Lifeboat Foundation

So, 22% increase. Roughly like a 120 person, which means if this literally translates to people it means a maximizing of our current lifespan. The rest is just a rundown of Aubrey’s experiment.

Dr Katcher’s lifespan experiment has come to an end as the last remaining rat, Sima, has died. She was 1,464 days old which is a record for Sprague-Dawley rats. We also talk about the exciting Robust Mouse Rejuvenation project at the LEV Foundation.

Continue reading “Dr Katcher’s E5 Lifespan Experiment Final Result | 22% Lifespan Extension” »

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Martian soil is generally poor for growing plants, but researchers have used CRISPR to create gene-edited rice that might be able to germinate and grow despite the hostile habitat.

By Leah Crane

Continue reading “Gene-edited rice may be able to grow on Mars” »

The research team used a new CRISPR-based genome editing system named PESpRY.

Scientists in China have effectively treated retinitis pigmentosa.

The research team utilized a novel form of CRISPR-based genome editing that is exceptionally adaptable and could potentially remedy numerous genetic mutations responsible for causing different diseases.

Summary: Using a highly versatile form of CRISPR gene editing, researchers successfully restored vision in mice with retinitis pigmentosa.

Source: Rockefeller University Press.

Researchers in China have successfully restored the vision of mice with retinitis pigmentosa, one of the major causes of blindness in humans.

Researchers in China have successfully restored the vision of mice with retinitis pigmentosa, one of the major causes of blindness in humans. The study, to be published March 17 in the Journal of Experimental Medicine, uses a new, highly versatile form of CRISPR-based genome editing with the potential to correct a wide variety of disease-causing genetic mutations.

Researchers have previously used genome editing to restore the vision of mice with genetic diseases, such as Leber congenital amaurosis, that affect the retinal pigment epithelium, a layer of non-neuronal cells in the eye that supports the light-sensing rod and cone photoreceptor cells. However, most inherited forms of blindness, including retinitis pigmentosa, are caused by genetic defects in the neural photoreceptors themselves.

“The ability to edit the genome of neural retinal cells, particularly unhealthy or dying photoreceptors, would provide much more convincing evidence for the potential applications of these genome-editing tools in treating diseases such as retinitis pigmentosa,” says Kai Yao, a professor at the Wuhan University of Science and Technology.

A study of the electron excitation response of DNA to proton radiation has elucidated mechanisms of damage incurred during proton radiotherapy.

Radiobiology studies on the effects of ionizing radiation on human health focus on the deoxyribonucleic acid (DNA) molecule as the primary target for deleterious outcomes. The interaction of ionizing radiation with tissue and organs can lead to localized energy deposition large enough to instigate double strand breaks in DNA, which can lead to mutations, chromosomal aberrations, and changes in gene expression. Understanding the mechanisms behind these interactions is critical for developing radiation therapies and improving radiation protection strategies. Christopher Shepard of the University of North Carolina at Chapel Hill and his colleagues now use powerful computer simulations to show exactly what part of the DNA molecule receives damaging levels of energy when exposed to charged-particle radiation (Fig. 1) [1]. Their findings could eventually help to minimize the long-term radiation effects from cancer treatments and human spaceflight.

The interaction of radiation with DNA’s electronic structure is a complex process [2, 3]. The numerical models currently used in radiobiology and clinical radiotherapy do not capture the detailed dynamics of these interactions at the atomic level. Rather, these models use geometric cross-sections to predict whether a particle of radiation, such as a photon or an ion, crossing the cell volume will transfer sufficient energy to cause a break in one or both of the DNA strands [4– 6]. The models do not describe the atomic-level interactions but simply provide the probability that some dose of radiation will cause a population of cells to lose their ability to reproduce.

Our trusted and proven sources were correct once again, as just hours after we broke the news that a Gattaca series is in development at Showtime, The Hollywood Reporter confirmed our exclusive. One of our writers here at Giant Freakin Robot wrote just two weeks ago that the 1997 dystopian sci-fi classic would be perfect as a television series, and it’s amazing how quickly we went from hoping it would happen to confirming that it is. The new series will be coming from the creators of Homeland, Howard Gordan and Alex Gansa.

As noted in our initial report, this is not the first time the film, starring Ethan Hawke, Uma Thurman, and Jude Law, has been optioned as a series. Back in 2009, Sony attempted to turn the movie into a procedural from Gil Grant, a writer on 24 and NCIS. The underrated cult-classic movie is ideal for transforming into a prestige series on a premium network as its themes on transhumanism, genetic manipulation, and a stratified society have become more relevant as technology leaps forwards every year.

In Gattaca, eugenics separates society into “valids” and “in-valids,” even if genetic discrimination is illegal; that hasn’t stopped businesses from profiling, giving the best jobs to the former and only menial labor opportunities to the latter. Ethan Hawke plays Vincent, an in-valid with a heart defect that uses samples from Jude Law’s Jerome Morrow, a paralyzed Olympic champion swimmer that’s also a valid. Using the purloined DNA, Vincent cons his way into a job at Gattaca Aerospace Corporation, eventually being selected as a navigator for a trip to Saturn’s moon, Titan.

A new study published in Nature reports that a technology known as spatial omics can be used to map simultaneously how genes are switched on and off and how they are expressed in different areas of tissues and organs. This improved technology, developed by researchers at Yale University and Karolinska Institutet, could shed light on the development of tissues, as well as on certain diseases and how to treat them.

Almost all cells in the body have the same set of genes and can in principle become any kind of cell. What distinguishes the cells is how the genes in our DNA are used. In recent years, spatial omics have given us a deeper understanding of how cells read the genome in precise locations in tissues. Now, researchers have further evolved this technology to increase knowledge of how tissues develop and how different diseases arise.

A key part of the study is the researchers’ ability to spatially map simultaneously two crucial components of our genetic makeup, the epigenome and the transcriptome. The epigenome controls the switching mechanisms that turn genes on and off in individual cells, whereas the transcriptome is the result of those gene expressions and what makes each cell unique.