Use code coolworlds at https://incogni.com/coolworlds to get an exclusive 60% off an annual Incogni plan. Nuclear weapons are the most terrifying invention of humanity. Could our genius to create such weapons also end them? Today we explore how neutrinos could be used to do just that, fizzling out nukes anywhere on Earth and with no defense. Written & presented by Prof. David Kipping, edited by Jorge Casas. Special thanks to Sam Gregson ( / @badboyofscience) for fact checking. → Support our research: https://www.coolworldslab.com/support → Get merch: https://teespring.com/stores/cool-wor… Check out our podcast: / @coolworldspodcast THANK-YOU to D. Smith, M. Sloan, L. Sanborn, C. Bottaccini, D. Daughaday, A. Jones, S. Brownlee, N. Kildal, Z. Star, E. West, T. Zajonc, C. Wolfred, L. Skov, G. Benson, A. De Vaal, M. Elliott, B. Daniluk, S. Vystoropskyi, S. Lee, Z. Danielson, C. Fitzgerald, C. Souter, M. Gillette, T. Jeffcoat, J. Rockett, D. Murphree, T. Donkin, K. Myers, A. Schoen, K. Dabrowski, J. Black, R. Ramezankhani, J. Armstrong, K. Weber, S. Marks, L. Robinson, S. Roulier, B. Smith, J. Cassese, J. Kruger, S. Way, P. Finch, S. Applegate, L. Watson, E. Zahnle, N. Gebben, J. Bergman, E. Dessoi, C. Macdonald, M. Hedlund, P. Kaup, C. Hays, W. Evans, D. Bansal, J. Curtin, J. Sturm, RAND Corp., M. Donovan, N. Corwin, M. Mangione, K. Howard, L. Deacon, G. Metts, R. Provost, B. Sigurjonsson, G. Fullwood, B. Walford, J. Boyd, N. De Haan, J. Gillmer, R. Williams, E. Garland, A. Leishman, A. Phan Le, R. Lovely, M. Spoto, A. Steele, K. Yarbrough, A. Cornejo, D. Compos, F. Demopoulos, G. Bylinsky, J. Werner, B. Pearson, S. Thayer, T. Edris, B. Seeley, F. Blood, M. O’Brien, P. Muzyka, D. Lee, J. Sargent, M. Czirr, F. Krotzer, I. Williams, J. Sattler, J. Smallbon, B. Reese, J. Yoder, O. Shabtay, X. Yao, S. Saverys, M. Pittelli, A. Nimmerjahn & C. Seay. CHAPTERS 0:00 Neutrinos 3:39 Incogni 5:08 Neutrino Factories 9:11 Applications 14:19 My Take 16:17 Outro & Credits #nuclearwar #nuke #coolworlds
The new findings could lead to better treatments for rheumatoid arthritis, lupus and other inflammatory diseases – and may even help us slow aging.
Researchers have discovered how “leaky” mitochondria can drive harmful inflammation responsible for diseases such as lupus and rheumatoid arthritis. Scientists may be able to leverage the findings to develop better treatments for those diseases, improve our ability to fight off viruses and even slow aging.
The new discovery reveals how genetic material can escape from our cellular batteries, known as mitochondria, and prompt the body to launch a damaging immune response. By developing therapies to target this process, doctors may one day be able to stop the harmful inflammation and prevent the toll it takes on our bodies.
A new study provided light on the role of the protein STAP-1 in activating certain immune cells. Understanding STAP-1’s involvement in these cells may help researchers gain a better understanding of immune-related diseases and potential treatments.
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The researchers discovered that STAP-1 plays a key role in the activation of T cells, which are white blood cells that help the body defend itself against infections and preserve overall health. T cells are capable of identifying foreign substances that elicit an immune response (antigens) and developing tailored responses to destroy pathogens like bacteria and viruses.
Two early clinical trials that together included nine patients suggest that a treatment called CAR-T therapy could treat glioblastoma, but its long-term effects are unknown.
According to the CDC, more than 140,000 Americans are dying each year from alcohol-related causes, and the rate of deaths has been rising for years, especially during the pandemic.
The idea: For occasional drinkers, alcohol causes the brain to release more dopamine, a chemical that makes you feel good. Chronic alcohol use, however, causes the brain to produce, and process, less dopamine, and this persistent dopamine deficit has been linked to alcohol relapse.
There is currently no way to reverse the changes in the brain brought about by AUD, but a team of US researchers suspected that an in-development gene therapy for Parkinson’s disease might work as a dopamine-replenishing treatment for alcoholism, too.
Researchers at Virginia Commonwealth University unveiled a genetic bullseye—a key gene that plays a pivotal role in initiating a genetic domino cascade, driving bone metastasis in prostate cancer.
A key gene that fuels the molecular cascade driving prostate cancer bone metastasis progression may open avenues for targeted therapies.
They treated three patients with recurrent glioblastoma using a variant of an existing CAR-T therapy, adding additional antibodies to the treatment — and the results were truly astounding.
According to the paper published in The New England Journal of Medicine, one patient saw their tumor decrease in size by 18.5% two days after the treatment, and by day 69, the tumor had decreased by 60.7%, while another saw their ‘tumor regress rapidly’, according to Mass General Brigham.
After the third patient was treated, an MRI showed that a single infusion had led to a ‘near-complete tumor regression’ in just five days.
Scientists have categorized different types of CRISPR systems into two classes based on how their Cas nucleases function. In class 1 (types I, III, and IV), different Cas proteins form a complex machinery to identify and cut foreign DNA; in class 2 CRISPR systems (types II, V, and VI), a single Cas protein effector recognizes and cleaves DNA.9
After characterizing CRISPR’s role as a defense mechanism in bacteria, researchers soon realized that they could harness this system for gene manipulation in any cell. All they needed to do was design a CRISPR gRNA sequence that bound to a specific DNA sequence and triggered the Cas nuclease, which would then cut precisely at that location. With CRISPR, researchers routinely knock out gene function by cutting out a DNA fragment, or they insert a desired genetic sequence into the genome by providing a reference DNA template along with the CRISPR components. While editing eukaryotic cells has been the focus for tackling diseases, many researchers now use CRISPR to edit bacterial communities.
“It’s almost like back to the beginning or back to the origins. There’s some irony in bringing CRISPR back to where it came from,” said Rodolphe Barrangou, a functional genomics researcher at North Carolina State University, who helped characterize the immune function of CRISPR and has been working with it for more than 20 years.
