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Scientists are working to end the need for human heart transplants by 2028. A team of researchers in the UK, Cambridge, and the Netherlands are developing a robot heart that can pump blood through the circulatory network but is soft and pliable. The first working model should be ready for implantation into animals within the next 3 years, and into humans within the next 8 years. The device is so promising that it is among just 4 projects that have made it to the shortlist for a £30-million prize, called the Big Beat Challenge for a therapy that can change the game in the treatment of heart disease.

The other projects include a genetic therapy for heart defects, a vaccine against heart disease, and wearable technology for early preclinical detection of heart attacks and strokes.

The need

There are about 7 million patients with heart and circulatory issues in the UK of which over 150,000 die every year. About 200 heart transplants occur each year in the UK alone, yet about 20 patients die in the same period while waiting for one. This is especially true if the patient waiting for one is a baby who was born with a defective heart, since babies need to have hearts transplanted from other babies – who must have died. And even with a successful transplant, strong immunosuppressive drugs must be started and often continued lifelong so that immune rejection does not occur. This is, however, accompanied by a higher risk of infectious and other complications.

In the underground movement known as, people are taking their health into their own hands. Biohacking ranges from people making simple lifestyle changes to extreme body modifications.

One popular form of focuses on nutrigenomics, where biohackers study how the foods they eat affect their genes over time. They believe they can map and track the way their diet affects genetic function. They use dietary restrictions and blood tests, while tracking their moods, energy levels, behaviors, and cognitive abilities.

Then there are grinders, a subculture of A grinder believes there’s a hack for every part of the body. Rather than attempting to modify our existing biology, grinders seek to enhance it with implanted technology.

Huntington’s disease (HD) is a neurological disorder that causes progressive loss of movement, coordination and cognitive function. It is caused by a mutation in a single gene called huntingtin (HTT). More than 200,000 people worldwide live with the genetic condition, approximately 30,000 in the United States. More than a quarter of a million Americans are at risk of inheriting HD from an affected parent. There is no cure.

But in a new study, published December 12, 2022 in Nature Neuroscience, researchers at University of California San Diego School of Medicine, with colleagues elsewhere, describe using RNA-targeting CRISPR/Cas13D technology to develop a new therapeutic strategy that specifically eliminates toxic RNA that causes HD.

CRISPR is known as a genome-editing tool that allows scientists to add, remove or alter genetic material at specific locations in the genome. It is based on a naturally occurring immune defense system used by bacteria. However, current strategies run the risk of off-target edits at unintended sites that may cause permanent and inheritable chromosomal insertions or genome alterations. Because of this, significant efforts have focused on identifying CRISPR systems that target RNA directly without altering the genome.

An international research team led by Dr. Ana Guadaño at the Alberto Sols Biomedical Research Institute (IIBM, a combined CSIC-UAM center) and involving the Complutense University of Madrid (UCM), used CRISPR gene editing techniques to incorporate into mice a mutation of the MCT8 protein responsible for transporting thyroid hormones to the interior of the cell.

Patients with mutations in this protein suffer from Allan-Herndon-Dudley syndrome, a that takes the form of serious neurological alterations, in which each patient may reveal a different mutation of MCT8.

This study, published in Neurobiology of Disease, describes the first avatar model for the disease—in other words, the first animal model with the same as various .

These genetically engineered plants can take over the work of 30 houseplants.

A bioengineered plant is able to clean the air by doing the work of over 30 houseplantsIt could be the start of a bold new industry that develps over the next 15 to 20 years.

The Neo P1 is the first of its kind.

A startup in Paris has developed a plant that could take over the work of 30 houseplants — and it’s just the beginning.


Yuri_Arcurs/iStock.

Neo P1, effectively a super-efficient air purifier, can metabolize four major indoor air pollutants and absorb certain volatile organic compounds, or VOCs. It’s the start of a revolution in plants that could lead to a dramatic new industry.

Northwestern University researchers have discovered a previously unknown mechanism that drives aging.

In a new study, researchers used artificial intelligence to analyze data from a wide variety of tissues, collected from humans, mice, rats and killifish. They discovered that the length of can explain most molecular-level changes that occur during aging.

All cells must balance the activity of long and short genes. The researchers found that longer genes are linked to longer lifespans, and shorter genes are linked to shorter lifespans. They also found that aging genes change their activity according to length. More specifically, aging is accompanied by a shift in activity toward short genes. This causes the gene activity in cells to become unbalanced.

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Northwestern University researchers have discovered a previously unknown mechanism that drives aging.

In a new study, researchers used artificial intelligence to analyze data from a wide variety of tissues, collected from humans, mice, rats and killifish. They discovered that the length of genes can explain most molecular-level changes that occur during aging.

All cells must balance the activity of long and short genes. The researchers found that longer genes are linked to longer lifespans, and shorter genes are linked to shorter lifespans. They also found that aging genes change their activity according to length. More specifically, aging is accompanied by a shift in activity toward short genes. This causes the gene activity in cells to become unbalanced.

Tournament selection, roulette selection, mutation, crossover — all processes used in genetic algorithms. Dr Alex Turner explains using the Knapsack Problem.

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This video was filmed and edited by Sean Riley.

Computer Science at the University of Nottingham: https://bit.ly/nottscomputer.

Computerphile is a sister project to Brady Haran’s Numberphile. More at http://www.bradyharan.com