Vitamin D Linked to Lower Diabetes Risk in People with VDR Gene Variant

A genetic analysis of a large U.S. clinical trial suggests that vitamin D supplementation may reduce the risk of progression from prediabetes to type 2 diabetes, but only for those people who harbor specific variants of the vitamin D receptor gene. The study, led by researchers at Tufts University and published in JAMA Network Open, found that daily high-dose vitamin D lowered diabetes risk by 19% in participants with certain genotypes, opening the possibility of using vitamin D as a diabetes prevention strategy.

The new findings build on data from the Vitamin D and Type 2 Diabetes (D2d) clinical trial, a multi-site randomized study that enrolled more than 2,000 U.S. adults with prediabetes. Study participants were assigned to receive either 4,000 IU of vitamin D3 daily or a placebo. The subjects were then followed for a median of 2.5 years to assess progression to diabetes. The original trial did not show a statistically significant reduction in diabetes risk across all participants.

“But the D2d results raised an important question: Could vitamin D still benefit some people?” said lead author Bess Dawson-Hughes, MD, a senior scientist at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University. “Diabetes has so many serious complications that develop slowly over years. If we can delay the time period that an individual will spend living with diabetes, we can stop some of those harmful side effects or lessen their severity.”

In their follow-on research, the Tufts noted that subsequent analysis of the D2d trial data showed that outcomes varied based on achieved blood levels of vitamin D in participants. The new study also found a genetic link to those who had improved outcomes.

To explore the role genetics might play, the investigators conducted a post hoc analysis of 2,098 D2d participants who consented to genetic testing. They focused on three common polymorphisms in the vitamin D receptor (VDR) gene: ApaI, BsmI, and FokI. The researchers first examined how vitamin D levels correlated with diabetes risk across genotypes, then evaluated how genetic variants influenced response to supplementation.

The data showed that the ApaI polymorphism is a key determinant of response. Participants with the AA genotype, which was about 30% of the cohort, did not experience a reduction in diabetes risk with vitamin D supplementation. By comparison, those with the AC or CC genotypes, the remaining 70% of participants, showed a 19% lower risk of developing diabetes when treated with vitamin D compared with placebo.

The biological basis for this effect is linked to the role the VDR gene plays in pancreatic β cells, where it influences insulin secretion and glucose regulation. Variations in the receptor may alter how effectively vitamin D exerts these effects, explaining why some individuals benefit from supplementation while others do not.

Earlier research has suggested there is a connection between vitamin D and diabetes risk. In earlier analyses of the D2d trial, participants who maintained higher blood levels of vitamin D experienced substantial reductions in diabetes incidence. These findings were supported by meta-analyses and observational studies, including research from the UK Biobank, which found that genetic variation in VDR could modify its activity.

“We hypothesized that VDR gene variants modify the association between achieved intratrial 25-hydroxyvitamin D (25(OH)D) level and diabetes risk and may modify the effect of vitamin D3 supplementation on the risk of developing diabetes,” the researchers wrote. 25(OH)D is the main form of vitamin D circulating in the blood.

The current study broadens knowledge on the role vitamin D can play in diabetes prevention by identifying the specific polymorphisms at play. The overlap between ApaI and BsmI variants provides further evidence of the role of VDR genetics, although the researchers noted that ApaI alone may be sufficient to identify likely responders.

“This genetic association analysis of the D2d study suggests that genetic variation in the VDR, specifically the ApaI polymorphism, is associated with diabetes risk at higher intratrial 25(OH)D levels and is associated with response to 4000 IU/d of vitamin D3 supplementation among adults with prediabetes,” the researchers wrote.

The implications for clinical care include the potential use of genetic testing to guide preventive treatment. A single test for the ApaI polymorphism could help identify patients with prediabetes who are most likely to benefit from higher-dose vitamin D supplementation.

While the results have established a link between variations in the VDR gene and diabetes development, the research noted that the study was not designed to assess the mechanisms underlying the genetic effects. Further, its sample size limited subgroup analyses by race and ethnicity.

