Catherine McKenna says the Paris Agreement was an incredible feat. “Now: Do the work.”

U.S. withdrawal from the Paris climate agreement would erase another 0.1 C of progress.

Diet is the main factor to consider, but the type of pet, its breed and where it came from all affect its impact.

“We have received so many calls from people asking us to rescue them from roofs and from their houses, but it’s impossible,” said the Philippine Red Cross secretary-general.

What if clinicians could place tiny electronic chips in the brain that electrically stimulate a precise target, through a simple injection in the arm? This may someday help treat deadly or debilitating brain diseases, while eliminating surgery-related risks and costs.

MIT researchers have taken a major step toward making this scenario a reality. They developed microscopic, wireless bioelectronics that could travel through the body’s circulatory system and autonomously self-implant in a target region of the brain, where they would provide focused treatment.

In a study on mice, the researchers show that after injection, these miniscule implants can identify and travel to a specific brain region without the need for human guidance. Once there, they can be wirelessly powered to provide electrical stimulation to the precise area. Such stimulation, known as neuromodulation, has shown promise as a way to treat brain tumors and diseases like Alzheimer’s and multiple sclerosis.

Moreover, because the electronic devices are integrated with living, biological cells before being injected, they are not attacked by the body’s immune system and can cross the blood-brain barrier while leaving it intact. This maintains the barrier’s crucial protection of the brain.

The researchers demonstrated the use of this technology, which they call “circulatronics,” to target brain inflammation, a major factor in the progression of many neurological diseases. They show that the implants can provide localized neuromodulation deep inside the brain achieving high precision, to within several microns around the target area.

In addition, the biocompatible implants do not damage surrounding neurons.

While brain implants usually require hundreds of thousands of dollars in medical costs and risky surgical procedures, circulatronics technology holds the potential to make therapeutic brain implants accessible to all by eliminating the need for surgery, says Deblina Sarkar, the AT&T Career Development Associate Professor in the MIT Media Lab and MIT Center for Neurobiological Engineering, head of the Nano-Cybernetic Biotrek Lab, and senior author of a study on the work.

She is joined on the paper by lead author Shubham Yadav, an MIT graduate student; as well as others at MIT, Wellesley College, and Harvard University. The research appears today in Nature Biotechnology.

Hybrid implants

The team has been working on circulatronics for more than six years. The electronic devices, each about one-billionth the length of a grain of rice, are composed of organic semiconducting polymer layers sandwiched between metallic layers to create an electronic heterostructure.

They are fabricated using CMOS-compatible processes in the MIT.nano facilities, and then integrated with living cells to create cell-electronics hybrids. To do this, the researchers lift the devices off the silicon wafer on which they are fabricated, so they are free-floating in a solution.

“The electronics worked perfectly when they were attached to the substrate, but when we originally lifted them off, they didn’t work anymore. Solving that challenge took us more than a year,” Sarkar says.

Key to their operation is the high wireless power conversion efficiency of the tiny electronics. This enables the devices to work deep inside the brain and still harness enough energy for neuromodulation.

The researchers use a chemical reaction to bond the electronic devices to cells. In the new study, they fused the electronics with a type of immune cell called monocytes, which target areas of inflammation in the body. They also applied a fluorescent dye, allowing them to trace the devices as they crossed the intact blood-brain barrier and self-implanted in the target brain region.

While they explored brain inflammation in this study, the researchers hope to use different cell types and engineer the cells to target specific regions of the brain.

“Our cell-electronics hybrid fuses the versatility of electronics with the biological transport and biochemical sensing prowess of living cells,” Sarkar says. “The living cells camouflage the electronics so that they aren’t attacked by the body’s immune system and they can travel seamlessly through the bloodstream. This also enables them to squeeze through the intact blood-brain barrier without the need to invasively open it.”

Over the course of about four years, the team tried many methods to autonomously and noninvasively cross the blood-brain barrier before they perfected this cellular integration technique.

In addition, because the circulatronics devices are so tiny, they offer much higher precision than conventional electrodes. They can self-implant, leading to millions of microscopic stimulation sites that take the exact shape of the target region.

