace
• What: Gravity 1 rocket
• When: Unknown
• Where: Yellow Sea
• Why: The Gravity 1 rocket will perform its first flight and tak 17 satellites into orbit. It will be launching from a sea platform this time but it can also do land launches. One of the satellites it’ll launch is called Jilin Gaofen 05.

Monday, 18 December

• Who: SpaceX
• What: Falcon 9 B5
• When: 4:00 - 8:31 a.m. UTC
• Where: Space Launch Complex 40, Cape Canaveral, Florida, US
• Why: SpaceX will be launching 23 Starlink satellites into a low Earth orbit. These satellites will join the huge Starlink constellation to beam internet to customers on Earth. This batch of satellites is designated as Starlink Group 6-34; this can be used to track the satellites on apps like ISS Detector.

Friday, 22 December

• Who: SpaceX
• What: Falcon 9 B5
• When: 9:46 - 11:45 p.m. UTC
• Where: Space Launch Complex 40, Cape Canaveral, Florida, US
• Why: SpaceX will launch the Ovzon 3 satellite into orbit before the satellite moves itself into a final orbit over the next several months. It will be the first commercial satellite to use a Roll-Out Solar Array. Ovzon will offer mobile broadband service via satellite combining high bandwidth satellite communication services with highly mobile terminals.

Recap

• The first launch we got this week was a Chinese Long March 2D carrying the Yaogan-39 05 satellite to orbit from the Xichang Satellite Launch Center. It is a remote sensing satellite.

• Next up, Chinese company iSpace launched the Hyperbola-2 in a vertical takeoff, vertical landing (VTVL) test, which it completed successfully. The rocket is a small two-stage launch vehicle that will be able to launch 1.9 tons into a low-Earth orbit and then land again for reuse.

• The third launch of the week was Rocket Lab’s Electron rocket carrying the QPS-SAR-5 satellite for iQPS. The mission was called “The Moon God Awakens” and the satellite is called TSUKUYOMI-I. It took off from Pad B at the Rocket Lab Launch Complex 1 in Mahia, New Zealand.

• The final launch this week was a Long March 5 carrying the Yaogan-41 high-orbit optical remote sensing satellite.

That’s all for this week, check back next time.

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Our B cells help prevent us from getting sick. Their job is to make antibodies, immune system proteins that fight off viruses and other foreign invaders. And they make a lot of antibodies—thousands of them every second. What if these antibody factories could be harnessed to make other things the body needs?

That’s the idea behind a trial launched by Seattle-based biotech company Immusoft. The company announced today that its scientists have genetically programmed a patient’s B cells and put them back in his body in an effort to treat disease. It’s the first time engineered B cells have been tested in a person.

The patient has a genetic disorder known as mucopolysaccharidosis type I, or MPS I. His body doesn’t produce an essential enzyme that helps to break down long-chain sugars inside cells. Without this enzyme, these sugars build up in the eyes, heart, bones, and elsewhere.

The effects are life-threatening. Patients have cloudy eyes, respiratory problems, cognitive issues, and enlarged organs. Those with the most severe form of the disease die in childhood. Others may live to their twenties or thirties.

Patients are currently treated with weekly infusions of the enzyme their body lacks. The therapy must be given for the entirety of a patient’s life. Typically, a gene called IDUA provides instructions for making this enzyme, but people with MPS I have a mutation in this gene. Immusoft’s aim is to override this problem by prompting a person’s B cells to make the enzyme instead. B cells appealed to Immusoft because of their ability to pump out lots of proteins. If a person’s B cells could provide a continuous supply of this enzyme, it could eliminate the need for regular infusions.

Sean Ainsworth, CEO of Immusoft, says the initial patient is doing well after receiving the experimental therapy in mid-November. “So far, so good,” he says.

Researchers at the company collected the patient’s B cells using a machine that removes blood, separates out a particular component, then returns the rest to circulation. There are billions of B cells in the body; Immusoft uses only a portion. “The body is constantly regenerating and producing new B cells,” Ainsworth says.

To get the B cells to produce the missing enzyme in addition to antibodies, scientists had to add new genetic instructions to them in the lab. They packaged those instructions into a transposon, a DNA sequence that can naturally integrate into a cell’s genome using a cut-and-paste mechanism.

Several commercially available therapies involve genetically engineering a patient’s cells outside the body to treat disease. A newly approved treatment for sickle cell disease uses Crispr to edit a patient’s blood-forming stem cells. And a type of “living drug” known as CAR-T cell therapy supercharges a patient’s T cells against cancer. No current therapies use a person’s B cells.

“It seems to me it was the obvious thing to move from T cells to B cells,” says Abla Creasey, vice president of therapeutics development at the California Institute for Regenerative Medicine, which has awarded $12 million in grants to Immusoft. She says B cells represent an exciting new strategy to treat disorders in which the body doesn’t make enough of a certain protein or enzyme.

