By John Sanford
Researchers from across Stanford’s campus gathered May 7 for a symposium focused on ways synthetic biology can promote a sustainable world.
By John Sanford
Researchers from across Stanford’s campus gathered May 7 for a symposium focused on ways synthetic biology can promote a sustainable world.
It represents a huge achievement, and the culmination of a long team effort.
A pregnant woman’s blood sample taken in 1972 was mysteriously missing a surface molecule found on all other known red blood cells at the time.
More than 50 years later, that strange absence finally led researchers from the UK and Israel to describe a new blood group system in humans. The team published a paper on the discovery in 2024.
“It represents a huge achievement, and the culmination of a long team effort, to finally establish this new blood group system and be able to offer the best care to rare, but important, patients,” hematologist Louise Tilley from the UK National Health Service said in September 2024, after nearly 2 decades of personally researching this bloody quirk.
Improvements in public health have allowed humankind to survive to older ages than ever before, but, for many people, these added golden years are not spent in good health. Aging is a natural part of life, but it is associated with a greatly increased incidence of most chronic diseases, including various cancers, diabetes, and Alzheimer’s disease.
The laboratory of Kris Burkewitz, assistant professor of cell and developmental biology, wants to figure out if there is a way to break the links between the aging process and disease so that we can stay healthy longer, allowing us to better enjoy our later years. To accomplish this goal, the Burkewitz lab focuses on how cells organize their internal compartments, or organelles, and how organelle structures can influence cellular function, metabolism, and disease risk.
In his most recent paper, published in Nature Cell Biology, Burkewitz describes a new way by which cells adapt to the aging process: by actively remodeling the endoplasmic reticulum, one of the cell’s largest and most complex organelles. His team found that aging cells remodel their ER through a process called ER-phagy, which selectively targets specific ER subdomains for breakdown. The discovery that ER-phagy is involved in aging highlights this process as a possible drug target for age-related chronic conditions such as neurodegenerative diseases and various metabolic disease contexts.
“One of the biggest challenges in treating asthma is that we currently have no effective way to tell which patient is going to have a severe attack in the near future,” says the senior author. “Our findings solve a critical unmet need. By measuring the balance between specific sphingolipids and steroids in the blood, we can identify high-risk patients with 90 per cent accuracy, allowing clinicians to intervene before an attack occurs.”
The team discovered that while individual metabolite levels provided some insight, the ratio between sphingolipids and steroids was the most powerful predictor of future health. ScienceMission sciencenewshighlights.
Researchers have identified a new method to predict asthma exacerbations with a high degree of accuracy. The study is published in Nature Communications.
Asthma is one of the world’s most common chronic diseases, affecting over 500 million people. Asthma exacerbations – commonly known as asthma attacks – are a major cause of disease morbidity and healthcare costs. Despite the prevalence of asthma, clinicians currently lack reliable biomarkers to identify which patients are at high risk for future attacks. Current methods often fail to distinguish between stable patients and those prone to severe exacerbations.
The study analysed data from three large asthma cohorts totalling over 2,500 participants, backed by decades of electronic medical records. Researchers used a high throughput approach called metabolomics to measures small molecules in the blood of individuals with asthma. They identified an important relationship between two classes of metabolites, sphingolipids and steroids, and asthma control. Specifically, they identified that sphingolipid to steroid ratios could predict exacerbation risk over a 5-year period. In some cases, the model could differentiate the time-to-first exacerbation between high-and low-risk groups by nearly a full year.
Researchers publishing in Aging Cell have discovered that cells derived from the human placenta may be useful in estimating the effects of potential anti-aging treatments.
A seemingly odd choice
Of all the organs in the body, the placenta may be the least concerning with regards to aging; it only exists for at most 10 months, after which it is discharged as part of the birthing process. The researchers openly admit that this lifespan difference may make placenta-related aging processes distinct from those in other tissues, which harms translation and generalizability.
Many fans expected Valve to announce Half-Life 3 in 2025, and Gabe Follower believes the news was delayed, which was the reason the second edition of Half-Life 2: Raising the Bar was postponed: he thinks the book will be out once the game is revealed.
For now, we can get glimpses of HL3 features in the updates to Valve’s Source 2 engine. Based on mentions of HLX in the code, Gabe Follower says that the game will offer dynamic physics and gravitational anomalies, where gravity no longer pulls objects in one direction but can be tied to a point, making objects’ gravitational pulls affect each other.
Characters will now have more accurate hitboxes that adjust to their limbs instead of simple boxes.
This screening platform washed cells with a broad range of retroviruses to determine which ones affect tau. In follow-up testing, the gene CUL5 was singled out as being crucial for tau degradation. Mitochondrial function was also found to be a key part of preventing tau pathology.
Using an ingenious CRISPR-based screening technique, scientists have found a protein that tags tau for degradation and is more strongly expressed in tau-resilient neurons [1].
Some neurons are more equal than others
The accumulation of tau protein fibrils in neurons is a hallmark of Alzheimer’s and several other diseases [2]. Scientists have long noticed that even in the brains of people who died of Alzheimer’s, some neurons are markedly healthier than others, suggesting that neurons differ in how they handle tau and that these differences may explain selective vulnerability in tauopathies [3].