Their small size also enables the biocompatible devices to live alongside neurons without causing harmful effects. Through a series of biocompatibility tests, the researchers found that circulatronics can safely integrate among neurons without impacting the brain processes behind cognition or motion.

After the devices have self-implanted in the target region, a clinician or researcher uses an external transmitter to provide electromagnetic waves, in the form of near-infrared light, that power the technology and enable electrical stimulation of the neurons.

Targeting deadly diseases

The Sarkar lab is currently working on developing their technology to treat multiple diseases including brain cancer, Alzheimer’s disease, and chronic pain.

The tiny size and self-implantation capabilities of circulatronics devices could make them well-suited to treat brain cancers such as glioblastoma that cause tumors at multiple locations, some of which may be too small to identify with imaging techniques. They may also provide new avenues for treating especially deadly cancers like diffuse intrinsic pontine glioma, an aggressive type of tumor found in the brain stem that usually cannot be surgically removed.

“This is a platform technology and may be employed to treat multiple brain diseases and mental illnesses,” Sarkar says. “Also, this technology is not just confined to the brain but could also be extended to other parts of the body in future.”

The researchers hope to move the technology into clinical trials within three years through the recently launched startup Cahira Technologies.

They are also exploring integration of additional nanoelectronic circuits into their devices to enable functionalities including sensing, feedback based on-chip data analysis, and capabilities such as creating synthetic electronic neurons.

“Our tiny electronic devices seamlessly integrate with the neurons and co-live and co-exist with the brain cells creating a unique brain-computer symbiosis. We are working dedicatedly to employ this technology for treating neural diseases, where drugs or standard therapies fail, for alleviating human suffering and envision a future where humans could transcend beyond diseases and biological limitations,” says Sarkar.

One of the highest-risk components of nuclear waste is iodine-129 (I-129), which stays radioactive for millions of years and accumulates in human thyroids when ingested. In the U.S., nuclear waste containing I-129 is scheduled to be disposed of in deep underground repositories, which scientists say will sufficiently isolate it.

Meanwhile, across the globe, France routinely releases low-level radioactive effluents containing iodine-129 and other radionuclides into the ocean. France recycles its spent nuclear fuel, and the reprocessing plant discharges about 153 kilograms of iodine-129 each year, under the French regulatory limit.

Is dilution a good solution? What’s the best way to handle spent nuclear fuel? A new study by MIT researchers and their collaborators at national laboratories quantifies I-129 release under three different scenarios: the U.S. approach of disposing spent fuel directly in deep underground repositories, the French approach of dilution and release, and an approach that uses filters to capture I-129 and disposes of them in shallow underground waste repositories.

The researchers found France’s current practice of reprocessing releases about 90 percent of the waste’s I-129 into the biosphere. They found low levels of I-129 in ocean water around France and the U.K.’s former reprocessing sites, including the English Channel and North Sea. Although the low level of I-129 in the water in Europe is not considered to pose health risks, the U.S. approach of deep underground disposal leads to far less I-129 being released, the researchers found.

The researchers also investigated the effect of environmental regulations and technologies related to I-129 management, to illuminate the tradeoffs associated with different approaches around the world.

“Putting these pieces together to provide a comprehensive view of Iodine-129 is important,” says MIT Assistant Professor Haruko Wainwright, a first author on the paper who holds a joint appointment in the departments of Nuclear Science and Engineering and of Civil and Environmental Engineering. “There are scientists that spend their lives trying to clean up iodine-129 at contaminated sites. These scientists are sometimes shocked to learn some countries are releasing so much iodine-129. This work also provides a life-cycle perspective. We’re not just looking at final disposal and solid waste, but also when and where release is happening. It puts all the pieces together.”

MIT graduate student Kate Whiteaker SM ’24 led many of the analyses with Wainwright. Their co-authors are Hansell Gonzalez-Raymat, Miles Denham, Ian Pegg, Daniel Kaplan, Nikolla Qafoku, David Wilson, Shelly Wilson, and Carol Eddy-Dilek. The study appears today in Nature Sustainability.

Managing waste

Iodine-129 is often a key focus for scientists and engineers as they conduct safety assessments of nuclear waste disposal sites around the world. It has a half-life of 15.7 million years, high environmental mobility, and could potentially cause cancers if ingested. The U.S. sets a strict limit on how much I-129 can be released and how much I-129 can be in drinking water — 5.66 nanograms per liter, the lowest such level of any radionuclides.