“Our findings suggest we may eventually be able to identify which patients with prediabetes are most likely to benefit from additional vitamin D supplementation,” Dawson-Hughes said. “In principle, this could involve a single, relatively inexpensive genetic test.”

Next steps in this line of research include replicating the findings in independent cohorts and conducting prospective trials designed to test genotype-guided supplementation strategies.

The post Vitamin D Linked to Lower Diabetes Risk in People with <i>VDR</i> Gene Variant appeared first on Inside Precision Medicine.

Heart’s beat may help it beat cancer, mouse research suggests

Heart disease and cancer are the leading causes of death in the United States, but it is rare that cancer makes its way to the heart. 

It’s an observation that clinicians have been grateful for, though largely unable to explain. But in a paper published Thursday in Science, researchers propose one potential explanation: The constant pressure that the organ is under from beating thousands of times a day and pushing gallons of blood creates an environment that is hostile to cancers. The study, which was conducted in mice, is preliminary, but outside experts said it points to potential new approaches for cancer treatments. 

Read the rest…

STAT+: Trump’s boosting of psychedelics, cannabis signal a new era in GOP drug policy

The days of “Just Say No,” it seems, are long gone. 

Over the weekend, President Trump signed an executive order to increase the availability of certain psychedelics as treatments for mental health conditions, ordering that $50 million be spent, and that the Food and Drug Administration fast-track reviews to usher in their approval. At one point, the president joked to the motley assembly of administration officials, a former Navy SEAL, and the podcaster Joe Rogan:  “Can I have some, please?” 

On Wednesday, the Trump administration announced it had downgraded medical marijuana from the highest tier of controlled substances, and was pushing the Drug Enforcement Administration to do the same for recreational marijuana.

The president’s lenient tack on some mind-altering drugs ushers in a new world of right-wing drug policy. While the administration has emphasized hardline, militaristic tactics when it comes to fentanyl, its recent actions on “softer” drugs could represent a new era not just for Republican politics but also for American drug policy writ large. 

“With this imminent move, we are now confronted with the most pro-drug administration in our history,” Kevin Sabet, the CEO of the anti-legalization advocacy group Smart Approaches to Marijuana, said in a statement. “Policy is now being dictated by marijuana CEOs, psychedelics investors, and podcasters in active addiction — it is a travesty and injustice to the American people of unprecedented proportions. The marijuana industry is the new Big Tobacco, and President Trump is welcoming them to the homes of families across this country with open arms.”

Continue to STAT+ to read the full story…

Regenerative Medicine: Promise, Hype, and What Actually Works

From stem cells to platelet-rich plasma, regenerative medicine is often positioned as the future of healthcare. But not all approaches deliver on that promise. As interest grows, so do questions regarding what actually works. GEN’s Editor in Chief John Sterling spoke with Thomas Buchheit, MD, founder and medical director of the Triangle Regen Medicine and Biologics Center in Chapel Hill, NC, in relation to the science, the hype, and the realities shaping the field today.

 

GEN: How do you define regenerative medicine?

Buchheit: Many people think of regenerative medicine as growing new organs, but I define it more broadly as any therapy that improves tissue health or function. With that definition, we can include platelet-rich plasma (PRP), stem cells, and autologous conditioned serum (ACS). These approaches aim to enhance tissue health and improve function.

GEN: The field is promising, but also sometimes criticized as overhyped. Which areas deserve that criticism, and which have gained credibility through clinical validation?

Buchheit: Some criticism is valid, especially around stem cells. We’ve all seen claims over “miracle” stem cells that regrow cartilage. In reality, while these cells can be therapeutic, they typically don’t survive long after injection. Instead, they work by activating the body’s immune-based healing mechanisms. They can improve tissue health, but they’re not the miracle cures they were once portrayed to be.

On the other hand, therapies like PRP and ACS have gained credibility when properly applied and studied, particularly in musculoskeletal conditions.

GEN: How do you incorporate regenerative medicine into your practice?

Buchheit: I focus on patient function—what people can do now and what they want to achieve. Then tailor therapies accordingly. I prioritize treatments with strong evidence. One example is ACS, also known as the Regenokine* program. It’s highly standardized and supported by over 20 years of research in osteoarthritis, sciatica, and radiculopathy.

