Michael Kratsios testified Tuesday before the Senate Commerce, Science and Transportation Committee.

The administration’s moves to slash Forest Service personnel and pause wildfire-related grants have left states to pick up the pieces on prevention and mitigation.

The 2040 target “will be presented soon,” said a European Commission spokesperson.

One German aluminum factory decided to go green and close its smelter. The EU faces a similar choice, with Europe’s future at stake.

The discussion in Rome will focus on how to spend what’s been pledged so far and how to raise a lot more to help preserve plant and animal life on Earth.

About 60 percent of all cancer patients in the United States receive radiation therapy as part of their treatment. However, this radiation can have severe side effects that often end up being too difficult for patients to tolerate.

Drawing inspiration from a tiny organism that can withstand huge amounts of radiation, researchers at MIT, Brigham and Women’s Hospital, and the University of Iowa have developed a new strategy that may protect patients from this kind of damage. Their approach makes use of a protein from tardigrades, often also called “water bears,” which are usually less than a millimeter in length.

When the researchers injected messenger RNA encoding this protein into mice, they found that it generated enough protein to protect cells’ DNA from radiation-induced damage. If developed for use in humans, this approach could benefit many cancer patients, the researchers say.

“Radiation can be very helpful for many tumors, but we also recognize that the side effects can be limiting. There’s an unmet need with respect to helping patients mitigate the risk of damaging adjacent tissue,” says Giovanni Traverso, an associate professor of mechanical engineering at MIT and a gastroenterologist at Brigham and Women’s Hospital.

Traverso and James Byrne, an assistant professor of radiation oncology at the University of Iowa, are the senior authors of the study, which appears today in Nature Biomedical Engineering. The paper’s lead authors are Ameya Kirtane, an instructor in medicine at Harvard Medical School and a visiting scientist at MIT’s Koch Institute for Integrative Cancer Research, and Jianling Bi, a research scientist at the University of Iowa.

Extreme survival

Radiation is often used to treat cancers of the head and neck, where it can damage the mouth or throat, making it very painful to eat or drink. It is also commonly used for gastrointestinal cancers, which can lead to rectal bleeding. Many patients end up delaying treatments or stopping them altogether.

“This affects a huge number of patients, and it can manifest as something as simple as mouth sores, which can limit a person’s ability to eat because it’s so painful, to requiring hospitalization because people are suffering so terribly from the pain, weight loss, or bleeding. It can be pretty dangerous, and it’s something that we really wanted to try and address,” Byrne says.

Currently, there are very few ways to prevent radiation damage in cancer patients. There are a handful of drugs that can be given to try to reduce the damage, and for prostate cancer patients, a hydrogel can be used to create a physical barrier between the prostate and the rectum during radiation treatment.

For several years, Traverso and Byrne have been working on developing new ways to prevent radiation damage. In the new study, they were inspired by the extraordinary survival ability of tardigrades. Found all over the world, usually in aquatic environments, these organisms are well known for their resilience to extreme conditions. Scientists have even sent them into space, where they were shown to survive extreme dehydration and cosmic radiation.

One key component of tardigrades’ defense systems is a unique damage suppressor protein called Dsup, which binds to DNA and helps protect it from radiation-induced damage. This protein plays a major role in tardigrades’ ability to survive radiation doses 2,000 to 3,000 times higher than what a human being can tolerate.

When brainstorming ideas for novel ways to protect cancer patients from radiation, the researchers wondered if they might be able to deliver messenger RNA encoding Dsup to patient tissues before radiation treatment. This mRNA would trigger cells to transiently express the protein, protecting DNA during the treatment. After a few hours, the mRNA and protein would disappear.

For this to work, the researchers needed a way to deliver mRNA that would generate large amounts of protein in the target tissues. They screened libraries of delivery particles containing both polymer and lipid components, which have been used separately to achieve efficient mRNA delivery. From these screens, they identified one polymer-lipid particle that was best-suited for delivery to the colon, and another that was optimized to deliver mRNA to mouth tissue.

“We thought that perhaps by combining these two systems — polymers and lipids — we may be able to get the best of both worlds and get highly potent RNA delivery. And that’s essentially what we saw,” Kirtane says. “One of the strengths of our approach is that we are using a messenger RNA, which just temporarily expresses the protein, so it’s considered far safer than something like DNA, which may be incorporated into the cells’ genome.”

