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Category: genetics – Page 226

Our bodies can’t plug-and-play organs like replacement computer parts. The first rule of organ transplant is that the donor organs need to “match” with the host to avoid rejection. That is, the protein molecules that help the body discriminate between self and other need to be similar—a trait common (but not guaranteed) among members of the same family.

The key for getting an organ to “take” is reducing destructive immune attacks—the holy grail in transplantation. One idea is to genetically engineer the transplanted organ so that it immunologically “fits” better with the recipient. Another idea is to look beyond the organ itself to the source of rejection: haemopoietic stem cells, nestled inside the bone marrow, that produce blood and immune cells.

DISOT’s theory is simple but clever: swap out the recipient’s immune system with the donor’s, then transplant the organ. The recipient’s bone marrow is destroyed, but quickly repopulates with the donor’s stem cells. Once the new immune system takes over, the organ goes in.

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Yet when faced with enormous protein complexes, AI faltered. Until now. In a mind-bending feat, a new algorithm deciphered the structure at the heart of inheritance—a massive complex of roughly 1,000 proteins that helps channel DNA instructions to the rest of the cell. The AI model is built on AlphaFold by DeepMind and RoseTTAfold from Dr. David Baker’s lab at the University of Washington, which were both released to the public to further experiment on.

Our genes are housed in a planet-like structure, dubbed the nucleus, for protection. The nucleus is a high-security castle: only specific molecules are allowed in and out to deliver DNA instructions to the outside world—for example, to protein-making factories in the cell that translate genetic instructions into proteins.

At the heart of regulating this traffic are nuclear pore complexes, or NPCs (wink to gamers). They’re like extremely intricate drawbridges that strictly monitor the ins and outs of molecular messengers. In biology textbooks, NPCs often look like thousands of cartoonish potholes dotted on a globe. In reality, each NPC is a massively complex, donut-shaped architectural wonder, and one of the largest protein complexes in our bodies.

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When something goes wrong in mitochondria, the tiny organelles that power cells, it can cause a bewildering variety of symptoms such as poor growth, fatigue and weakness, seizures, developmental and cognitive disabilities, and vision problems. The culprit could be a defect in any of the 1,300 or so proteins that make up mitochondria, but scientists have very little idea what many of those proteins do, making it difficult to identify the faulty protein and treat the condition.

Researchers at Washington University School of Medicine in St. Louis and the University of Wisconsin–Madison systematically analyzed dozens of mitochondrial proteins of unknown function and suggested functions for many of them. Using these data as a starting point, they identified the genetic causes of three and proposed another 20 possibilities for further investigation. The findings, published May 25 in Nature, indicate that understanding how mitochondria’s hundreds of proteins work together to generate power and perform the organelles’ other functions could be a promising path to finding better ways to diagnose and treat such conditions.

“We have a parts list for mitochondria, but we don’t know what many of the parts do,” said co-senior author David J. Pagliarini, Ph.D., the Hugo F. and Ina C. Urbauer Professor and a BJC Investigator at Washington University. “It’s similar to if you had a problem with your car, and you brought it to a mechanic, and upon opening the hood they said, ‘We’ve never seen half of these parts before.’ They wouldn’t know how to fix it. This study is an attempt to define the functions of as many of those mitochondrial parts as we can so we have a better understanding of what happens when they don’t work and, ultimately, a better chance at devising therapeutics to rectify those problems.”

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As they grow, solid tumors surround themselves with a thick, hard-to-penetrate wall of molecular defenses. Getting drugs past that barricade is notoriously difficult. Now, scientists at UT Southwestern have developed nanoparticles that can break down the physical barriers around tumors to reach cancer cells. Once inside, the nanoparticles release their payload: a gene editing system that alters DNA inside the tumor, blocking its growth and activating the immune system.

