Lifeboat Foundation

Proteins are made from chains of amino acids that fold into three-dimensional shapes, which in turn dictate protein function. Those shapes evolved over billions of years and are varied and complex, but also limited in number. With a better understanding of how existing proteins fold, researchers have begun to design folding patterns not produced in nature.

But a major challenge, says Kim, has been to imagine folds that are both possible and functional. “It’s been very hard to predict which folds will be real and work in a protein structure,” says Kim, who is also a professor in the departments of molecular genetics and computer science at U of T. “By combining biophysics-based representations of protein structure with diffusion methods from the image generation space, we can begin to address this problem.”

The new system, which the researchers call ProteinSGM, draws from a large set of image-like representations of existing proteins that encode their structure accurately. The researchers feed these images into a generative diffusion model, which gradually adds noise until each image becomes all noise. The model tracks how the images become noisier and then runs the process in reverse, learning how to transform random pixels into clear images that correspond to fully novel proteins.

In a study of 17 people from five families, Johns Hopkins Medicine researchers say they found that ultra-lengthy DNA endcaps called telomeres fail to provide the longevity presumed for such people. Instead, people with long telomeres tend to develop a range of benign and cancerous tumors, as well as the age-related blood condition clonal hematopoiesis.

Reporting in the May 4 issue of the New England Journal of Medicine, the Johns Hopkins researchers say clonal hematopoiesis is common among this long-telomere group, and the blood condition combined with long telomeres may help mutations stick around longer in blood cells.

“Our findings challenge the idea that long telomeres protect against aging,” says Mary Armanios, M.D., professor of oncology at the Johns Hopkins Kimmel Cancer Center, and professor of genetic medicine, molecular biology and genetics, and pathology at the Johns Hopkins University School of Medicine. “Rather than long telomeres protecting against aging, long telomeres allowed cells with mutations that arise with aging to be more durable.”

Join us on Patreon!
https://www.patreon.com/MichaelLustgartenPhD

Discount Links:
NAD+ Quantification: https://www.jinfiniti.com/intracellular-nad-test/
Use Code: ConquerAging At Checkout.

Continue reading “Quantifying Biological Age: Blood Test #3 in 2023” »

Sure could’ve used this a few years ago.

A study has found that a mitochondrial disease in newborns shows cancer-like changes in proliferating cells, causing tissues to age prematurely. The finding is a significant step forward in understanding the syndrome and developing treatments for mitochondrial diseases.

GRACILE syndrome, a mitochondrial disease that is one of the Finnish heritage diseases, shows altered cell metabolism and proliferation resembling that of cancer cells. In the future, similar mitochondrial diseases could potentially be treated by limiting excessive cell proliferation. This is demonstrated in a study led by docent Jukka Kallijärvi and professor emerita Vineta Fellman that was carried out at the Folkhälsan Research Center and the University of Helsinki and published in Nature Communications in April 2023.

Mitochondria are organelles responsible for a large portion of cellular energy metabolism. Mutations in genes required for mitochondrial functions cause mitochondrial diseases in humans. GRACILE syndrome is caused by a malfunction in the respiratory chain, the very system the mitochondria utilize to generate cellular energy. The onset of the syndrome is in the fetal period, manifesting after birth as a liver and kidney disease with severe metabolic complications. Newborns with the syndrome usually only survive a few weeks.

Our cells naturally degrade over time, which is part of the reason we’re not as mobile and sprightly aged 80 as we are aged 8. Now scientists have figured out a way to boost cell lifespan and longevity using a synthetic genetic ‘clock’.

Researchers from the University of California San Diego based their findings on the yeast Saccharomyces cerevisiae, making it unlikely that humans might live forever any time soon – but the team thinks that the work could be developed to eventually help the human body age in a healthier way.

By ‘rewiring’ the yeast cells, the researchers were able to boost their lifespan by 82 percent on average. It’s a promising development in the control of cellular aging and treating age-related conditions.

Neural networks are distributed computing structures inspired by the structure of a biological brain and aim to achieve cognitive performance comparable to that of humans but in a much shorter time.

These technologies now form the basis of machine learning and artificial intelligence systems that can perceive the environment and adapt their own behavior by analyzing the effects of previous actions and working autonomously. They are used in many areas of application, such as speech and image recognition and synthesis, autonomous driving and augmented reality systems, bioinformatics, genetic and molecular sequencing, and high-performance computing technologies.

Compared to conventional computing approaches, in order to perform complex functions, neural networks need to be initially “trained” with a large amount of known information that the network then uses to adapt by learning from experience. Training is an extremely energy-intensive process and as computing power increases, the neural networks’ consumption grows very rapidly, doubling every six months or so.

In a recent study published in the journal Cell Stem Cell, researchers hypothesized that pacemaker-like activity of human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) resulted in engraftment arrhythmias (EAs), which hampers the clinical use of cell-based therapy using hPSC-CMs for treatment of myocardial infarction (MI).

Study: Gene editing to prevent ventricular arrhythmias associated with cardiomyocyte cell therapy. Image Credit: FrentaN / Shutterstock.

Scientists are still determining whether humans will reach a maximum possible age or if we can extend lifespan indefinitely. One thing we know is that the aging we see and feel in our bodies is connected to aging that individual cells experience. Yeast is a common model in molecular biology that is often used to study aging. In 2020, scientists found that yeast cells could go down one of two aging paths; in one, structures called nucleoli were degraded and ribosomal DNA experienced less silencing; in the other, mitochondria were affected and heme accumulation was reduced. The researchers suggested that these were two distinct types of terminal aging.

In follow-up work, the research team has manipulated the genetics of those pathways, and have extended the lifespan of cells by doing so. The work has been reported in Science. The investigators applied a solution to the cells that altered gene circuits to stop the cells from deteriorating.