“Iodine-129 is very mobile, so it is usually the highest-dose contributor in safety assessments,” Wainwright says.

For the study, the researchers calculated the release of I-129 across three different waste management strategies by combining data from current and former reprocessing sites as well as repository assessment models and simulations.

The authors defined the environmental impact as the release of I-129 into the biosphere that humans could be exposed to, as well as its concentrations in surface water. They measured I-129 release per the total electrical energy generated by a 1-gigawatt power plant over one year, denoted as kg/GWe.y.

Under the U.S. approach of deep underground disposal with barrier systems, assuming the barrier canisters fail at 1,000 years (a conservative estimate), the researchers found 2.14 x 10–8 kg/GWe.y of I-129 would be released between 1,000 and 1 million years from today.

They estimate that 4.51 kg/GWe.y of I-129, or 91 percent of the total, would be released into the biosphere in the scenario where fuel is reprocessed and the effluents are diluted and released. About 3.3 percent of I-129 is captured by gas filters, which are then disposed of in shallow subsurfaces as low-level radioactive waste. A further 5.2 percent remains in the waste stream of the reprocessing plant, which is then disposed of as high-level radioactive waste.

If the waste is recycled with gas filters to directly capture I-129, 0.05 kg/GWe.y of the I-129 is released, while 94 percent is disposed of in the low-level disposal sites. For shallow disposal, some kind of human disruption and intrusion is assumed to occur after government or institutional control expires (typically 100-1,000 years). That results in a potential release of the disposed amount to the environment after the control period.

Overall, the current practice of recycling spent nuclear fuel releases the majority of I-129 into the environment today, while the direct disposal of spent fuel releases around 1/100,000,000 that amount over 1 million years. When the gas filters are used to capture I-129, the majority of I-129 goes to shallow underground repositories, which could be accidentally released through human intrusion down the line.

The researchers also quantified the concentration of I-129 in different surface waters near current and former fuel reprocessing facilities, including the English Channel and the North Sea near reprocessing plants in France and U.K. They also analyzed the U.S. Columbia River downstream of a site in Washington state where material for nuclear weapons was produced during the Cold War, and they studied a similar site in South Carolina. The researchers found far higher concentrations of I-129 within the South Carolina site, where the low-level radioactive effluents were released far from major rivers and hence resulted in less dilution in the environment.

“We wanted to quantify the environmental factors and the impact of dilution, which in this case affected concentrations more than discharge amounts,” Wainwright says. “Someone might take our results to say dilution still works: It’s reducing the contaminant concentration and spreading it over a large area. On the other hand, in the U.S., imperfect disposal has led to locally higher surface water concentrations. This provides a cautionary tale that disposal could concentrate contaminants, and should be carefully designed to protect local communities.”

Fuel cycles and policy

Wainwright doesn’t want her findings to dissuade countries from recycling nuclear fuel. She says countries like Japan plan to use increased filtration to capture I-129 when they reprocess spent fuel. Filters with I-129 can be disposed of as low-level waste under U.S. regulations.

“Since I-129 is an internal carcinogen without strong penetrating radiation, shallow underground disposal would be appropriate in line with other hazardous waste,” Wainwright says. “The history of environmental protection since the 1960s is shifting from waste dumping and release to isolation. But there are still industries that release waste into the air and water. We have seen that they often end up causing issues in our daily life — such as CO2, mercury, PFAS and others — especially when there are many sources or when bioaccumulation happens. The nuclear community has been leading in waste isolation strategies and technologies since the 1950s. These efforts should be further enhanced and accelerated. But at the same time, if someone does not choose nuclear energy because of waste issues, it would encourage other industries with much lower environmental standards.”

The work was supported by MIT’s Climate Fast Forward Faculty Fund and the U.S. Department of Energy.

Nature Climate Change, Published online: 05 November 2025; doi:10.1038/s41558-025-02473-0

A decade ago, the Paris Agreement was adopted, which was a landmark for international climate governance. In this infographic, we reflect on the progress that has been made as well as some of the challenges that still lie ahead, such as policy agenda, social change and technology development.