Protection from radiation

After showing that these particles could successfully deliver mRNA to cells grown in the lab, the researchers tested whether this approach could effectively protect tissue from radiation in a mouse model.

They injected the particles into either the cheek or the rectum several hours before giving a dose of radiation similar to what cancer patients would receive. In these mice, the researchers saw a 50 percent reduction in the amount of double-stranded DNA breaks caused by radiation.

“This study shows great promise and is a really novel idea leveraging natural mechanisms of protection again DNA damage for the purpose of protecting healthy cells during radiation treatments for cancer,” says Ben Ho Park, director of the Vanderbilt-Ingram Cancer Center at Vanderbilt University Medical Center, who was not involved in the study.

The researchers also showed that the protective effect of the Dsup protein did not spread beyond the injection site, which is important because they don’t want to protect the tumor itself from the effects of radiation. To make this treatment more feasible for potential use in humans, the researchers now plan to work on developing a version of the Dsup protein that would not provoke an immune response, as the original tardigrade protein likely would.

If developed for use in humans, this protein could also potentially be used to protect against DNA damage caused by chemotherapy drugs, the researchers say. Another possible application would be to help prevent radiation damage in astronauts in space.

Other authors of the paper include Netra Rajesh, Chaoyang Tang, Miguel Jimenez, Emily Witt, Megan McGovern, Arielle Cafi, Samual Hatfield, Lauren Rosenstock, Sarah Becker, Nicole Machado, Veena Venkatachalam, Dylan Freitas, Xisha Huang, Alvin Chan, Aaron Lopes, Hyunjoon Kim, Nayoon Kim, Joy Collins, Michelle Howard, Srija Manchkanti, and Theodore Hong.

The research was funded by the Prostate Cancer Foundation Young Investigator Award, the U.S. Department of Defense Prostate Cancer Program Early Investigator Award, a Hope Funds for Cancer Research Fellowship, the American Cancer Society, the National Cancer Institute, MIT’s Department of Mechanical Engineering, and the U.S. Advanced Research Projects Agency for Health. 

In addition to patrolling the body for foreign invaders, the immune system also hunts down and destroys cells that have become cancerous or precancerous. However, some cancer cells end up evading this surveillance and growing into tumors.

Once established, tumor cells often send out immunosuppressive signals, which leads T cells to become “exhausted” and unable to attack the tumor. In recent years, some cancer immunotherapy drugs have shown great success in rejuvenating those T cells so they can begin attacking tumors again.

While this approach has proven effective against cancers such as melanoma, it doesn’t work as well for others, including lung and ovarian cancer. MIT Associate Professor Stefani Spranger is trying to figure out how those tumors are able to suppress immune responses, in hopes of finding new ways to galvanize T cells into attacking them.

“We really want to understand why our immune system fails to recognize cancer,” Spranger says. “And I’m most excited about the really hard-to-treat cancers because I think that’s where we can make the biggest leaps.”

Her work has led to a better understanding of the factors that control T-cell responses to tumors, and raised the possibility of improving those responses through vaccination or treatment with immune-stimulating molecules called cytokines.

“We’re working on understanding what exactly the problem is, and then collaborating with engineers to find a good solution,” she says.

Jumpstarting T cells

As a student in Germany, where students often have to choose their college major while still in high school, Spranger envisioned going into the pharmaceutical industry and chose to major in biology. At Ludwig Maximilian University in Munich, her course of study began with classical biology subjects such as botany and zoology, and she began to doubt her choice. But, once she began taking courses in cell biology and immunology, her interest was revived and she continued into a biology graduate program at the university.

During a paper discussion class early in her graduate school program, Spranger was assigned to a Science paper on a promising new immunotherapy treatment for melanoma. This strategy involves isolating tumor-infiltrating T-cells during surgery, growing them into large numbers, and then returning them to the patient. For more than 50 percent of those patients, the tumors were completely eliminated.

“To me, that changed the world,” Spranger recalls. “You can take the patient’s own immune system, not really do all that much to it, and then the cancer goes away.”

Spranger completed her PhD studies in a lab that worked on further developing that approach, known as adoptive T-cell transfer therapy. At that point, she still was leaning toward going into pharma, but after finishing her PhD in 2011, her husband, also a biologist, convinced her that they should both apply for postdoc positions in the United States.