The new , described in Nature Nanotechnology, effectively stopped the growth and spread of ovarian and liver tumors in mice. The system offers a new path forward for the use of the gene editing tool known as CRISPR-Cas9 in , said study leader Daniel Siegwart, Ph.D., Associate Professor of Biochemistry at UT Southwestern.

“Although CRISPR offers a new approach for treating , the technology has been severely hindered by the low efficiency of delivering payloads into tumors,” said Dr. Siegwart, a member of the Harold C. Simmons Comprehensive Cancer Center.

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Superhumans are coming! Various technological advances in the field of medicine through AI and CRISPR are going to radically alter our understanding of what it means to be human. AI and Crispr technology have been making revolutionary changes to the field of medicine. Artificial intelligence is being applied in identification of harmful genes and treatment of disease.

Multiple new gene editing technologies in addition to artificial intelligence will cause major changes in healthcare.
The gene-editing tool CRISPR, short for clustered regularly interspaced short palindromic repeats, could help us to reprogram life. It gives scientists more power and precision than they have ever had to alter human DNA.

Could it be conceivable that at one point in the future we could increase the average IQ of the population?
CRISPR technology in the future could enable efficient and affordable treatment of many diseases. It will be also probably used to enhance our intelligence.

CRISPR was originally designed as a technique for editing the DNA of living organisms, but its uses and capabilities have expanded substantially. It is now used widely in biomedical research, including research into human genetics. One of the main issues concerning technologies such as CRISPR-Cas9 is accuracy and safety, as mistakes can have significant and dangerous consequences when it comes to an individual’s genome.

Continue reading “The Age of Superhumans — Gene Editing Through CRISPR & AI” | >

Artificial Intelligence is touching almost every aspect of our lives. It’s reasonable to expect AI influence will only increase in the future. One of many fields heavily influenced by AI is the military. Particularly in the development of Supersoldiers. The notion of super-soldiers enhanced with biotechnology and cybernetics was once only possible in the realm of science fiction. But it may not be too long before these concepts become a reality.

A new worldwide arms race is pitting countries against each other to be the first to successfully create real genetically modified super soldiers by using tools such as CRISPR. Understandably many of these human enhancement technologies raise health and safety questions and it is more likely these enhancements will first gain traction in countries that do not place as much weight on ethical concerns.

According to US Intelligence, China has conducted “human testing” on members of the People’s Liberation Army in hope of developing soldiers with “biologically enhanced capabilities.

This has made the U.S. military’s top intelligence agencies increasingly worried but the Pentagon has significantly invested in its own research in AI and in the extension of the human senses beyond their current physical limitations, to provide soldiers with superhuman abilities.

Continue reading “The Rise of Supersoldiers — How AI Changes Everything” | >

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia, affecting more than 5.8 million individuals in the U.S. Scientists have discovered some genetic variants that increase the risk for developing Alzheimer’s; the most well-known of these for people over the age of 65 is the APOE ε4 allele. Although the association between APOE4 and increased AD risk is well-established, the mechanisms responsible for the underlying risk in human brain cell types has been unclear until now.

Researchers from Boston University School of Medicine (BUSM) have discovered two important novel aspects of the gene: 1) human genetic background inherited with APOE4 is unique to APOE4 patients and 2) the mechanistic defects due to APOE4 are unique to human cells.

Our study demonstrated what the APOE4 gene does and which brain cells get affected the most in humans by comparing human and mouse models. These are important findings as we can find therapeutics if we understand how and where this risk gene is destroying our brain.

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A new theory suggests that mutations have few straightforward ways to establish themselves in cells and cause tumors.

For many researchers, the road to cancer prevention is long and difficult, but a recent study by Rice University scientists suggests that there may be shortcuts.

A theoretical framework is being developed by Rice scientist Anatoly Kolomeisky, postdoctoral researcher Hamid Teimouri, and research assistant Cade Spaulding that will explain how cancers brought on by several genetic mutations might be more readily recognized and perhaps prevented.

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