Nature Climate Change, Published online: 05 November 2025; doi:10.1038/s41558-025-02488-7

Microbes wake up

Nature Climate Change, Published online: 05 November 2025; doi:10.1038/s41558-025-02490-z

Climate anxiety and parenting practices

Nature Climate Change, Published online: 05 November 2025; doi:10.1038/s41558-025-02489-6

Bees already fly in sub-optimal conditions

Nature Climate Change, Published online: 05 November 2025; doi:10.1038/s41558-025-02491-y

Expanding storms

Nature Climate Change, Published online: 05 November 2025; doi:10.1038/s41558-025-02492-x

December 2025 marks the tenth anniversary of adoption of the Paris Agreement. Although we have seen both achievements and disappointments in the past decade, we believe that the Paris Agreement will keep playing a key role in international climate actions.

Nature Climate Change, Published online: 05 November 2025; doi:10.1038/s41558-025-02477-w

To mark the tenth anniversary of the Paris Agreement, Nature Climate Change asked experts to reflect on the progress of and barriers to several of its key Articles. They share their thoughts on important policy implications, what has been achieved and missed, as well as future directions.

Nature Climate Change, Published online: 05 November 2025; doi:10.1038/s41558-025-02471-2

How mesoscale horizontal stirring changes with warming is not well understood. Here the authors present high-resolution simulations that show that mesoscale horizontal stirring increases in the Arctic Ocean and around Antarctica, mainly due to sea ice reduction.

Although heart cells and skin cells contain identical instructions for creating proteins encoded in their DNA, they’re able to fill such disparate niches because molecular machinery can cut out and stitch together different segments of those instructions to create endlessly unique combinations.

The ingenuity of using the same genes in different ways is made possible by a process called splicing and is controlled by splicing factors; which splicing factors a cell employs determines what sets of instructions that cell produces, which, in turn, gives rise to proteins that allow cells to fulfill different functions. 

In an open-access paper published today in Nature Biotechnology, researchers in the MIT Department of Biology outlined a framework for parsing the complex relationship between sequences and splicing regulation to investigate the regulatory activities of splicing factors, creating models that can be applied to interpret and predict splicing regulation across different cell types, and even different species. Called Knockdown Activity and Target Models from Additive regression Predictions, KATMAP draws on experimental data from disrupting the expression of a splicing factor and information on which sequences the splicing factor interacts with to predict its likely targets. 

Aside from the benefits of a better understanding of gene regulation, splicing mutations — either in the gene that is spliced or in the splicing factor itself — can give rise to diseases such as cancer by altering how genes are expressed, leading to the creation or accumulation of faulty or mutated proteins. This information is critical for developing therapeutic treatments for those diseases. The researchers also demonstrated that KATMAP can potentially be used to predict whether synthetic nucleic acids, a promising treatment option for disorders including a subset of muscular atrophy and epilepsy disorders, affect splicing.

Perturbing splicing 

In eukaryotic cells, including our own, splicing occurs after DNA is transcribed to produce an RNA copy of a gene, which contains both coding and non-coding regions of RNA. The noncoding intron regions are removed, and the coding exon segments are spliced back together to make a near-final blueprint, which can then be translated into a protein. 

According to first author Michael P. McGurk, a postdoc in the lab of MIT Professor Christopher Burge, previous approaches could provide an average picture of regulation, but could not necessarily predict the regulation of splicing factors at particular exons in particular genes.

KATMAP draws on RNA sequencing data generated from perturbation experiments, which alter the expression level of a regulatory factor by either overexpressing it or knocking down its levels. The consequences of overexpression or knockdown are that the genes regulated by the splicing factor should exhibit different levels of splicing after perturbation, which helps the model identify the splicing factor’s targets. 

Cells, however, are complex, interconnected systems, where one small change can cause a cascade of effects. KATMAP is also able to distinguish between direct targets from indirect, downstream impacts by incorporating known information about the sequence the splicing factor is likely to interact with, referred to as a binding site or binding motif.

“In our analyses, we identify predicted targets as exons that have binding sites for this particular factor in the regions where this model thinks they need to be to impact regulation,” McGurk says, while non-targets may be affected by perturbation but don’t have the likely appropriate binding sites nearby. 