Thomas Buchheit, MD
Thomas Buchheit, MD

I also use PRP, which can be effective, but only when properly dosed. That’s been a major challenge since there are many ways to prepare PRP. We now know that dose matters. For example, treating knee osteoarthritis typically requires close to 10 billion platelets. At our clinic, we measure platelet counts before and after preparation to ensure accuracy, something often not done enough or at all.

GEN: Where did these approaches originate, and how widely are they used?

Buchheit: ACS originated in Germany in the 1990s with Dr. Peter Wehling. It was initially developed as an alternative to steroids for treating sciatica. The process involves incubating whole blood under controlled conditions, which stimulates the release of anti-inflammatory proteins, growth factors, and exosomes.

It became popular as patients, including athletes, traveled to Germany for treatment. Today, it’s available in the United States, though still more common in Europe. We now better understand how it works. Our research shows that exosomes play a key role in long-term benefits. If you remove them, effectiveness drops significantly.

GEN: Your new book Healing Joints and Nerves—who is it for?

Buchheit: It’s written for patients and a broad audience. I focused on authoring a book on regenerative medicine based on scientific accuracy and depth. I wanted to create a resource that explains these therapies clearly and truthfully—what they can and cannot do. It took over six years to complete. The book covers the history of stem cells and concludes with ACS, including both research and my personal experience with it as an avid runner and bicycle rider.

GEN: You often mention “good” vs. “bad” inflammation. What’s the difference?

Buchheit: Chronic inflammation is harmful. It damages tissue, drives pain, and contributes to diseases like osteoarthritis. But acute, controlled inflammation is essential for healing. It triggers the body’s repair processes. Exercise is a good example. It creates cycles of inflammation and recovery that make us stronger. Regenerative therapies aim to harness this same mechanism.

Interestingly, suppressing inflammation too aggressively can backfire. Studies show that patients who take anti-inflammatories after acute injuries may have a higher risk of chronic pain. Repeated steroid injections can also worsen joint damage over time.

GEN: Does all PRP work for osteoarthritis?

Buchheit: No. PRP must contain a sufficient platelet dose to be effective. Research shows that below approximately three billion platelets, it’s unlikely to work. Above four billion, effectiveness improves, and near 10 billion provides optimal results.

A practical tip: patients should ask how much blood is drawn. If only 10 mL is used to produce PRP, it’s mathematically impossible to achieve a high dose. Proper preparation typically requires 60–120 mL. Patients should also ask whether platelet counts are measured.

GEN: Please talk a bit more about Regenokine.

Buchheit: The program is based on ACS, enhanced through a controlled incubation process. This stimulates cells to release anti-inflammatory proteins, growth factors, and exosomes. Treatment typically takes roughly a week. Patients often come to the clinic for that duration. We’ve seen strong results in osteoarthritis and spine conditions, especially in patients who haven’t responded to other treatments, including stem cells.

GEN: What about safety, efficacy, and durability of results?

Buchheit: Outcomes vary by patient, but the primary goal is restoring function—whether that’s walking a dog or running a marathon. My approach is to stay as evidence-based as possible. That’s critical in a field where there is some overpromise or poorly validated treatments.

There are real concerns regarding product quality, sourcing, and transparency in some parts of the market. We need to know exactly what we’re using, how it works, and what evidence supports it. That’s how regenerative medicine will continue to advance responsibly.

Thomas Buchheit, MD, founded the Triangle Regen Medicine and Biologics Center in Chapel Hill, NC, to bring a range of regenerative therapies to patients. He now serves as an adjunct associate professor at Duke and continues to work with scientists at the Center for Translational Pain Medicine.

Buchheit began studying nerve injury pain and served as chief of pain medicine at Duke University Medical Center. He investigated the immune basis of pain relief following injury and the mechanisms behind regenerative therapies, including platelet-rich plasma, stem cells, and autologous conditioned serum. He has led several studies funded by the NIH and the Department of Defense.

