2 Department of Breast Surgery of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
3Department of Radiation Oncology, Zhejiang Cancer Hospital, Hangzhou Institute of Medicine, Chinese Academy of Sciences, Zhejiang Key Laboratory of Particle Radiotherapy Equipment, Hangzhou, China.
In a world first, scientists led by a team from Stanford University have created 16 viable viruses that do not exist in nature and were designed by AI. Their experiment, which is published in Science, could help in the fight against superbugs by allowing researchers to design customized viruses to kill drug-resistant bacteria. Thomas Inglesby and Moritz S. Hanke have published a Perspective piece on the work and its implications in the same edition of the journal.
Artificial intelligence is already helping to speed up drug discovery by analyzing massive genetic data sets, predicting protein shapes and identifying potential medicines. But in this research, the team wanted to see if AI could go a step further by creating an entire functioning genome based on a natural virus template.
One of the hallmarks of Alzheimer’s disease is the accumulation of a peptide in the brain known as amyloid beta. A new study published in Nature Communications on July 22 has uncovered the atomic structure of the peptide in its harmful form.
Amyloid beta is a naturally occurring peptide that exists in healthy brains. But in Alzheimer’s disease, these peptides clump together abnormally and form large plaques. Scientists have known about the association between these plaques and Alzheimer’s disease for over a century, but whether this buildup is actually damaging the brain or simply a byproduct of the disease has been hotly debated.
There is also an intermediate state of amyloid beta that exists between the healthy peptides and the large plaques. Emerging evidence suggests that it is these intermediates—so-called “oligomeric” amyloid beta—that drive damage to the brain, but their structure has remained unknown. Now, a team of researchers at Yale School of Medicine has characterized this intermediate form for the first time.
A human kidney is built once, before birth, and the rules guiding its construction have been largely inferred from animal models. Researchers at Penn Medicine have now read those rules directly in human tissue. They found that developing cells are steered by soluble signals released by their neighbors—and identified insulin-like growth factor 2 (IGF2) as a key signal that sustains the kidney’s stem-like cells.
Their study is published in Nature Genetics and was conducted by the Penn-CHOP Kidney Innovation Center, a research collaboration between the Perelman School of Medicine and Children’s Hospital of Philadelphia, working with bioengineers from Penn’s School of Engineering and Applied Science and the Institute for Regenerative Medicine.
How well a kidney is built before birth matters for the rest of a person’s life. Healthy people are born with anywhere from 200,000 to 2 million nephrons—the microscopic filtering units that clear waste from the blood—and no more are made after birth. A low nephron endowment carries a higher lifetime risk of high blood pressure and chronic kidney disease, and severe disruptions of kidney formation are the leading cause of chronic kidney disease in children.
A novel prostate cancer treatment—225 Ac-PSMA-617 radioligand therapy—has been shown to increase the progression free survival (PFS) and overall survival (OS) of metastatic castration-resistant prostate cancer (mCRPC) patients, according to research published by The Journal of Nuclear Medicine. Ninety-one percent of patients experienced a greater than 50% reduction of their initial PSA (prostate specific antigen) value after treatment with 225 Ac-PSMA-617, resulting in a PFS of 22 months and an OS not yet reached at the conclusion of the study.
While the five-year survival rate of localized prostate cancer is nearly 100%, for mCRPC patients it is only 30%. Clinical studies have demonstrated the efficacy and safety of several therapies, including 177 Lu-PSMA in the post-androgen deprivation therapy (ADT) setting in patients with mCRPC. Additional therapies, such as 225 Ac-PSMA-617, are often considered once the disease begins to progress again.
“Previous research has shown a remarkable therapeutic efficacy of 225 Ac-PSMA-617 in heavily pre-treated mCRPC patients, as demonstrated by the initial work from Kratochwil et al. from Germany,” said Mike Sathekge, professor and head of the Nuclear Medicine Department at the University of Pretoria and Steve Biko Academic Hospital in Pretoria, South Africa. “In this study we sought to compare 225 Ac-PSMA-617 to other common post-ADT treatments, such as chemotherapy, enzalutamide, and abiraterone acetate or docetaxel, administered in a comparable setting.”
Results from a small clinical trial suggest it may be possible to reduce the risk of dementia by eating during fewer hours of the day. The pilot study, which involved a weight-loss program for older women with overweight or obesity, showed modest cognitive improvements among those who limited their daily eating window instead of just reducing their calorie intake.
“Losing weight alone will ward off some of the aging-related cognitive decline, and these data suggest that there may be additional benefits if you stop eating four hours before going to sleep and reduce food intake to 8–9 hours per day, compared with the usual eating window of 12 hours per day,” said Sue Shapses, Ph.D., RD, DFASN, professor at Rutgers University and Rutgers-RWJ Medical Center and the study’s principal investigator.
Shapses’ group will present the findings at NUTRITION 2026, the flagship annual meeting of the American Society for Nutrition, held July 25–28 in National Harbor, Maryland, just outside Washington, D.C.
