Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog

Category: health

Clinician–scientists identify brain network linked to deadliest childhood brain cancer

A human brain network associated with survival in children with diffuse midline glioma (DMG), the deadliest childhood brain cancer, has been identified by UCL clinician-scientists, raising the possibility of entirely new treatment approaches. The researchers found that DMG tumors seem to exploit the brain’s existing neural circuitry to drive tumor growth and progression. Tumors that were more strongly connected to this network were associated with significantly shorter patient survival.

The study, published in Nature, builds on pioneering work in the field of cancer neuroscience, which shows that brain tumors, including DMG, dynamically interact with the otherwise healthy brain.

The study was led by Dr. Jai Sidpra and Dr. Valentina Lind, medical students enrolled in the MBPhD Program within the UCL Division of Medicine and senior author Professor Darren Hargrave’s group at the UCL Great Ormond Street Institute of Child Health.

New tool to help build more reliable DNA nanostructures

Scaffolded DNA and RNA origami is a technique that allows scientists to build tiny, highly precise two- and three-dimensional objects. Because these nanostructures can interact naturally with biological systems, they could have important future uses in health care and agritech.

AI repurposes routine chest X-rays to catch silent bone loss before fracture

Osteoporosis is a silent disease where bone loss develops gradually before fractures occur. Current clinical screening recommendations mainly focus on older women and selected high-risk groups, leaving some men, younger adults, and individuals with normal body weight completely outside routine screening pathways.

To close this care gap, researchers from St. Paul’s Hospital and National Taiwan University have demonstrated how AI can leverage routine chest X-rays to detect asymptomatic bone loss, closing critical gaps in screening healthy Asian populations. Their paper is published in the journal npj Digital Medicine.

Strikingly, the study found that more than half of the confirmed abnormal bone-density cases occurred in people with a normal body mass index (BMI). This reveals a severe diagnostic blind spot in conventional, guideline-based screening. By relying strictly on traditional criteria, health care systems routinely overlook healthy-weight individuals, younger adults, and men who are secretly losing bone density but remain completely off the clinical radar.

Popular joint supplement glucosamine linked to faster Alzheimer’s progression

Because glucosamine is widely available and frequently used by older adults to support joint health, the researchers wanted to determine whether it could influence Alzheimer’s disease and related dementias (ADRD).

Working with collaborators Yi Guo, Ph.D., and Jiang Bian, Ph.D., the team used artificial intelligence to analyze deidentified UF Health records collected between 2012 and 2024. They focused on patients diagnosed with either ADRD or mild cognitive impairment (MCI).

Among those patients, researchers found that glucosamine use was relatively common. A total of 1,896 patients with ADRD and 2,750 patients with MCI reported taking the supplement, representing about 8% of each group.

Canada’s National Artificial Intelligence Strategy: AI for All

Message from the minister The Government’s vision: AI for All Key pillars of the strategy Priority sectors Pillar 1: Protecting Canadians and safeguarding democracy Pillar 2: Ensuring AI empowers Canadians Pillar 3: Powering AI adoption for shared prosperity Pillar 4: Building the Canadian sovereign AI foundation Pillar 5: Scaling Canadian champions Pillar 6: Building trusted partnerships and global alliances Conclusion

An innovative Canada is a stronger Canada. And AI is the major driver of innovation in Canada and around the world. But to understand the potential of Canadian AI, you have to see how it is already working to improve the lives of people. How a Canadian pediatric cardiologist in Halifax named Dr. Robert Chen is using the AI application he built to diagnose heart murmurs in newborns. His technology could cut down wait times by many months for anxious parents to see a specialist, saving our health care system tens of millions of dollars.

You have to see how a Canadian AI company called Croptimistic is helping farmers precisely map their soil. This technology allows them to use less fertilizer, while increasing crop yield, making our food system more resilient and more affordable.

The AI tools shaping patient care may be operating outside regulatory oversight. MIT researchers say it’s time to change that

Every day, across thousands of American hospitals, artificial intelligence quietly shapes decisions that determine patient outcomes. An algorithm flags a patient as high risk for sepsis; a risk score informs whether a woman receives additional cancer screening; a deterioration model triggers an alert that sends a care team to a bedside. These tools are embedded in the workflows of nearly two-thirds of US hospitals, integrated into the electronic health record systems clinicians rely on daily. But many have never been reviewed by the FDA.

A new viewpoint in The Lancet Digital Health, co-authored by researchers at MIT’s Computer Science and Artificial Intelligence Laboratory (CSAIL) and Jameel Clinic, traces how this problem took root, why it carries serious consequences, and what genuine transparency would require to fix it.