*Regenokine was developed by Peter Wehling, MD, in Germany, originally in the 1990s. It utilizes a patient’s own blood to create a serum rich in anti-inflammatory proteins, particularly the interleukin 1 receptor antagonist (IL-1Ra), which helps reduce inflammation and promote healing in joints and tendons. The treatment is used for conditions like osteoarthritis and has gained popularity among athletes seeking pain relief. While it has shown promise in small studies, it is not yet FDA-approved and is not covered by insurance in the United States.

 

 

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Trelleborg Costa Rica site earns ISO 13485 certification

NEWS RELEASE: Trelleborg strengthens quality compliance with ISO certification in Costa Rica Plymouth, Minnesota — Trelleborg Medical Solutions’ manufacturing site in Costa Rica earns its ISO 13485:2016 certification helping ensure product consistency and compliance. ISO 13485:2016 is a process-focused quality framework that ensures medical devices are designed and manufactured under controlled conditions, risks to patients and…

The post Trelleborg Costa Rica site earns ISO 13485 certification appeared first on Medical Design and Outsourcing.

Stryker pay drops for top executives and the median employee

Stryker has disclosed lower compensation for its top executives and median employee in a recent filing with the U.S. Securities and Exchange Commission. Median employee pay dropped for the second consecutive year, while executive compensation decreased due to lower cash performance bonuses and option awards. Stryker was the world’s fifth-largest medical device company in our…

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How Geospatial Science is Reshaping Cancer Epidemiology: Three Perspectives from the Front Lines

The intersection of geography and oncology is no longer a speculative frontier—it is rapidly becoming the new standard in understanding who gets cancer, who survives it, and why. At a recent session at AACR 2026 bringing together leading researchers from the Fred Hutch Cancer Center, Harvard, and UCSF, the consensus was clear: geospatial methods are fundamentally altering how epidemiologists interrogate the cancer continuum, from incidence to mortality, from prevention to palliative care.

Trang VoPham, PhD, from Fred Hutch opened proceedings with a sweeping overview of how location data is being weaponized against cancer disparities. Her team’s work exemplifies the field’s evolution beyond crude ecological fallacies toward granular, individual-level exposure assessment. “We linked geospatial data on agricultural pesticide operations with all death certificates in the U.S. from 1989 to 2023,” she explained, detailing their findings that higher linuron use correlated with a 16% increased risk of colorectal cancer mortality among under-50s—higher than the 11% seen in older populations. The precision matters: “It is absolutely critical… can you access or generate residential address histories, not just baseline, not just at diagnosis, to consider life course exposures, timing of exposures, during relevant and critical time periods?”

Trang VoPham, PhD, Fred Hutch Cancer Center

VoPham’s lab is already translating these insights into population health interventions. Their GeoXMap web application—developed with community advisory boards across Washington State—enables neighborhood-level mapping of over 175 health variables, each paired with actionable mitigation strategies. “When you map radon, you can click on the tips button and see strategies for exposure mitigation, like where to get free radon test kits,” she noted. During 2023’s wildfire season, her team used Epic electronic health records to identify and contact 64,000 high-risk patients, resulting in over 4,000 same-day virtual primary care appointments. “This approach could absolutely be scaled to target other populations… to empower high-risk patients with information to help protect themselves from environmental hazards.”

Jaime Hart, ScD, from Harvard, shifted focus to the atmospheric dimensions of cancer risk, tracing how air pollution research has matured since IARC’s 2013 carcinogen declaration. She noted that evidence at the time was largely restricted to lung cancer data. Today, the picture has broadened considerably. Hart highlighted recent consortium work linking traffic-related nitrogen dioxide with premenopausal and Black women’s breast cancer risk—”mostly being driven by premenopausal breast cancer and breast cancer among Black women and non-Hispanic white women”—while PM2.5 associations remain more equivocal for this site.

Jaime Hart, ScD, Harvard T.H. Chan School of Public Health

The mechanistic sophistication has advanced in parallel. Hart detailed how particulate matter can “translocate across your lungs, get into your circulation and deposit in every tissue in your body,” even ascending the nasal pathway to breach the blood-brain barrier. Her collaboration with VoPham on wildfire-specific PM2.5 revealed that “even for the same increase in air pollution exposure… if that PM2.5 is coming more from wildfires than not, you saw an elevated risk,” suggesting source-specific toxicity profiles that carry profound regulatory implications.

