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Russian chemists synthesize silver compounds that outperform main tuberculosis drug Three-out-of-five new silver complexes show higher activity against tuberculosis bacteria than rifampicin — the frontline antibiotic One compound completely kills the bacteria, and doesn't just stops their growth 🔸 It uses myrtenic acid and attacks two key targets: cell...

11,938 views • 11 days ago •via X (Twitter)

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🚨 SCIENTISTS MAY HAVE FOUND A NEW WAY TO KILL DRUG-RESISTANT BACTERIA. And it doesn't rely on traditional antibiotics. Researchers repurposed a ruthenium-based anticancer drug and activated it using ultrasound deep inside infected tissue. Why this matters: • Antibiotic resistance is one of the fastest-growing threats to global health • Drug-resistant infections could kill more people than cancer by 2050 • Many antibiotics are losing effectiveness • Deep-tissue infections are difficult to target safely • Bacteria continue evolving resistance to conventional treatments The breakthrough: Scientists used a compound called TLD1433, originally developed for cancer therapy. By itself, the drug is largely inactive. But when exposed to focused ultrasound... it generates highly reactive oxygen molecules that attack bacterial DNA and destroy protective biofilms. Unlike antibiotics, the treatment doesn't target a single bacterial pathway. Instead, it creates widespread oxidative damage that bacteria struggle to evolve resistance against. The results were remarkable: • Outperformed conventional antibiotics in laboratory tests • Reduced survival of pneumonia-causing bacteria to just 14% • Broke down oxygen-starved bacterial biofilms • In animal studies, every treated mouse survived • Only 25% of untreated controls survived The deeper implication is enormous: For decades we've searched for new antibiotics. But the future may not be finding stronger drugs. It may be activating existing drugs only where they're needed. By combining chemistry with precisely targeted ultrasound... scientists could attack dangerous infections deep inside the body while minimizing damage to healthy tissue. The real question is: Could sound become one of medicine's most powerful weapons against antibiotic resistance? Follow for more frontier science and technology discoveries.

TheNewPhysics

10,651 views • 1 month ago

🚨 SCIENTISTS JUST CREATED A WAY TO KILL ANTIBIOTIC-RESISTANT BACTERIA USING NOTHING BUT LIGHT. Researchers have developed graphene quantum dots that destroy over 99.9% of antibiotic-resistant S. aureus and E. coli when hit with low-intensity blue light without using any antibiotics at all. The dots work by generating reactive oxygen species that rip apart bacterial cells. After chemically modifying them, the team made the dots over 20 times more efficient, allowing them to work at very low concentrations. Because they’re made from graphene instead of toxic heavy metals, they’re also much safer for medical use. Why this matters: • Antibiotic resistance is one of the fastest-growing threats to global health • This offers a completely different weapon light instead of drugs • The dots could be used in wound dressings, creams, gels, and coatings for implants and catheters • Graphene is cheap, stable, and biocompatible The deeper implication: We’re running out of effective antibiotics, and bacteria are evolving faster than we can develop new drugs. This approach flips the script: instead of fighting bacteria with chemicals they can eventually resist, we use light to trigger a physical attack they can’t easily adapt to. If this scales, it could become a powerful new tool in the fight against superbugs especially for wound infections and medical devices, where resistant bacteria are hardest to treat. Sometimes the solution isn’t a better drug. It’s a better way to attack. Would you trust a light-activated treatment over traditional antibiotics if it worked this well? Follow for more frontier nanotechnology and breakthroughs in the fight against antibiotic resistance.

