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Cells have surface receptors called integrins that bind to repetitive domains present on the extracellular matrix (ECM) surrounding the cells, allowing them to grow and spread. A new study from the Department of Bioengineering (BE), Indian Institute of Science (IISc) and collaborators shows that tweaking the spacing between these binding domains on the ECM can boost the efficiency of ultrasound treatment applied to kill cancer cells.

“In a normal tissue, the spacing on the ECM is around 50–70 nanometers (nm), but in the , severe choking occurs due to excessive ECM secretion, which may reduce the binding spacing to below 50 nm,” explains Ajay Tijore, Assistant Professor in BE and corresponding author of a related study published in Nano Letters. “We found more being killed when the binding spacing is increased to around 50–70 nm.”

Low-frequency ultrasound waves (39 kHz) can disrupt the and trigger cell death in cancer cells. It is a relatively low-cost and non-invasive approach. Unlike normal cells, cancer cells do not have repair mechanisms that help them withstand the exerted by ultrasound waves.

Mammoth Biosciences researchers have developed NanoCas, an ultracompact CRISPR nuclease, demonstrating its ability to perform gene editing in non-liver tissues, including skeletal muscle, using a single adeno-associated virus (AAV) vector. Experiments in non-human primates (NHPs) resulted in editing efficiencies exceeding 30% in muscle tissues.

CRISPR gene editing has revolutionized genetics, but delivery challenges have restricted its clinical applications primarily to ex vivo and liver-directed therapies. Conventional CRISPR nucleases, including Cas9 and Cas12a, exceed the packaging limits of a single AAV vector, necessitating dual-AAV strategies that reduce efficiency.

Smaller CRISPR systems such as Cas12i and CasX have been identified, but they remain too large or exhibit low editing efficiency. Existing compact systems like Cas14 and IscB have not demonstrated robust efficacy in large animal models.

In 1978, parvovirus—then common to cats—started infecting dogs in Europe. The virus spread quickly around the globe, killing hundreds of thousands of dogs, mostly puppies—until a team of Cornell researchers led by the late Leland “Skip” Carmichael developed a vaccine, the derivatives of which are still used today.

“It was really at the time a worldwide relief, a miracle,” said Colin Parrish, interim director of the Baker Institute for Animal Health, who joined Carmichael’s lab as a graduate student in 1980 and is now senior author of a new study that continues to advance our understandings of the virus and how the vaccine works.

The paper, published Feb. 14 in Proceedings of the National Academy of Sciences, shows how host antibodies bind to parvovirus and neutralize it. The findings shed light on fundamental interactions between viruses and their hosts, and open new doors for improving current vaccines and treatments for infected animals.

Humans have been poisoning rodents for centuries. But fast-breeding rats and mice have evolved resistance to earlier poisons. In response, manufacturers have produced second generation anticoagulant rodenticides such as bromadiolone, widely used in Australian households.

Unfortunately, these potent poisons do not magically disappear after the is dead. For example, it’s well known who eat poisoned rodents suffer the same slow death from .

Our new research, published in the journal Science of The Total Environment, shows the problem is much bigger than owls. We found Australia’s five largest marsupial predators—the four quoll species and the Tasmanian devil—are getting hit by these poisons too.

Researchers from the National University of Singapore (NUS) and University of New South Wales (UNSW) Sydney have proven that a spinning atomic nucleus really is fundamentally a quantum resource. The teams were led respectively by Professor Valerio Scarani, from NUS Department of Physics, and Scientia Professor Andrea Morello from UNSW Engineering. The paper was published in the journal Newton on 14 February 2025.

It has long been inferred that tiny particles such as electrons or protons are indeed quantum due to the way they get deflected in a magnetic field. However, when left to spin freely, they appear to behave in exactly the same way as a classical spinning item, such as a Wheel of Fortune turning on its axis. For more than half a century, experts in spin resonance have taken this fact as a universal truth.

For the same reason, a technician or a doctor operating a (MRI) machine at the hospital never needed to understand quantum mechanics—the spinning of the protons inside the patient’s body produces the same kind of magnetic field that would be created by attaching a fridge magnet to a spinning wheel.

Technically this year we have a global pandemic but with 11 different viruses that have evolved.


For the first time the pandemic began, deaths from influenza have outpaced deaths from COVID-19 in 22 states, plus New York City and Washington, D.C. Dr. Jon LaPook has the latest numbers.

Selective serotonin reuptake inhibitor (SSRI) antidepressants are some of the most widely prescribed drugs in the world, and new research suggests they could also protect against serious infections and life-threatening sepsis. Scientists at the Salk Institute studying a mouse model of sepsis uncovered how the SSRI fluoxetine can regulate the immune system and defend against infectious disease, and found that this protection is independent to peripheral serotonin. The findings could encourage additional research into the potential therapeutic uses of SSRIs during infection.

“When treating an infection, the optimal treatment strategy would be one that kills the bacteria or virus while also protecting our tissues and organs,” commented professor Janelle Ayres, PhD, holder of the Salk Institute Legacy Chair and Howard Hughes Medical Institute Investigator. “Most medications we have in our toolbox kill pathogens, but we were thrilled to find that fluoxetine can protect tissues and organs, too. It’s essentially playing offense and defense, which is ideal, and especially exciting to see in a drug that we already know is safe to use in humans.”

Ayres is senior author of the team’s report in Science Advances. In their paper, titled “Fluoxetine promotes IL-10–dependent metabolic defenses to protect from sepsis-induced lethality,” the investigators stated, “Our work reveals a beneficial ‘off-target’ effect of fluoxetine, and reveals a protective immunometabolic defense mechanism with therapeutic potential.”

Artificial intelligence (AI) has the potential to revolutionize the drug discovery process, offering improved efficiency, accuracy, and speed. However, the successful application of AI is dependent on the availability of high-quality data, the addressing of ethical concerns, and the recognition of the limitations of AI-based approaches. In this article, the benefits, challenges, and drawbacks of AI in this field are reviewed, and possible strategies and approaches for overcoming the present obstacles are proposed. The use of data augmentation, explainable AI, and the integration of AI with traditional experimental methods, as well as the potential advantages of AI in pharmaceutical research, are also discussed. Overall, this review highlights the potential of AI in drug discovery and provides insights into the challenges and opportunities for realizing its potential in this field.

Summary: A new study reveals how AI-driven deep learning models can decode the genetic regulatory switches that define brain cell types across species. By analyzing human, mouse, and chicken brains, researchers found that some brain cell types remain highly conserved over 320 million years, while others have evolved uniquely.

This regulatory code not only sheds light on brain evolution but also provides new tools for studying gene regulation in health and disease. The findings highlight how AI can identify preserved and divergent genetic instructions controlling brain function across species.

The study also has implications for understanding neurological disorders by linking genetic variants to cognitive traits. Researchers are now expanding their models to study the brains of various animals and human disease states like Parkinson’s.