The argument, the scientists say, is not that AI has no place in clinical decision-making. It is that a $4 billion market of clinical decision support tools operates largely beyond public accountability, leaving patients and providers often unable to know whether the tools influencing their care have been validated, by whom, or for which populations they work as intended.

Sleep and exercise may curb heart risk from mutant white blood cells

Healthy sleep and regular exercise can work to counteract genetic mutations in white blood cells that are associated with cardiovascular disease and are most common among older people, Mount Sinai researchers have found. In a study published in Nature, the team reported for the first time that sufficient sleep and exercise can help reduce the cancer-like cell expansion and atherosclerotic risk linked to mutations that spontaneously occur in white blood cells.

These mutations accumulate over our lifetimes and occur most often in hematopoietic stem cells, which are the cells in bone marrow that make blood cells, including macrophages and monocytes, immune cells that help defend the body. When these cells develop mutations, they start to proliferate, multiplying faster than they should, and become more inflammatory, irritating or damaging tissues in the body.

This condition, known as clonal hematopoiesis (CH), is detectable in a quarter of people over age 70 and half of people over 80, the researchers say, though it is infrequent in young, healthy people.

New antibody may boost KRAS-targeted lung cancer treatment after resistance emerges

An experimental antibody treatment that binds to a protein known as PCDH7 shrank tumors in preclinical models of non-small cell lung cancer (NSCLC), including those resistant to a targeted therapy, a study led by UT Southwestern Medical Center researchers showed. The findings, published in Science Advances, could eventually lead to a new class of drugs to treat NSCLC and potentially other cancers.

“Overcoming resistance to molecularly targeted therapies is a critical unmet need for lung cancer patients. We are excited that these antibodies may open another therapeutic avenue for lung cancer, especially for patients whose cancers have become resistant to KRAS inhibitors,” said Kathryn O’Donnell, Ph.D., associate professor of molecular biology and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. O’Donnell co-led the study with first author Nicole Novaresi, Ph.D., a postdoctoral researcher in the O’Donnell Lab, and collaborators at the University of Texas Health Science Center at Houston.

NSCLC accounts for about 85% of lung cancer cases in the U.S. and is the leading cause of cancer-related deaths. The O’Donnell Lab focuses on identifying and characterizing proteins on the surface of NSCLC and other cancer cells because of their potential as therapeutic targets. In 2017, O’Donnell and her colleagues identified PCDH7 as a driver of NSCLC, especially in tumors with mutations in a gene called KRAS. Found in about 25% of NSCLC cases, these mutations cause uncontrolled cell proliferation that propels tumor growth.

Faulty protein cleanup gene tied to severe early-onset neurological disorders

Though protein clumps associated with Alzheimer’s and Parkinson’s were discovered more than a century ago, researchers remain largely unable to prevent them from forming or eliminate them from the brain. And though a variety of therapies have taken aim at tau tangles, beta-amyloid plaques and Lewy bodies, among other notorious aggregates, none have been very effective at stopping disease progression.

Rockefeller’s Hermann Steller and his team in the Strang Laboratory of Apoptosis and Cancer Biology have long been focused on understanding how the cell’s protein-degrading machines, called proteasomes, are regulated. His lab discovered that a transporter protein termed PI31 shuttles proteasomes over long distances from the nerve cell body to synapses. When this system fails, synapses become depleted of degradative capacity, and proteins that should have been eliminated accumulate. As a result, synaptic communication breaks down, protein clumps form and neuronal health deteriorates.

Now a new study in Nature Communications, led by researchers from University College London and contributed to by Steller’s lab, has identified mutations in PSMF1, the gene that produces PI31, that cause the protein to malfunction. Moreover, the scientists demonstrated that these mutations cause a spectrum of severe, very early-onset neurological disorders.

Genomes from Oceania offer new clues to human evolution

A new Yale-led study provides one of the most detailed and comprehensive analyses to date of genetic variation in human populations in Oceania, filling a major gap in representation in genomics research. Despite harboring remarkable diversity, populations in this vast region in the South Pacific historically have been overlooked in global human genetic studies, which have often focused largely on people of European descent, researchers say. The study is published in the journal Science.

“The drastic underrepresentation of Oceanians limits our understanding of human evolution and could exacerbate health inequalities as genomic research is used to develop novel medical treatments,” said lead author Serena Tucci, assistant professor of anthropology in Yale’s Faculty of Arts and Sciences and principal investigator of the Yale Human Evolutionary Genomics Laboratory. “To fill that gap, my research team embarked on a large-scale project to expand what is known about human genetic variation, including genetic variants inherited from extinct hominins.”

The work shows how the genes that ancient humans acquired after mating with extinct hominins continue to shape the biology, health and survival of our species today.

/* */