The field is still new, says David Rawlings, an immunologist at Seattle Children’s Hospital who is working on engineered B cell therapies. That’s in part because B cells proved more difficult to manipulate than other types of cells. His lab is using Crispr to modify B cells, and he cofounded a company, Be Biopharma, to further develop them.

“The uses are really broad because you can think of them as a drug-secreting platform that lasts for a long time,” Rawlings says.

Existing engineered cell therapies have shown miraculous effects, but they come with downsides. In the case of the Crispr treatment, patients first undergo chemotherapy, which can cause hair loss, nausea, and other unpleasant side effects. After treatment, they must then stay in the hospital for weeks while their edited stem cells take up residence in the bone marrow. With CAR-T cell therapy, serious immune or nervous system effects can occur, so patients must be monitored in the hospital.

By contrast, Immusoft’s engineered B cells are given as an IV infusion in an outpatient procedure, Ainsworth says.

Paul Orchard, the doctor running the trial at the University of Minnesota Medical School, says the original plan was to treat children with the disease. “It’s easier to prevent complications than it is to reverse them after they’ve already happened,” he says. “If you can identify kids and intervene relatively early in life, they’re more likely to get benefits.” However, the US Food and Drug Administration has limited the team to working with adults initially, until the therapy is shown to be safe.

He says one concern the FDA has with engineering B cells is the possibility that they could turn cancerous, giving rise to lymphoma or leukemia. The transposon system Immunosoft uses inserts the new genetic material in a random fashion, so Orchard says there’s a theoretical risk that it could do so near a cancer-causing gene. This is also a known risk with current CAR-T cell therapies, which use viruses to deliver new genetic material to cells. Scientists can’t precisely control where in the genome viruses drop off their payload.

Immusoft’s initial trial is meant to test safety of its engineered B cell approach, so patients will continue receiving their usual enzyme infusions for now. The next step will be to take patients off the infusions to see whether the modified B cells are doing what they’re supposed to do. Orchard says they’ll measure enzyme levels in the blood and also look for improvement in patients’ symptoms, including movement and heart function.

One big question investigators are hoping to answer is how long the engineered B cells stick around in the body. Some B cells last for decades, Orchard says. “We’ll have to see. Obviously, it would be better if it's a definitive therapy and a one-time administration.”

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Reading print texts improves comprehension more than reading digital materials does, according to a new study.

Researchers at the University of Valencia analysed more than two dozen studies on reading comprehension published between 2000 and 2022, which assessed nearly 470,000 participants. Their findings suggest that print reading over a long period of time could boost comprehension skills by six to eight times more than digital reading does.

“The association between frequency of digital reading for leisure and text comprehension abilities is close to 0,” said Ladislao Salmerón, a professor at the University of Valencia who co-authored the paper. This may be because the “linguistic quality of digital texts tends to be lower than that traditionally found in printed texts”, he added. Text on social media, for example, may be conversational and lack complex syntax and reasoning.

Salmerón said that the “reading mindset” for digital texts also tends to be more shallow than that for printed materials, with scanning being more common. This can mean the reader “doesn’t fully get immersed in the narration, or doesn’t fully capture the complex relations in an informative text”.

The study, published in the Review of Educational Research, also found that while there is a negative relationship between digital reading and comprehension for primary school students, the relationship turns positive for secondary school and undergraduate students.

Salmerón suggests that this may be because young children are less able to navigate the distractions, such as incoming messages, that might come with reading on a digital device. “We know that our ability to regulate our cognition evolves during adolescence,” he said. Young children “may not be fully equipped to self-regulate their activity during digital leisure reading”.

The authors also said that young children engaging in frequent digital reading may learn less academic vocabulary “in a critical period when they are shifting from learning to read to reading to learn”.

The researchers are not “against digital reading”, said Lidia Altamura, a PhD student who co-authored the paper. “It’s just that, based on what we have found, digital reading habits do not pay off as much as print reading. That is why, when recommending reading activities, schools and school leaders should emphasise print reading more than digital reading, especially for younger readers.”

Salmerón added that one surprising finding was that the relatively small association between digital reading for leisure and comprehension stands regardless of the type of reading people engage in, across both social media and educational websites such as Wikipedia. “We expected that the latter would be much more positively associated with text comprehension, but our data says that is not the case.”

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Unfortunately, as the temperature falls, the risk of heart problems heats up. Even if you live far from the nearest iceberg, cold weather can pose problems. Studies have linked low temperatures to an increased risk of stroke, heart-related chest pain, heart rhythm problems and deaths from heart failure and cardiac arrest.

Cardiologist Dr. Sherrie Khadanga said an increased risk of heart attack is a top concern in cold weather. "Usually that ends up due to a patient overexerting themselves doing strenuous physical activity, such as shoveling or walking through heavy snow," said Khadanga, an assistant professor of medicine at the University of Vermont's Larner College of Medicine in Burlington.

Dr. Richard Gumina, an interventional cardiologist and associate professor at The Ohio State University Wexner Medical Center in Columbus, said cardiac arrest – a sudden stoppage of the heart – is a related concern in the cold. "Sometimes cardiac arrest can be due to a heart attack," said Gumina, who also is associate dean for convergent research at Ohio State's College of Medicine. "Other times it can be due to heart rhythm problems that can be brought on by doing strenuous activity and cold weather."