They ended up at the University of Chicago, where Spranger worked in a lab that studies how the immune system responds to tumors. There, she discovered that while melanoma is usually very responsive to immunotherapy, there is a small fraction of melanoma patients whose T cells don’t respond to the therapy at all. That got her interested in trying to figure out why the immune system doesn’t always respond to cancer the way that it should, and in finding ways to jumpstart it.

During her postdoc, Spranger also discovered that she enjoyed mentoring students, which she hadn’t done as a graduate student in Germany. That experience drew her away from going into the pharmaceutical industry, in favor of a career in academia.

“I had my first mentoring teaching experience having an undergrad in the lab, and seeing that person grow as a scientist, from barely asking questions to running full experiments and coming up with hypotheses, changed how I approached science and my view of what academia should be for,” she says.

Modeling the immune system

When applying for faculty jobs, Spranger was drawn to MIT by the collaborative environment of MIT and its Koch Institute for Integrative Cancer Research, which offered the chance to collaborate with a large community of engineers who work in the field of immunology.

“That community is so vibrant, and it’s amazing to be a part of it,” she says.

Building on the research she had done as a postdoc, Spranger wanted to explore why some tumors respond well to immunotherapy, while others do not. For many of her early studies, she used a mouse model of non-small-cell lung cancer. In human patients, the majority of these tumors do not respond well to immunotherapy.

“We build model systems that resemble each of the different subsets of non-responsive non-small cell lung cancer, and we’re trying to really drill down to the mechanism of why the immune system is not appropriately responding,” she says.

As part of that work, she has investigated why the immune system behaves differently in different types of tissue. While immunotherapy drugs called checkpoint inhibitors can stimulate a strong T-cell response in the skin, they don’t do nearly as much in the lung. However, Spranger has shown that T cell responses in the lung can be improved when immune molecules called cytokines are also given along with the checkpoint inhibitor.

Those cytokines work, in part, by activating dendritic cells — a class of immune cells that help to initiate immune responses, including activation of T cells.

“Dendritic cells are the conductor for the orchestra of all the T cells, although they’re a very sparse cell population,” Spranger says. “They can communicate which type of danger they sense from stressed cells and then instruct the T cells on what they have to do and where they have to go.”

Spranger’s lab is now beginning to study other types of tumors that don’t respond at all to immunotherapy, including ovarian cancer and glioblastoma. Both the brain and the peritoneal cavity appear to suppress T-cell responses to tumors, and Spranger hopes to figure out how to overcome that immunosuppression.

“We’re specifically focusing on ovarian cancer and glioblastoma, because nothing’s working right now for those cancers,” she says. “We want to understand what we have to do in those sites to induce a really good anti-tumor immune response.”

UK Prime Minister Keir Starmer made a public commitment on February 14 to Laila Soueif, the mother of Alaa Abd El Fattah, stating “I will do all that I can to secure the release of her son Alaa Abd el-Fattah and reunite him with his family.” While that commitment was welcomed by the family, it is imperative that it now be followed up with concrete action.

Laila has called on PM Starmer to speak directly to President Sisi of Egypt. Starmer has written to Sisi twice, in December and January, and his National Security Adviser, Jonathan Powell, discussed Alaa with Egyptian authorities in Cairo on January 2. UK authorities have not made public any further contact with Egypt since.

“all she wants is for [Alaa] to be free now that he served the full five year sentence, and after they stole 11 years of his and [his son] Khaled’s life.”

Laila, who has been on hunger strike since Alaa’s intended release date in September, was hospitalized on Monday night after her blood sugar dropped to worrying new levels. A letter published today from her NHS doctor states that there is now immediate risk to her life including further deterioration or death. Nevertheless, Laila remains steadfast in her commitment to refrain from eating until her son is freed.

In the words of Alaa’s sister Mona Seif: “all she wants is for [Alaa] to be free now that he served the full five year sentence, and after they stole 11 years of his and [his son] Khaled’s life.”

Alaa is a British citizen, and as such his government owes him more than mere lip service. The UK government can and must use every tactic available to them, including:

• Changing travel advice on the Foreign Office’s website to reflect the fact that citizens arrested in Egypt cannot be guaranteed consular access
• Convening a joint meeting of ministers and officials of the Foreign, Commonwealth and Development Office; Ministry of Defence; and Department of Business and Trade to discuss a unified strategy toward Alaa’s case
• Summoning the Egyptian ambassador in London and restricting his access to Whitehall if Alaa is not released and returned to the UK
• Announcing a moratorium on any governmental assistance or promotion of new Foreign Direct Investments into Egypt, as called for by 15 NGOs in November.

