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Researchers at Tufts University and Harvard University’s Wyss Institute have created tiny biological robots that they call Anthrobots from human tracheal cells that can move across a surface and have been found to encourage the growth of neurons across a region of damage in a lab dish.

The multicellular robots, ranging in size from the width of a human hair to the point of a sharpened pencil, were made to self-assemble and shown to have a remarkable healing effect on other . The discovery is a starting point for the researchers’ vision to use patient-derived biobots as new therapeutic tools for regeneration, healing, and treatment of disease.

The work follows from earlier research in the laboratories of Michael Levin, Vannevar Bush Professor of Biology at Tufts University School of Arts & Sciences, and Josh Bongard at the University of Vermont in which they created multicellular biological robots from frog embryo cells called Xenobots, capable of navigating passageways, collecting material, recording information, healing themselves from injury, and even replicating for a few cycles on their own.

Regenerative medicine might just have had a new tool added to its arsenal: Scientists have created tiny biological robots out of living human cells. Though they may be small, the self-assembling bots are mighty, with a study demonstrating their potential for healing and treating disease.

The team had already proven their biological robotics chops back in 2020 with the creation of Xenobots, made from frog embryonic cells. They even managed to design Xenobots so that they could reproduce in a way that no living animal or plant does, something that had never been seen before.

The researchers weren’t sure whether the incredible capabilities of the Xenobots were in some way down to their amphibious origins, so they wanted to find out if biobots could also be created from the cells of other organisms. And why not begin with humans?

Additionally, GAI helps radiologists cross-reference comorbidities in a way that was not possible before. For instance, people with certain types of autoimmune arthritis have an increased risk of cardiovascular disease (atherosclerosis, hypertension, and type 2 diabetes). These conditions might seem unrelated, but if a CT scan reveals calcifications in the coronary arteries, GAI can facilitate informing the radiologist and treating physician of this important biomarker. These types of added value are not just consumer conveniences. As potentiators of clinical research and effectuators of episodes of care, they can save the lives of patients.

Leaning into the whole.

It should be clear to most in the industry that AI is knocking at the door, and those who do not adopt new technology will be left behind. What seems less clear is how that design and implementation should move forward. Laying AI functions on top of already outdated systems or relying on separate solutions that do not play into the unified stack system–especially given the volume of data, delicate privacy issues and the need for constant updates–does not optimally contribute to advancement. Instead, we should embrace the vision as a whole and build for unification and GAI, rather than jury-rig a square peg in a round hole.

A cancer diagnosis can greatly disrupt treatment with methadone, a medication used to treat patients with opioid use disorder, according to a perspective piece published in the New England Journal of Medicine by University of Pittsburgh researchers.

Through the lens of a specific patient treated with methadone for many years and later diagnosed with head and , the authors discuss how segregating methadone distribution from general medical care is problematic and emphasize the need to integrate opioid use disorder treatment and improve .

Before his diagnosis, the patient was afforded a 28-day supply of take-home methadone doses, which he self-administered and, per clinic and federal regulations, returned to the clinic every 28 days for monitoring and refills.

The hypertension drug rilmenidine has been shown to slow down aging in worms, an effect that in humans could hypothetically help us live longer and keep us healthier in our latter years.

Previous research has shown rilmenidine mimics the effects of caloric restriction on a cellular level. Reducing available energy while maintaining nutrition within the body has been shown to extend lifespans in several animal models.

Whether this translates to human biology, or is a potential risk to our health, is a topic of ongoing debate. Finding ways to achieve the same benefits without the costs of extreme calorie cutting could lead to new ways to improve health in old age.

An international team of researchers has used time-resolved ultrafast crystallography to follow the progress of DNA repair by a photolyase enzyme. The work is ‘the first structural characterisation of a full enzyme reaction cycle,’ says Manuel Maestre-Reyna, who led the research.

Photolyases repair DNA damage caused by ultraviolet light in bacteria, fungi, plants and some animals including marsupials. Humans and other mammals don’t contain these enzymes, but we too incur light-induced damage. One common outcome is the formation of cyclobutane pyrimidine dimers (CPDs), where two adjacent pyrimidine bases (thymine or cytosine) fuse together via a four-membered cyclobutane ring. ‘CPD formation is the main cause of skin cancer, and sunburnt skin always contains CPD lesions’, says Maestre-Reyna, a biochemist at the Institute of Biological Chemistry in Taipei, Taiwan.