Iona Cheng, PhD, from University of California, San Francisco, anchored the session in the structural determinants that underlie these spatial patterns. Her work on redlining—historical mortgage discrimination encoded into contemporary health disparities—demonstrates how geospatial tools can excavate systemic injustice. “In Detroit… about 70% [of non-Hispanic white men with prostate cancer] do live in an area that has not been redlined, in contrast to about 30%,” she reported, whereas “almost 60%” of African American patients resided in the most heavily denied neighborhoods. The mortality gradient was stark: “Higher prostate cancer mortality, or lower survival, associated with living in neighborhoods with more redlining, for both Black and white men.”

Iona Cheng, PhD, University of California, San Francisco

Cheng emphasized that these are not proxy measures for individual behavior but independent contextual effects. “We do see that the neighborhood itself has contributions,” she said, describing how her team is developing racially-ethnic-specific composite indices of structural racism across housing, education, employment, and judicial domains. The community-engaged methodology proved essential: working with Hawaiian advisory boards revealed that non-Hispanic white reference groups made little demographic sense for the islands, prompting recalibration.

The session closed with a palpable sense of acceleration. From Google’s nascent geospatial reasoning AI to wearable sensor validation of satellite models; from street-view imagery classifying 350 million U.S. locations to ecological momentary assessment tracking real-time exposures, the toolkit is expanding exponentially. As Hart observed: “The places where we live, work, and play influence our risk of cancer, impose diagnostic outcomes. There are robust biological mechanisms that underlie this.” The geospatial revolution in cancer epidemiology, it seems, is only getting started.

The post How Geospatial Science is Reshaping Cancer Epidemiology: Three Perspectives from the Front Lines appeared first on Inside Precision Medicine.

AACR 2026 Video Update: Cancer Research Edges Toward an AI-Driven Era

SAN DIEGO – At the American Association for Cancer Research (AACR) Annual Meeting 2026, the conversation around AI-driven cancer research has moved decisively past theory. Now the focus is on what’s being deployed and how to gain researchers’ and clinicians’ trust.

Fay Lin, PhD, senior editor, technology at GEN, and Jonathan D. Grinstein, PhD, North American editor at Inside Precision Medicine, discuss how AI is increasingly embedded across cancer research areas, from organoid models to pathology. Yet challenges such as data integration, longitudinal patient tracking, and clinician confidence continue to hinder its impact on patient outcomes.

Watch the full discussion below for a clearer view of the trends, tensions, and inflection points in AI shaping the future of cancer research:

 

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New ADC Yields Encouraging Clinical Benefit in Platinum-Resistant Ovarian Cancer

Patients with advanced platinum-resistant ovarian cancer whose disease had progressed on standard therapy experienced clinical benefit when treated with the investigational antibody-drug conjugate (ADC) QLS5132.

This finding is according to results from a Phase I clinical trial presented at the American Association for Cancer Research (AACR) Annual Meeting 2026, held in San Diego.

Patients diagnosed with platinum-resistant ovarian cancer face both a poor prognosis and limited treatment options, explained Tao Zhu, MD, chief physician and vice president of Zhejiang Cancer Hospital in China, who presented the study.

Zhu and collaborators tested an investigational ADC, QLS5132, which targets the protein CLDN6. QLS5132 combines a CLDN6-targeting monoclonal antibody with a cytotoxic payload, topoisomerase-1 inhibitor, at a drug-to-antibody ratio of 8:1. CLDN6, Zhu said, makes an ideal target as a protein with very high expression on the surface of ovarian cancer cells and minimal cell-surface expression in healthy tissues.

“The primary purpose of this first-in-human study was to evaluate the safety, tolerability, and pharmacokinetic profile of QLS5132 in patients with platinum-resistant ovarian cancer and determine the recommended Phase II dose for future clinical development,” Zhu said. “Additionally, we aimed to assess preliminary antitumor activity to establish an early signal of clinical benefit in this heavily pretreated population with limited options.”