This is especially helpful for splicing factors that aren’t as well-studied. 

“One of our goals with KATMAP was to try to make the model general enough that it can learn what it needs to assume for particular factors, like how similar the binding site has to be to the known motif or how regulatory activity changes with the distance of the binding sites from the splice sites,” McGurk says. 

Starting simple

Although predictive models can be very powerful at presenting possible hypotheses, many are considered “black boxes,” meaning the rationale that gives rise to their conclusions is unclear. KATMAP, on the other hand, is an interpretable model that enables researchers to quickly generate hypotheses and interpret splicing patterns in terms of regulatory factors while also understanding how the predictions were made. 

“I don’t just want to predict things, I want to explain and understand,” McGurk says. “We set up the model to learn from existing information about splicing and binding, which gives us biologically interpretable parameters.” 

The researchers did have to make some simplifying assumptions in order to develop the model. KATMAP considers only one splicing factor at a time, although it is possible for splicing factors to work in concert with one another. The RNA target sequence could also be folded in such a way that the factor wouldn’t be able to access a predicted binding site, so the site is present but not utilized.

“When you try to build up complete pictures of complex phenomena, it’s usually best to start simple,” McGurk says. “A model that only considers one splicing factor at a time is a good starting point.” 

David McWaters, another postdoc in the Burge Lab and a co-author on the paper, conducted key experiments to test and validate that aspect of the KATMAP model.

Future directions

The Burge lab is collaborating with researchers at Dana-Farber Cancer Institute to apply KATMAP to the question of how splicing factors are altered in disease contexts, as well as with other researchers at MIT as part of an MIT HEALS grant to model splicing factor changes in stress responses. McGurk also hopes to extend the model to incorporate cooperative regulation for splicing factors that work together. 

“We’re still in a very exploratory phase, but I would like to be able to apply these models to try to understand splicing regulation in disease or development. In terms of variation of splicing factors, they are related, and we need to understand both,” McGurk says.

Burge, the Uncas (1923) and Helen Whitaker Professor and senior author of the paper, will continue to work on generalizing this approach to build interpretable models for other aspects of gene regulation.

“We now have a tool that can learn the pattern of activity of a splicing factor from types of data that can be readily generated for any factor of interest,” says Burge, who is also an extra-mural member of the Koch Institute for Integrative Cancer Research and an associate member of the Broad Institute of MIT and Harvard. “As we build up more of these models, we’ll be better able to infer which splicing factors have altered activity in a disease state from transcriptomic data, to help understand which splicing factors are driving pathology.”

MIT engineers have developed a flexible drug-delivery patch that can be placed on the heart after a heart attack to help promote healing and regeneration of cardiac tissue.

The new patch is designed to carry several different drugs that can be released at different times, on a pre-programmed schedule. In a study of rats, the researchers showed that this treatment reduced the amount of damaged heart tissue by 50 percent and significantly improved cardiac function.

If approved for use in humans, this type of patch could help heart attack victims recover more of their cardiac function than is now possible, the researchers say.

“When someone suffers a major heart attack, the damaged cardiac tissue doesn’t regenerate effectively, leading to a permanent loss of heart function. The tissue that was damaged doesn’t recover,” says Ana Jaklenec, a principal investigator at MIT’s Koch Institute for Integrative Cancer Research. “Our goal is to restore that function and help people regain a stronger, more resilient heart after a myocardial infarction.”

Jaklenec and Robert Langer, the David H. Koch Institute Professor at MIT and a member of the Koch Institute, are the senior authors of the new study, which appears today in Cell Biomaterials. Former MIT postdoc Erika Wangis the lead author of the paper.

Programmed drug delivery

After a heart attack, many patients end up having bypass surgery, which improves blood flow to the heart but doesn’t repair the cardiac tissue that was damaged. In the new study, the MIT team wanted to create a patch that could be applied to the heart at the same time that the surgery is performed.

This patch, they hoped, could deliver drugs over an extended time period to promote tissue healing. Many diseases, including heart conditions, require phase-specific treatment, but most systems release drugs all at once. Timed delivery better synchronizes therapy with recovery.