EFF once again calls on Prime Minister Starmer to pick up the phone and call Egyptian President Sisi to free Alaa and save Laila—before it’s too late.

Earlier this month, the Senate passed the TAKE IT DOWN Act (S. 146), by a voice vote. The bill is meant to speed up the removal of non-consensual intimate imagery, or NCII, including videos that imitate real people, a technology sometimes called “deepfakes.” 

Protecting victims of these heinous privacy invasions is a legitimate goal. But good intentions alone are not enough to make good policy. As currently drafted, the TAKE IT DOWN Act mandates a notice-and-takedown system that threatens free expression, user privacy, and due process, without addressing the problem it claims to solve. 

This misguided bill can still be stopped in the House of Representatives. Help us speak out against it now. 

take action

"Take It Down" Has No real Safeguards  

Before this vote, EFF, along with the Center for Democracy & Technology (CDT), Authors Guild, Demand Progress Action, Fight for the Future, Freedom of the Press Foundation, New America’s Open Technology Institute, Public Knowledge, Restore The Fourth, SIECUS: Sex Ed for Social Change, TechFreedom, and Woodhull Freedom Foundation, sent a letter to the Senate, asking them to change this legislation to protect legitimate speech that is not NCII. Changes are also needed to protect users who rely on encrypted services.

The letter explains that the bill’s “takedown” provision applies to a much broader category of content—potentially any images involving intimate or sexual content at all—than the narrower NCII definitions found elsewhere in the bill. The bill contains no protections against frivolous or bad-faith takedown requests. Lawful content—including satire, journalism, and political speech—could be wrongly censored. The legislation requires that apps and websites remove content within 48 hours, meaning that online service providers, particularly smaller ones, will have to comply so quickly to avoid legal risk that they won’t be able to verify claims

This would likely lead to the use of often-inaccurate automated filters that are infamous for flagging legal content, from fair-use commentary to news reporting. Communications providers that offer users end-to-end encrypted messaging, meanwhile, may be served with notices they simply cannot comply with, given the fact that these providers cannot view the contents of messages on their platforms. Platforms may respond by abandoning encryption entirely in order to be able to monitor content—turning private conversations into surveilled spaces. 

Congress should focus on enforcing and improving the many existing civil and criminal laws that address NCII, rather than opting for a broad takedown regime that is bound to be abused. Tell your Member of Congress to oppose censorship and to oppose S. 146. 

take action

Tell the house to stop "Take it down" 

Further reading:

• EFF and allies letter opposing S. 146, the TAKE IT DOWN Act. 

It looks like a very sophisticated attack against the Dubai-based exchange Bybit:

Bybit officials disclosed the theft of more than 400,000 ethereum and staked ethereum coins just hours after it occurred. The notification said the digital loot had been stored in a “Multisig Cold Wallet” when, somehow, it was transferred to one of the exchange’s hot wallets. From there, the cryptocurrency was transferred out of Bybit altogether and into wallets controlled by the unknown attackers.

[…]

…a subsequent investigation by Safe found no signs of unauthorized access to its infrastructure, no compromises of other Safe wallets, and no obvious vulnerabilities in the Safe codebase. As investigators continued to dig in, they finally settled on the true cause. Bybit ultimately said that the fraudulent transaction was “manipulated by a sophisticated attack that altered the smart contract logic and masked the signing interface, enabling the attacker to gain control of the ETH Cold Wallet.”...

With the rise of digital surveillance, securing our health data is no longer just a privacy issue—it's a matter of personal safety. In the wake of the Supreme Court's reversal of Roe v. Wade and the growing restrictions on abortion and gender-affirming care, protecting our personal health data has never been more important. And in a world where nearly half of U.S. states have either banned or are on the brink of banning abortion, unfettered access to personal health data is an even more dangerous threat.

That’s why EFF joins the New York Civil Liberties Union (NYCLU) in urging Governor Hochul to sign the New York Health Information Privacy Act (A.2141/S.929). This legislation is a crucial step toward safeguarding the digital privacy of New Yorkers at a time when health data is increasingly vulnerable to misuse.