The Phase I, single-arm, dose-escalation trial enrolled 28 patients with a median age of 57.5 who had been diagnosed with advanced platinum-resistant ovarian cancer and who had experienced progression while on standard therapy. The research team administered QLS5132 as an intravenous infusion every three weeks at dose levels of 1.6 mg/kg, 3.2 mg/kg, 4.8 mg/kg, 5.6 mg/kg, and 6.4 mg/kg.

Treatment-related adverse events (TRAEs) occurred in 26 (92.9%) patients, with nausea, anorexia, anemia, and weakness occurring most frequently. Nine (32.1%) patients experienced TRAEs of grade 3 or higher, and of those grade ≥3 TRAEs, seven were instances of hematological toxicity. No TRAEs led to treatment discontinuation or death, and no patients experienced interstitial lung disease, ocular toxicity, or febrile neutropenia, Zhu said.

After a median follow-up of 2.2 months, nine patients had a partial response at various dose levels. Two of these partial responses occurred in patients who had no detectable CLDN6 expression.

Across all dose levels, 18 evaluable patients experienced an objective response rate of 50% and a disease control rate of 94.4%. When calculated for the 17 evaluable patients who had received dose levels ≥3.2 mg/kg, the objective response rate and disease control rate rose to 52.9% and 100%, respectively. These responses to QLS5132 occurred irrespective of patients’ CLDN6 expression levels at baseline.

“The most encouraging finding from our study was that QLS5132 demonstrated compelling antitumor activity in patients with platinum-resistant ovarian cancer, with an objective response rate exceeding 50%,” said Zhu. “Equally important, at the potential recommended Phase II dose, we observed a favorable safety profile with no reported cases of interstitial lung disease, ocular toxicity, oral mucositis, or febrile neutropenia.”

Zhu also noted that, though more research would be needed to confirm, preliminary data indicated antitumor activity from QLS5132 regardless of CLDN6 expression levels—which, he said, could expand its potential as a treatment option to a broad cohort of patients with platinum-resistant ovarian cancer.

Zhu acknowledged that further research would be needed to fully understand why QLS5132 can have anticancer effects in patients with undetectable CLDN6 tumoral expression. But he suggested the phenomenon may have a few explanations, including tumor heterogeneity, as well as a potent bystander effect resulting in antitumor efficacy even in cells with low or no CLDN6 expression.

“These findings support the advancement of QLS5132 into Phase III studies, with the goal of providing a much-needed new treatment option for these patients,” said Zhu.

Some limitations of this study include a small sample size and an exploratory single-arm design.

This study was funded by Qilu Pharmaceutical. Zhu discloses no conflicts of interest.

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The Download: introducing the Nature issue

This is today’s edition of The Download, our weekday newsletter that provides a daily dose of what’s going on in the world of technology.

Introducing: the Nature issue

When we talk about “nature,” we usually mean something untouched by humans. But little of that world exists today. 

From microplastics in rainforest wildlife to artificial light in the Arctic Ocean, human influence now reaches every corner of Earth. In this context, what even is nature? And should we employ technology to try to make the world more “natural”?  

In our new Nature issue, MIT Technology Review grapples with these questions. We investigate birds that can’t sing, wolves that aren’t wolves, and grass that isn’t grass. We look for the meaning of life under Arctic ice, within ourselves, and in the far future on a distant world, courtesy of new fiction by the renowned author Jeff VanderMeer. 

Together, these stories examine how technology has altered our planet—and how it might be used to repair it. Subscribe now to read the full print issue.

What’s next for large language models?

After ChatGPT launched in late 2022, the OpenAI chatbot became an everyday everything app for hundreds of millions of people. It led to LLMs being heralded as the new future. The entire tech industry was consumed by the inferno, with companies racing to spin up rival products.

But what’s the next big thing after LLMs? More LLMs—but better. Let’s call them LLMs+. Find out how they’re set to become cheaper, more efficient, and more powerful.

—Will Douglas Heaven

LLMs+ is on our list of the 10 Things That Matter in AI Right Now, MIT Technology Review’s guide to what’s really worth your attention in the busy, buzzy world of AI. We’ll be unpacking one item from the list each day here in The Download, so stay tuned.