TheNewPhysics

35,112 views • 1 month ago

BREAKING: President Donald J. Trump just signed an executive order implementing Most Favored Nation prescription drug pricing — which will deliver dramatically lower drug prices for the American people. Here's what it does: REDUCING DRUG PRICES FOR AMERICANS AND TAXPAYERS: Today, President Donald J. Trump signed an Executive Order to bring the prices Americans and taxpayers pay for prescription drugs in line with those paid by similar nations. — The Order directs the U.S. Trade Representative and Secretary of Commerce to take action to ensure foreign countries are not engaged in practices that purposefully and unfairly undercut market prices and drive price hikes in the United States. — The Order instructs the Administration to communicate price targets to pharmaceutical manufacturers to establish that America, the largest purchaser and funder of prescription drugs in the world, gets the best deal. — The Secretary of Health and Human Services will establish a mechanism through which American patients can buy their drugs directly from manufacturers who sell to Americans at a “Most-Favored-Nation” price, bypassing middlemen. — If drug manufacturers fail to offer most-favored-nation pricing, the Order directs the Secretary of Health and Human Services to: (1) propose rules that impose most-favored-nation pricing; and (2) take other aggressive measures to significantly reduce the cost of prescription drugs to the American consumer and end anticompetitive practices. GETTING A BETTER DEAL FOR AMERICANS: President Trump is once again taking action to keep pharmaceutical manufacturers from charging Americans high drug prices while giving steep discounts to other wealthy nations. — According to recent data, the prices Americans pay for brand-name drugs are more than three times the price other OECD nations pay, even after accounting for discounts manufacturers provide in the U.S. — The United States has less than five percent of the world’s population, yet funds roughly 75% of global pharmaceutical profits. — Drug manufacturers discount their products to gain access to foreign markets and then subsidize those discounts through high prices charged in America—in essence, Americans are subsidizing drug-manufacturer profits and foreign health systems, despite drug manufacturers benefiting from generous research subsidies and enormous healthcare spending by the U.S. Government. — In his first term, President Trump took historic action to keep Medicare and seniors from paying more for drugs than economically comparable countries, which the Biden Administration rescinded before it could take effect. — Instead of fixing this problem, the Biden Administration’s greatest achievement was to negotiate prices that were, on average, 78 percent higher than in 11 comparable countries as part of Biden’s effort to “beat Medicare.” DELIVERING ON PROMISES TO PUT AMERICAN PATIENTS FIRST: President Trump is delivering on his promise to once again put America first by furthering efforts to get American patients and taxpayers a fair deal for prescription drugs. — This Order builds on actions from President Trump’s first term to make progress on reducing price disparities at home and expands those efforts by including Medicaid in addition to Medicare. — President Trump recently signed an Executive Order to take additional action to lower drug prices, including by providing massive discounts to low-income patients for lifesaving medicines, facilitating importation programs, and increasing the availability of generic and biosimilar medicines. — President Trump is also working to make drug prices radically transparent, as he recently signed an Executive Order to build on his historic price transparency efforts undertaken during his first term. — President Trump has been relentless in his effort to address the unfair and outrageous prices Americans pay for prescription drugs: — President Trump: “In case after case, our citizens pay massively higher prices than other nations pay for the same exact pill, from the same factory, effectively subsidizing socialism aboard [abroad] with skyrocketing prices at home. So we would spend tremendous amounts of money in order to provide inexpensive drugs to another country. And when I say the price is different, you can see some examples where the price is beyond anything — four times, five times different.”

