Lifeboat Foundation: Safeguarding Humanity
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Blog – Page 18

When Bluesky CEO Jay Graber took the SXSW stage this week, she managed to make fun of Mark Zuckerberg without mentioning Meta at all. Her black T-shirt was emblazoned with black text stretching across the chest and sleeves, similar to the style of a T-shirt that the billionaire founder wore at an event last year. Graber’s shirt declared in Latin, Mundus sine Caesaribus. Or, “a world without Caesars.”

On Bluesky, users expressed such excitement over Graber’s T-shirt that the platform decided to sell replicas to raise money for its developer ecosystem.

The $40 shirt, available in sizes S – XL, sold out in roughly 30 minutes.

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Proteins are long molecules that must fold into complex three-dimensional structures to perform their cellular functions. This folding process occasionally goes awry, resulting in misfolded proteins that, if not corrected, can potentially lead to disease. Now, a new study has described a potential mechanism that could help explain why some proteins refold in a different pattern than expected.

The researchers, led by chemists at Penn State, found that a type of misfolding, in which the proteins incorrectly intertwine their segments, can occur and create a barrier to the normal folding process. Correcting this misfold requires high-energy or extensive unfolding, which slows the folding process, leading to the unexpected pattern first observed in the 1990s.

“Misfolded proteins can malfunction and lead to disease,” said Ed O’Brien, professor of chemistry in the Eberly College of Science, a co-hire of the Institute for Computational and Data Sciences at Penn State, and leader of the research team. “So, understanding the mechanisms involved in the folding process can potentially help researchers prevent or develop treatments for diseases caused by misfolding.”

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Using a systems and synthetic biology approach to study the molecular determinants of conversion, Wang et al. find that proliferation history and TF levels drive cell fate in direct conversion to motor neurons.

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Scientists have devised a way to store and read data from individual atoms embedded in tiny crystals only a few millimeters in size (where 1 mm is 0.04 inches). If scaled up, it could one day lead to ultra-high density storage systems capable of holding petabytes of data on a single disc — where 1 PB is equivalent to approximately 5,000 4K movies.

Encoding data as 1s and 0s is as old as the entire history of computing, with the only difference being the medium used to store this data — moving from vacuum tubes flashing on and off, tiny electronic transistors, or even compact discs (CDs), with pits in the surface representing 1s and smoothness indicating 0.

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Battery waste has become an increasing problem in recent years due to the massive demand for consumer electronics like smartphones and laptops, as well as the electrification of the automotive industry.

A recent report from Stanford University in the US, published in the journal Nature Communications, found that recycling lithium-ion batteries is far more environmentally friendly than mining for new materials.

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Inside the human eye, the retina is made up of several types of cells, including the light-sensing photoreceptors that initiate the cascade of events that lead to vision. Damage to the photoreceptors, either through degenerative disease or injury, leads to permanent vision impairment or blindness.

David Gamm, director of UW–Madison’s McPherson Eye Research Institute and professor of ophthalmology and visual sciences, says that stem cell replacement therapy using lab-grown photoreceptors is a promising strategy to combat retinal disease. The challenge is that stem cell treatments aimed at replacing photoreceptors need to first be tested in animals. Since human cells are not compatible in other species and are quickly rejected when transplanted, it’s difficult to assess their potential.

Pig and human retinas share many key features, making pigs ideal for modeling human retinal disease and testing ocular therapeutics. By testing ‘human-equivalent’ photoreceptors in pigs, we can get a better sense of what these cells can do if they are not immediately attacked by the host animal.

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In research inspired by the principles of quantum mechanics, researchers from Pompeu Fabra University (UPF) and the University of Oxford reveal new findings to understand why the human brain is able to make decisions quicker than the world’s most powerful computer in the face of a critical risk situation. The human brain has this capacity despite the fact that neurons are much slower at transmitting information than microchips, which raises numerous unknown factors in the field of neuroscience.

The research is published in the journal Physical Review E.

It should be borne in mind that in many other circumstances, the human brain is not quicker than technological devices. For example, a computer or calculator can resolve mathematical operations far faster than a person. So, why is it that in critical situations—for example, when having to make an urgent decision at the wheel of a car—the human brain can surpass machines?

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Adding immunotherapy to a new type of inhibitor that targets multiple forms of the cancer-causing gene mutation KRAS kept pancreatic cancer at bay in preclinical models for significantly longer than the same targeted therapy by itself, according to researchers from the Perelman School of Medicine at the University of Pennsylvania and Penn Medicine’s Abramson Cancer Center. The results, published in Cancer Discovery, prime the combination strategy for future clinical trials.

Patients with pancreatic cancer have an overall poor prognosis: in most patients, the disease has already spread at the time of diagnosis, resulting in limited treatment options. Nearly 90 percent of pancreatic cancers are driven by KRAS mutations, the most common cancer-causing gene mutation across cancer types, which researchers long considered “undruggable.”

In 2021, the first KRAS inhibitor was approved to treat with KRAS G12C mutations, but with longer follow-up, it has become clear that KRAS-mutant cancers can quickly evolve to resist therapies targeted at one specific form of the gene mutation.

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