One of the main risk factors, Khadanga said, comes from your body's basic reaction to the cold. To conserve warmth, blood vessels constrict to limit blood flow to your skin, which raises your blood pressure. "And that, in and of itself, can increase the risk of a heart attack or a stroke," she said.

The lower the air temperature, the worse the problem, she said, and the concern is highest among people with existing heart disease, whose blood flow is already restricted. But many people are unaware they have heart disease until they start having symptoms such as chest pain, Gumina said.

Even people living in warm climates can be affected. A review of research, published in March in Frontiers in Cardiovascular Medicine, looked at data from several studies and found that overall, cold spells increased deaths from cardiovascular disease by 32%. The effect was more pronounced in areas where the weather is typically milder than areas that see cold regularly.

But, in news that should warm your heart, Gumina and Khadanga offered simple ways people can protect themselves.

Wear the gear

Khadanga tells her patients that when they're outside, "not only should they be wearing layers of clothing, but also hats, gloves and heavy socks" to stay warm.

To that, Gumina adds a mask, "so you're not taking in just cold air."

But don't overdo it, Khadanga said. "You want to dress warmly if you're outside, but you don't want to overheat."

Shoveling snow? Go slow

Several studies have linked snow shoveling to a higher risk of heart attacks. Part of the problem, Gumina said, is that people who aren't usually physically active will attempt it. The combination of a heart that is not conditioned for heavy lifting plus cold-constricted blood vessels that might also be partially blocked from plaque can leave a heart starving for the oxygen-rich blood it needs to function.

Gumina said he advises his patients with heart disease to get help to clear the driveway. But those who insist on doing it themselves need to be careful.

Just as you wouldn't jump on a treadmill set at the highest level and steepest angle and start running, he said, you shouldn't run right out to the driveway and vigorously attack the drifts. "Ensure that you've given yourself a little warmup period," he said.

Then, "bite it off in small pieces," he said, with frequent breaks. And know the symptoms of a heart attack, which can include chest discomfort, shortness of breath and nausea.

Stay active – carefully

In Vermont, Khadanga is surrounded by people who ski, snowboard and do other outdoor activities in the cold. Even for healthy, active people, taking breaks is important, she said. "You do a couple of runs down the hill, then you go back inside to warm up," she said.

Staying physically active is a crucial component of heart health, and you shouldn't be afraid to go out in the cold, Gumina said. But you have to be aware of potential problems.

Gumina said winter is the wrong time of year to plunge into an outdoor exercise routine. "You want to have a period ahead of time where you've been exercising, and then you can transition into something that is cold." And if you are going out in the cold weather, "I always tell people to go in pairs," because of the risk of slipping on ice.

And stay hydrated, he said. "You don't realize how much you sweat during that time when you're in cold weather."

Stock up on meds

Khadanga reminds her patients to make sure that they fill prescriptions before winter storms arrive. "Snow and ice can make the roads extra slippery, and I wouldn't want a patient to run out of necessary medication."

Vaccines are a heart health issue

Cold weather sends people indoors, which boosts the risk of catching the flu or COVID-19. Research shows the risk of having a heart attack is six times higher within a week of having the flu, and COVID-19 has been linked to substantial risk of heart problems and stroke.

"Everyone needs a flu shot and their COVID vaccination," Gumina said. "These are things that we know decrease your risk of having severe disease."

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A recent study suggests that dining after 9pm might elevate the risk of strokes and mini-strokes, shedding light on the potential health impacts of meal timing. 

Examining over 100,000 individuals in France, the research focused on participants' meal schedules through extensive food diaries. Those eating dinner after 9pm were found to be 28% more likely to experience a stroke or mini-stroke compared to those who dined before 8 pm.

The study, spanning an average of seven years, identified approximately 2,000 cases of cardiovascular disease, including heart attacks and strokes. 

Notably, the research emphasised the significance of meal timing, proposing that our evolutionary patterns favour earlier eating. While animal studies indicate potential associations between late-night digestion and elevated blood sugar and pressure, more research is required to draw conclusive links.

Dr Bernard Srour, the senior author of the study, highlighted the potential health risks associated with late-night dining, particularly for individuals who attribute their dining times to busy schedules. 

The findings underscore the importance of considering meal timing as a factor that may impact health, particularly in women, who constituted nearly 80% of the study participants.

The study, published in Nature Communications, delves into the relationship between breakfast and dinner timings and the risk of cardiovascular diseases. 

While no heightened risk of coronary heart problems was observed for those eating dinner after 9 pm, each hour delay in dinner was linked to an 8% increased risk of strokes or mini-strokes. 

Additionally, every hour delay in breakfast was associated with a 6% higher risk of various cardiovascular diseases, with significant implications for women participants. 

The study also supported earlier research suggesting that prolonged overnight fasting may contribute to better health outcomes, particularly for those who consume dinner early.

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