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In a bizarre experiment researchers from US and Russia connected the circulatory systems of young and old mice for a whole 12 weeks, slowing the older animals’ cellular aging and increasing their lifespan by as much as 10 percent.

The study expands on previous research showing there are components in young mammalian blood worth investigating for anti-aging health benefits.

As impressive as the results seem, they fall well short of supporting whole-blood transfusion treatments in humans. Putting aside the huge biological leap between mice and humans, there are numerous known and severe risks associated with such treatments for the receiver, not to mention questionable ethics of donation.

A team at Nottingham Trent University analyzed the full set of more than 11,000 gene transcripts inside muscle cells, finding that the ‘development pathways’—the different ways in which genes work together to regenerate muscle—become weakened in aged cells.

The study may help to shed some light on why take longer to recover from as we age. The study is published in the Journal of Tissue Engineering and Regenerative Medicine.

The researchers developed a new approach to examine in vitro in the laboratory to enable them to observe the different molecular mechanisms that drive aging.

Inaugurated in 2018, the Human BioMolecular Atlas Program (HuBMAP) endeavours to construct comprehensive spatial maps that feature a range of biomolecules such as RNA, proteins, and metabolites in human organs at single-cell resolution. This collection features the research, datasets, methods and tools generated by this project, accompanied by a Perspective, a News and Views, and links to other resources.

In a recent study published in the Journal of Biomedical Science, researchers investigate whether M2 macrophage-derived exosomes (M2-Exos) could prevent inflammation-associated damage during sepsis-associated acute lung injury (ALI) by modulating abnormal polymorphonuclear neutrophil (PMN) behaviors.

Study: Exosomal PGE2 from M2 macrophages inhibits neutrophil recruitment and NET formation through lipid mediator class switching in sepsis. Image Credit: Kateryna Kon / Shutterstock.com.

The Klotho gene has gained increasing attention for its anti-aging properties. In the most recent installment of this series, we explored the promising cognitive benefits of administering Klotho to both mice and monkeys, the results from which may be mirrored in humans. The benefits of this circulating hormone, however, extend beyond the brain.

Klotho was first discovered as the antiaging gene in 1997 when researchers found that enhancing its expression could increase the lifespan of mice by more than 30%. Although a variety of different genes and environmental factors can influence longevity, studies have shown that Klotho-deficient mice not only have shorter lifespans but also experience more age-related complications. Premature aging in these mice often was accompanied by loss of muscle and fat tissue, thinning skin, reduced fertility, cardiovascular complications, movement abnormalities, and bone disease. Since Klotho is primarily produced in the kidneys, it is not surprising that many of these age-related complications often result from kidney dysfunction.

The kidneys generate two types of Klotho: a transmembrane protein that inserts itself into the cell membrane and mediates kidney function, and a secreted hormone that is released into the bloodstream. Individuals with naturally high levels of the hormone in their blood seem to not only live longer and be more resistant to age-related complications but also perform better on learning and memory tasks. In fact, even when a relatively small dose of Klotho is administered, animal studies have shown that the brain undergoes significant changes that allow more connections to be made in the hippocampus, the brain’s learning and memory center.

The researchers were successful in showing the relationship between activin A and bone erosion in cholesteatoma. “Our study showed that targeting activin A is a potential treatment in the management of cholesteatomas,” says senior author Masaru Ishii, MD, PhD, professor.

Currently in clinical settings, the only effective treatment for cholesteatomas is complete surgical removal. However, the discovery of how a cholesteatoma can cause bone erosion in this study offers new hope for developing novel medical treatments as first-line management for cholesteatomas.

“A cholesteatoma can still return or happen again even after its surgical removal, so it is important to know what is actually causing it,” notes lead author Kotaro Shimizu.

This article is an installment of Future Explored, a weekly guide to world-changing technology. You can get stories like this one straight to your inbox every Thursday morning by subscribing here.

The Australian military is funding a project to grow intelligent “mini-brains” in petri dishes. The goal is to use these “DishBrains” to design better AIs — and, eventually, even combine the two, creating AIs merged with processing features of human brain cells.

By creating just the right conditions, scientists can coax stem cells into growing into “organoids,” three-dimensional tissues that resemble the structure and function of different organs — even brains.

A team of scientists led by the University of Oxford have achieved a significant breakthrough in detecting modifications on protein structures. The method, published in Nature Nanotechnology, employs innovative nanopore technology to identify structural variations at the single-molecule level, even deep within long protein chains.

Human cells contain approximately 20,000 -encoding genes. However, the actual number of proteins observed in cells is far greater, with over 1,000,000 different structures known. These variants are generated through a process known as post-translational modification (PTM), which occurs after a protein has been transcribed from DNA.

PTM introduces structural changes such as the addition of chemical groups or carbohydrate chains to the individual amino acids that make up proteins. This results in hundreds of possible variations for the same protein chain.