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4000 Times Fewer Gene Editing Errors Without Sacrificing Speed

Scientists at The University of Texas at Austin have redesigned a key component of a widely used CRISPR-based gene-editing tool, called Cas9, to be thousands of times less likely to target the wrong stretch of DNA while remaining just as efficient as the original version, making it potentially much safer.

Other labs have redesigned Cas9 to reduce off-target interactions, but so far, all these versions improve accuracy by sacrificing speed. SuperFi-Cas9, as this new version has been dubbed, is 4,000 times less likely to cut off-target sites but just as fast as naturally occurring Cas9. Bravo says you can think of the different lab-generated versions of Cas9 as different models of self-driving cars. Most models are really safe, but they have a top speed of 10 miles per hour.

“They’re safer than the naturally occurring Cas9, but it comes at a big cost: They’re going extremely slowly,” said Bravo. “SuperFi-Cas9 is like a self-driving car that has been engineered to be extremely safe, but it can still go at full speed.”

Deleting a Protein May Prevent Heart Attacks and Strokes

Macrophages travel through our arteries, gobbling fat the way Pac-man gobbled ghosts. But fat-filled macrophages can narrow blood vessels and cause heart disease. Now, UConn Health researchers describe in Nature Cardiovascular Research how deleting a protein could prevent this and potentially prevent heart attacks and strokes in humans.

Macrophages are large white blood cells that cruise through our body as a kind of clean-up crew, clearing hazardous debris. But in people with atherosclerosis—fatty deposits and inflammation in their blood vessels— macrophages can cause trouble. They eat excess fat inside artery walls, but that fat causes them to become foamy. And foamy macrophages tend to encourage inflammation in the arteries and sometimes bust apart plaques, freeing clots that can cause heart attack, stroke, or embolisms elsewhere in the body.

Changing how macrophages express a certain protein could prevent that kind of bad behavior, reports a team of researchers from UConn Health. They found that the protein, called TRPM2, is activated by inflammation. It signals macrophages to start eating fat. Since inflammation of the blood vessels is one of the primary causes of atherosclerosis, TRPM2 gets activated quite a bit. All that TRPM2 activation pushes macrophage activity, which leads to more foamy macrophages and potentially more inflamed arteries. The way that TRPM2 activated macrophage activity was surprising, says Lixia Yue, a UConn School of Medicine cell biologist.

How a Seagen cancer drug with Nobel Prize science might also work in diabetes

Some diabetes therapies work by ramping up the body’s secretion of insulin to counteract high blood sugar levels. | Preserving insulin-producing pancreatic beta cells—rather than exhausting them—might be a better strategy in the treatment of diabetes. Following that thinking, scientists at the Karolinska Institute found a cancer drug by Seagen holds promise for the metabolic disease.

Surgeons implant printed earlobe in a work-accident victim

A 55-year-old man who lost half of his external ear in a work accident in a carpentry shop that couldn’t be reattached nevertheless has a new ear lobe instead.

Plastic surgeons at Jerusalem’s Shaare Zedek Medical Center (SZMC) used advanced technology and artificial cartilage to sculpt a new earlobe and implant it on the side of the accident victim’s head.

The patient was rushed to SZMC’s emergency department after a wooden surface fell on him and caused the loss of the upp… See more.


“At first, I didn’t feel the lack of an ear,” said the patient, an Arab who works in the Jerusalem area.

Tiny Experimental Implant Could Treat Neuropathic Pain

𝐏𝐚𝐢𝐧 𝐍𝐞𝐰𝐬 𝐍𝐞𝐭𝐰𝐨𝐫𝐤:

The Neuro-Network.

𝐓𝐢𝐧𝐲 𝐄𝐱𝐩𝐞𝐫𝐢𝐦𝐞𝐧𝐭𝐚𝐥 𝐈𝐦𝐩𝐥𝐚𝐧𝐭 𝐂𝐨𝐮𝐥𝐝 𝐓𝐫𝐞𝐚𝐭 𝐍𝐞𝐮𝐫𝐨𝐩𝐚𝐭𝐡𝐢𝐜 𝐏𝐚𝐢𝐧

𝘼 𝙩𝙞𝙣𝙮 𝙬𝙞𝙧𝙚𝙡𝙚𝙨𝙨 𝙞𝙢𝙥𝙡𝙖𝙣𝙩 𝙩𝙝𝙖𝙩 𝙨𝙩𝙞𝙢𝙪𝙡𝙖𝙩𝙚𝙨 𝙥𝙚𝙧𝙞𝙥𝙝𝙚𝙧𝙖𝙡 𝙣𝙚𝙧𝙫𝙚𝙨 𝙛𝙧𝙤𝙢 𝙬𝙞𝙩𝙝𝙞𝙣 𝙗𝙡𝙤𝙤𝙙 𝙫𝙚𝙨𝙨𝙚𝙡𝙨 𝙨𝙝𝙤𝙬𝙨 𝙥𝙤𝙩𝙚𝙣𝙩𝙞𝙖𝙡 𝙖𝙨 𝙖 … See more.


