Lifeboat Foundation

Restraining or slowing ageing hallmarks at the cellular level have been proposed as a route to increased organismal lifespan and healthspan. Consequently, there is great interest in anti-ageing drug discovery. However, this currently requires laborious and lengthy longevity analysis. Here, we present a novel screening readout for the expedited discovery of compounds that restrain ageing of cell populations in vitro and enable extension of in vivo lifespan.

Using Illumina methylation arrays, we monitored DNA methylation changes accompanying long-term passaging of adult primary human cells in culture. This enabled us to develop, test, and validate the CellPopAge Clock, an epigenetic clock with underlying algorithm, unique among existing epigenetic clocks for its design to detect anti-ageing compounds in vitro. Additionally, we measured markers of senescence and performed longevity experiments in vivo in Drosophila, to further validate our approach to discover novel anti-ageing compounds. Finally, we bench mark our epigenetic clock with other available epigenetic clocks to consolidate its usefulness and specialisation for primary cells in culture.

We developed a novel epigenetic clock, the CellPopAge Clock, to accurately monitor the age of a population of adult human primary cells. We find that the CellPopAge Clock can detect decelerated passage-based ageing of human primary cells treated with rapamycin or trametinib, well-established longevity drugs. We then utilise the CellPopAge Clock as a screening tool for the identification of compounds which decelerate ageing of cell populations, uncovering novel anti-ageing drugs, torin2 and dactolisib (BEZ-235). We demonstrate that delayed epigenetic ageing in human primary cells treated with anti-ageing compounds is accompanied by a reduction in senescence and ageing biomarkers. Finally, we extend our screening platform in vivo by taking advantage of a specially formulated holidic medium for increased drug bioavailability in Drosophila. We show that the novel anti-ageing drugs, torin2 and dactolisib (BEZ-235), increase longevity in vivo.

Researchers have developed a genetic algorithm for designing phononic crystal nanostructures, significantly advancing quantum computing and communications.

The new method, validated through experiments, allows precise control of acoustic wave propagation, promising improvements in devices like smartphones and quantum computers.

Quantum Computing Revolution

Treating cancer can sometimes feel like a game of Whac-A-Mole. The disease can become resistant to treatment, and clinicians never know when, where and what resistance might emerge, leaving them one step behind. But a team led by Penn State researchers has found a way to reprogram disease evolution and design tumors that are easier to treat.

They created a modular genetic circuit that turns cancer cells into a “Trojan horse,” causing them to self-destruct and kill nearby drug-resistant cancer cells. Tested in human cell lines and in mice as proof of concept, the circuit outsmarted a wide range of resistance.

The findings were published today, July 4, in the journal Nature Biotechnology. The researchers also filed a provisional application to patent the technology described in the paper.

The advent of quantum computers promises to revolutionize computing by solving complex problems exponentially more rapidly than classical computers. However, today’s quantum computers face challenges such as maintaining stability and transporting quantum information.

Phonons, which are quantized vibrations in periodic lattices, offer new ways to improve these systems by enhancing qubit interactions and providing more reliable information conversion. Phonons also facilitate better communication within quantum computers, allowing the interconnection of them in a network.

Nanophononic materials, which are artificial nanostructures with specific phononic properties, will be essential for next-generation quantum networking and communication devices. However, designing phononic crystals with desired vibration characteristics at the nano-and micro-scales remains challenging.

A team of scientists from the University of Sharjah say they have invented a biosensor capable of detecting the gene mutations responsible for the loss of hearing.

Advances in Care Podcast — Episode 24In today’s world, genetic testing has become increasingly accessible for more people, creating an increased opportunity…

This prospective, multimodal neuroimaging study systematically assessed both intracerebellar pathology and cerebrocerebellar connectivity alterations in a genetically stratified cohort of amyotrophic lateral sclerosis:

Background and Objectives.

This single-center longitudinal cohort study has followed known carriers of PRNP pathogenic variants at risk for prion disease, individuals with a close relative who died of genetic prion disease but who have not undergone predictive genetic testing, and controls. All participants were asymptomatic at first visit and returned roughly annually. We determined PRNP genotypes, measured NfL and GFAP in plasma, and RT-QuIC, total PrP, NfL, T-tau, and beta-synuclein in CSF.

This study uncoversthe pivotal role of the enzyme METTL4 in promoting tumor metastasis through the mediation of nuclear N6-methyldeoxyadenosine (6mA) in mammalian cells. By utilizing cellular models, the study demonstrates how hypoxia induces METTL4 to mediate 6mA modifications. This process, in turn, activates genes essential for tumor metastasis, including the involvement of specific long noncoding RNA and a novel HIF-1α co-activator, ZMIZ1. These findings not only shed light on the epigenetic mechanisms driving tumor progression but also establish METTL4 as a prognostic marker for cancer and a potential target for therapeutic intervention. The promise of this discovery lies in its potential to inspire new strategies for combating hypoxia-induced tumor progression, opening avenues for further research and development in cancer treatment.

DNA N6-methyldeoxyadenosine (6mA) has been recognized in various organisms for its role in gene regulation. However, its function in mammalian cells, particularly in the context of cancer, has remained elusive. Previous studies have shown that 6mA modifications can influence gene expression and are present in several species, indicating a potential regulatory role in tumorigenesis. This research addresses a critical gap in understanding the nuclear role of 6mA and its enzymatic mediator METTL4, in mammalian tumor cells, particularly under hypoxia (a common condition in tumor microenvironments that promotes metastasis). The study posits that METTL4-mediated 6mA deposition is a key epigenetic modification that activates metastasis-inducing genes. This finding offers a new perspective on the mechanisms of tumor progression and identifying novel targets for therapeutic intervention.

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