Will fusion power get cheap? Don’t count on it.

Fusion power could provide a steady, zero-emissions source of electricity in the future—if companies can get plants built and running. But a new study published in Nature Energy suggests that even if that future arrives, it might not come cheap.

The research team aimed to improve predictions of fusion’s future price by estimating the technology’s experience rate—the percentage by which its cost declines every time capacity doubles. Their findings offer new clues on the technology’s path to deployment. Read the full story.

—Casey Crownhart

This story is from The Spark, our weekly climate newsletter. Sign up to receive it in your inbox every Wednesday.

The must-reads

I’ve combed the internet to find you today’s most fun/important/scary/fascinating stories about technology.

1 Trump signaled he’s open to reversing the Anthropic ban
What that really means in practice remains to be seen. (Reuters $)
+ Anthropic says there’s no “kill switch” for its AI. (Axios)
+ “Humans in the loop” in AI warfare is an illusion. (MIT Technology Review)

2 SpaceX plans to manufacture its own GPUs
To support the company’s growing AI ambitions. (Reuters $)
+ Musk is shifting SpaceX’s focus from Mars to AI ahead of its IPO. (NYT $)
+ SpaceX and Tesla may be on a collision course. (FT $)

3 Chinese tech giant Tencent has unveiled its first flagship AI model
A former OpenAI researcher is at the helm. (SCMP)
+ Chinese open models are spreading fast. (MIT Technology Review)

4 High earners are racing ahead on AI, deepening workplace divides
The division in adoption risks widening inequality. (FT $)
+ Startups are bragging they spend more on AI than staff. (404 Media)

5 Thousands of Samsung workers are demanding a new share of AI profits
Chip-division employees want 15% of the operating profit. (Bloomberg $)
+ Here’s why opinion on AI is so divided. (MIT Technology Review)

6 AI is helping mediocre Korean hackers steal millions
They’re vibe coding their malware. (Wired $)
+ AI is making online crimes easier. (MIT Technology Review)

7 Kalshi suspended three political candidates for betting on their own races
Including a Democrat and a Republican running for Congress. (CNN)
+ And an independent candidate who said he did it to make a point. (Gizmodo)
+ Lawmakers argue that prediction markets are a loophole for gambling. (NPR)

8 A ping-pong robot is beating elite human players for the first time
The Sony AI system was trained with reinforcement learning. (New Scientist)
+ Just days earlier, a humanoid smashed the human half-marathon record. (AP)

9 Crypto scammers are luring ships into the Strait of Hormuz
By falsely promising safe passage. (Ars Technica)

10 ‘Age tech’ could help us grow old comfortably at home
Apps, wearables, and remote monitoring could fill caregiving gaps. (NYT $)

 

Quote of the day

“It’s a hallucinogenic business plan.”

—Ross Gerber, the chief executive of Gerber Kawasaki, an investment firm that owns SpaceX shares, tells the New York Times that he’s unimpressed by Musk’s changing goals for the aerospace company. 

One More Thing

Photos of victims are displayed under white crosses at a memorial for the August 2023 wildfire victims

AP PHOTO/LINDSEY WASSON


This grim but revolutionary DNA technology is changing how we respond to mass disasters

After hundreds went missing in Maui’s deadly fires, victims were identified with rapid DNA analysis—an increasingly vital tool for putting names to the dead in mass-casualty events.

The technology helped identify victims within just a few hours and bring families some closure more quickly than ever before. But it also previews a dark future marked by the rising frequency of catastrophic events.

Find out how this forensic breakthrough is preparing us for a more volatile world.


—Erika Hayasaki

We can still have nice things

A place for comfort, fun and distraction to brighten up your day. (Got any ideas? Drop me a line.)

+ This fascinating dive into botanical history reveals the origins of the first true plants.
+ Here’s how to use Google’s reference desk to find what ordinary search engines miss.
+ Watch duct tape get deconstructed to reveal the physics behind its legendary stickiness.
+ When Radiohead covers Joy Division, the result is a beautiful intersection of two legendary musical eras.