“We wanted to see if it’s possible to deliver a precisely orchestrated therapeutic intervention to help heal the heart, right at the site of damage, while the surgeon is already performing open-heart surgery,” Jaklenec says.

To achieve this, the researchers set out to adapt drug-delivery microparticles they had previously developed, which consist of capsules similar to tiny coffee cups with lids. These capsules are made from a polymer called PLGA and can be sealed with a drug inside.

By changing the molecular weight of the polymers used to form the lids, the researchers can control how quickly they degrade, which enables them to program the particles to release their contents at specific times. For this application, the researchers designed particles that break down during days 1-3, days 7-9, and days 12-14 after implantation.

This allowed them to devise a regimen of three drugs that promote heart healing in different ways. The first set of particles release neuregulin-1, a growth factor that helps to prevent cell death. At the next time point, particles release VEGF, a growth factor that promotes formation of blood vessels surrounding the heart. The last batch of particles releases a small molecule drug called GW788388, which inhibits the formation of scar tissue that can occur following a heart attack.

“When tissue regenerates, it follows a carefully timed series of steps,” Jaklenec says. “Dr. Wang created a system that delivers key components at just the right time, in the sequence that the body naturally uses to heal.”

The researchers embedded rows of these particles into thin sheets of a tough but flexible hydrogel, similar to a contact lens. This hydrogel is made from alginate and PEGDA, two biocompatible polymers that eventually break down in the body. For this study, the researchers created compact, miniature patches only a few millimeters across.

“We encapsulate arrays of these particles in a hydrogel patch, and then we can surgically implant this patch into the heart. In this way, we’re really programming the treatment into this material,” Wang says.

Better heart function

Once they created these patches, the researchers tested them on spheres of heart tissue that included cardiomyocytes generated from induced pluripotent stem cells. These spheres also included endothelial cells and human ventricular cardiac fibroblasts, which are also important components of the heart.

The researchers exposed those spheres to low-oxygen conditions, mimicking the effects of a heart attack, then placed the patches over them. They found that the patches promoted blood vessel growth, helped more cells to survive, and reduced the amount of fibrosis that developed.

In tests in a rat model of heart attack, the researchers also saw significant improvements following treatment with the patch. Compared to no treatment or IV injection of the same drugs, animals treated with the patch showed 33 percent higher survival rates, a 50 percent reduction in the amount of damaged tissue, and significantly increased cardiac output.

The researchers showed that the patches would eventually dissolve over time, becoming a very thin layer over the course of a year without disrupting the heart’s mechanical function.

“This is an important way to combine drug delivery and biomaterials to potentially new treatments for patients,” Langer says.

Of the drugs tested in this study, neuregulin-1 and VEGF have been tested in clinical trials to treat heart conditions, but GW788388 has only been explored in animal models. The researchers now hope to test their patches in additional animal models in hopes of running a clinical trial in the future.

The current version of the patch needs to be implanted surgically, but the researchers are exploring the possibility of incorporating these microparticles into stents that could be inserted into arteries to deliver drugs on a programmed schedule.

Other authors of the paper include Elizabeth Calle, Binbin Ying, Behnaz Eshaghi, Linzixuan Zhang, Xin Yang, Stacey Qiaohui Lin, Jooli Han, Alanna Backx, Yuting Huang, Sevinj Mursalova, Chuhan Joyce Qi, and Yi Liu.

The researchers were supported by the Natural Sciences and Engineering Research Council of Canada and the U.S. National Heart, Lung, and Blood Institute.

Microsoft is warning of a scam involving online payroll systems. Criminals use social engineering to steal people’s credentials, and then divert direct deposits into accounts that they control. Sometimes they do other things to make it harder for the victim to realize what is happening.

I feel like this kind of thing is happening everywhere, with everything. As we move more of our personal and professional lives online, we enable criminals to subvert the very systems we rely on.

The move — revealed in emails and internal drafts — sidelined EPA's deep bench of career economists.

The budge office wanted to weaken curbs on cars' soot- and smog-forming air pollutants as it unraveled a key climate policy.

Negotiators at shipping talks in London were told both they and their countries could be punished unless they voted with the U.S.