By Pat Anson, PNN Editor.

A tiny wireless implant that stimulates peripheral nerves from within blood vessels shows potential as a treatment for neuropathic pain, according to a proof-of-concept study by a team of Texas researchers published in the journal Nature Biomedical Engineering.

Mark Zuckerberg — Founder and CEO of Meta | The Tim Ferriss Show

It’s a reference to the evil form in the ‘Lord of the Rings’ books. For those unfamiliar with the ‘Lord of the Rings” books and movies, the Eye of Sauron is the chief antagonist in the series, exemplified as a flaming eye and that is a metaphor for pure evil. It’s not something anyone would want to be compared to unless, of course, you are Meta founder and CEO Mark Zuckerberg.


Mark Zuckerberg on Long-Term Strategy, Business and Parenting Principles, Personal Energy Management, Building the Metaverse, Seeking Awe, the Role of Religion, Solving Deep Technical Challenges (e.g., AR), and More | Brought to you by Eight Sleep’s Pod Pro Cover sleeping solution for dynamic cooling and heating (http://eightsleep.com/Tim), Magic Spoon delicious low-carb cereal (http://magicspoon.com/tim), and Helium 10 all-in-one software suite to sell on Amazon (https://helium10.com/tim).

Mark Zuckerberg (FB/IG) is the founder, chairman, and CEO of Meta, which he originally founded as Facebook in 2004. Mark is responsible for setting the overall direction and product strategy for the company. In October 2021, Facebook rebranded to Meta to reflect all of its products and services across its family of apps and a focus on developing social experiences for the metaverse—moving beyond 2D screens toward immersive experiences like augmented and virtual reality to help build the next evolution in social technology.

He is also the co-founder and co-CEO of the Chan Zuckerberg Initiative with his wife Priscilla, which is leveraging technology to help solve some of the world’s toughest challenges—including supporting the science and technology that will make it possible to cure, prevent, or manage all diseases by the end of the twenty-first century.

Mark studied computer science at Harvard University before moving to Palo Alto, California, in 2004.

The Biggest Revolution Since the Computer Is Here — Synthetic Biology 🧫

Innovations in computing tech have improved the accuracy of DNA synthesis and enabled synthetic biology to work in the real world.


I don’t know about you, but I’m constantly looking for the “next big thing” in the stock market. And I think synthetic biology might just be it.

Why? If you invested just $10,000 into any of those world-changing stocks back in their early days, you’d have MILLIONS today. Forget the Iraq War, the housing crash, the European debt crisis. Forget the pandemic and the Russia-Ukraine war. Through it all, you’d have millions today.

Clinical Trials Targeting Aging

A miniature review of.


The risk of morbidity and mortality increases exponentially with age. Chronic inflammation, accumulation of DNA damage, dysfunctional mitochondria, and increased senescent cell load are factors contributing to this. Mechanistic investigations have revealed specific pathways and processes which, proposedly, cause age-related phenotypes such as frailty, reduced physical resilience, and multi-morbidity. Among promising treatments alleviating the consequences of aging are caloric restriction and pharmacologically targeting longevity pathways such as the mechanistic target of rapamycin (mTOR), sirtuins, and anti-apoptotic pathways in senescent cells. Regulation of these pathways and processes has revealed significant health-and lifespan extending results in animal models. Nevertheless, it remains unclear if similar results translate to humans. A requirement of translation are the development of age-and morbidity associated biomarkers as longitudinal trials are difficult and not feasible, practical, nor ethical when human life span is the endpoint. Current biomarkers and the results of anti-aging intervention studies in humans will be covered within this paper. The future of clinical trials targeting aging may be phase 2 and 3 studies with larger populations if safety and tolerability of investigated medication continues not to be a hurdle for further investigations.

As age increases, so does the susceptibility to a series of chronic diseases which ultimately result in fatal endings. This is such a basic part of life that we rarely consider if there is anything we can do to postpone it. So far, the principal of “one-disease-one-treatment” has brought medical sciences far but this line of thought may soon be outdated when it comes to aging related conditions. It is like fighting a many-headed monster: If one condition is treated successfully, another emerges shortly after. This point is illustrated as eradicating the two leading causes of death (cancer and cardiovascular disease) extends mean life span by 3.3 and 4 years, respectively (Arias et al., 2013). Interestingly, the gain of treating multiple diseases combined exceeds the sum of these numbers.

Aging is the greatest risk factor for most diseases likely because as aging progresses, cells and tissue undergo a series of processes which result in gradually declining functionality, accumulation of damage, increased inflammation, and cell death. If these processes are reversable or treatable, all aging related chronical diseases may potentially be simultaneously treated—or postponed—and healthy aging could be achieved. This approach to treating aging itself could effectively treat chronic diseases among the world’s elderly, shifting from treating symptoms of aging to treating the cause of it. The fact that the number and proportion of elderly people (65 years) is growing in every country in the world underlines the relevance of this field of research (World Population Prospects — Population Division, 2021).

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