Why Health Data Privacy Matters

When individuals seek reproductive health care or gender-affirming care, they leave behind a digital trail. Whether through search histories, email exchanges, travel itineraries, or data from period-tracker apps and smartwatches, every click, every action, and every step is tracked, often with little or no consent. And this kind of data—however collected—has already been used to criminalize individuals who were simply seeking health care. 

Unlike HIPAA, which regulates 'covered entities'—providers of treatment, payors/insurers—who are part of the traditional health care system and their ‘business associates,’ this bill would expand its reach to cover a broad range of 'new' entities. These include data brokers, tech companies, and others in the digital ecosystem, who can access and share this sensitive health information. The result is a growing web of entities collecting personal data, far beyond the scope of traditional health care providers.

For example, in some states, individuals have been investigated or even prosecuted based on their digital data, simply for obtaining abortion care. In a world where our health choices are increasingly monitored, the need for robust privacy protections is clearer than ever. The New York Health Information Privacy Act is the Empire State’s opportunity to lead the nation in protecting its residents.

What Does the Health Information Privacy Act Do?

At its core, the New York Health Information Privacy Act would provide vital protections for New Yorkers' electronic health data. Here’s what the bill does:

• Prohibits the sale of health data: Health data is not a commodity to be bought and sold. This bill ensures that your most personal information is not used for profit by commercial entities without your consent.
• Requires explicit consent: Before health data is processed, New Yorkers will need to provide clear, informed consent. The bill limits processing (storing, collecting, using) of personal data to “strictly necessary” purposes only, minimizing unnecessary collection.
• Data deletion rights: Health data will be deleted by default after 60 days, unless the individual requests otherwise. This empowers individuals to control their data, ensuring that unnecessary information doesn’t linger.
• Non-discrimination protections: Individuals will not face discrimination or higher costs for exercising their privacy rights. No one should be penalized for wanting to protect their personal information.

Why New York Needs This Bill Now

The need for these protections is urgent. As digital surveillance expands, so does the risk of personal health data being used against individuals. In a time when personal health decisions are under attack, it’s crucial that New Yorkers have control over their health information. By signing this bill, Governor Hochul would ensure that out-of-state actors cannot easily access New Yorkers’ health data without due process, protecting individuals from legal actions in states that criminalize reproductive and gender-affirming care.

However, this bill still faces a critical shortcoming—the absence of a private right of action (PRA). Without it, individuals cannot directly sue companies for privacy violations, leaving them vulnerable. Accountability would fall solely on the Attorney General, who would need the resources to quickly and consistently enforce the new law. Nonetheless, the Attorney General’s role will now be critical in ensuring this bill is upheld, and they must remain steadfast in implementing these protections effectively.

Governor Hochul: Sign A.2141/S.929

The importance of this legislation cannot be overstated—it is about protecting people from potential legal actions related to their health care decisions. By signing this bill, Governor Hochul would solidify New York’s position as a leader in health data privacy and take a firm stand against the misuse of personal information.

New York has the power to protect its residents and set a strong precedent for privacy protections across the nation. Let’s ensure that personal health data remains in the hands of those who own it—the individuals themselves.

Governor Hochul: This is your chance to make a difference. Let’s take action now to protect what matters most—our health, our data, and our rights. Sign A.2141/ S.929 today.

The bonds are considered a safe investment. The Los Angeles wildfires sparked concern that climate change is making them risky.

Graham Allen has called climate change an “attempt of the left to spin FEAR.” He also says Taylor Swift is a witch who attracted fans through “some kind of satanic music.”

The fund shows the aviation industry's interest in technology that uses fans, carbon-absorbing materials, heat and electricity to scrub CO2 from the skies.

“We have an obligation to fulfill” the grant agreement, Power Forward Communities CEO Tim Mayopoulos said in an interview with POLITICO.

EPA has been silent about the frozen funds. Nonprofit grant recipients say the agency and bank have been mum about what's happening.

The former Argus Insight leaders have taken key roles at the Republican National Committee and the White House.

The push by the Trump administration creates a “big risk” for financial stability, said Bank of France Gov. Francois Villeroy de Galhau.

A formal proposal to amend overarching climate law will accompany the Clean Industrial Deal.

The EU’s Carbon Border Adjustment Mechanism is currently set to go into full effect in 2026.