Rapid Response 47

611,256 views • 1 year ago

🚨 SCIENTISTS JUST DISCOVERED THAT BACTERIA HAVE BEEN USING A QUANTUM ENERGY TRICK FOR BILLIONS OF YEARS. In a breakthrough published in Nature Chemistry, researchers from the University of Sheffield (working with IBM and international collaborators) have shown that purple photosynthetic bacteria (Rhodobacter sphaeroides) use singlet fission (SF) as a functional mechanism to enhance light harvesting. When carotenoids absorb blue-green light (via their S₂ state), the energy rapidly undergoes heterofission: the singlet exciton splits into a pair of triplet excitons shared between a carotenoid and its neighboring bacteriochlorophyll (BChl) a molecule. These triplet pairs are long-lived and weakly coupled. They then recombine via triplet-triplet annihilation (TTA), efficiently populating the BChl a Qy singlet state which then transfers energy to the reaction center. This SF-mediated pathway contributes up to ~18% of total carotenoid-to-BChl energy transfer in some complexes and introduces a temporal “buffering” effect, staggering energy arrival at the reaction center. Why this matters: • It is the clearest demonstration yet that singlet fission plays a genuine, functional role in natural photosynthesis • The heterofission mechanism (triplets on adjacent Crt and BChl molecules) explains how bacteria achieve ultrafast SF while maintaining long-lived, harvestable triplet pairs • This pathway helps organisms make better use of blue-green light and may protect the reaction center during fluctuating light conditions The deeper implication: Nature has evolved a sophisticated way to temporarily store and then cooperatively release electronic energy using spin-protected triplet states. This biological strategy offers new inspiration for designing artificial light-harvesting and energy-conversion systems that can buffer and regulate energy flow something synthetic SF materials have struggled to achieve. We are learning that evolution solved some of the hardest problems in photophysics long before we started trying. How might understanding biological singlet fission change the way we design future solar energy or quantum-inspired technologies? Follow for more frontier photosynthesis research and natural quantum biology.

TheNewPhysics

75,999 views • 1 month ago

Some microbes carry a protein, called SNIPE, that "chops up" phage DNA as it's being injected into the cell. This is a new mechanism for phage defense! CRISPR–Cas and restriction enzymes also evolved to fight against phages, but they work by recognizing sequences. SNIPE works, instead, by sensing "touch." SNIPE is a protein with about 500 amino acids. After it's made by the ribosome, it latches onto ManYZ, two proteins which sit on the cell's inner membrane. (ManYZ is an importer; it brings mannose and other sugars into the cell.) Once attached to ManYZ, SNIPE sits and waits for an invading phage. Some phages, including lambda, actually infect cells by pushing their DNA through this ManYZ channel. Lambda uses its "tail" to reach inside the protein channel, basically, and inject its DNA. When this physical touch happens, though, SNIPE is waiting. As soon as the phage DNA starts entering the cell, and passes through ManYZ and SNIPE, it gets immediately destroyed. This means that SNIPE is the first phage defense system discovered, so far, that uses spatial positioning at the injection site to destroy invaders. But there are caveats, of course. If you untether SNIPE from ManYZ, such that it can freely diffuse through the cell, it will chew up the bacterium's genome. It is not a highly discerning nuclease! Also, SNIPE is not found in most bacteria. A prior pangenome study, which sequenced lots of different microbes, found that roughly a third of well-studied bacterial lineages had at least one member with a SNIPE-like protein. (For this paper, they just ported one of those homologs into an E. coli laboratory strain.) And finally, because SNIPE's mechanism is tightly tied to ManYZ, it cannot be used to defend against phages that enter the cell through different routes. T4 phages, for example, inject their DNA straight through the cell membrane and into the cytoplasm, without interacting with ManYZ. This is a nice basic science paper. Applications TBD. (Just remember that scientists figured out that bacteria had a phage defense system, called CRISPR-Cas, many years before it was repurposed into a gene-editing tool.) P.S. The video below shows how cells with the SNIPE gene (middle row) kill invading phages, and thus continue growing and dividing. Empty vector (top row) refers to bacteria carrying a plasmid with no SNIPE gene; this is a control group. And SNIPE E414A refers to cells which received a mutated SNIPE gene, where the glutamate at position 414 has been changed to an alanine, thus destroying the protein's nuclease activity. These cells also die when they get infected with a phage.

Niko McCarty.

20,516 views • 5 months ago

A single E. coli cell, placed on a dish, will become 70 billion cells in just 12 hours. That’s exponential growth. But a new preprint shows that it's possible to engineer E. coli to grow linearly instead, where only one daughter cell continues dividing and the other stops. First, some context. In nature, there is a bacterium called Mycobacterium smegmatis (initially discovered in 1884 in ulcers scraped from syphilis patients.) M. smegmatis is weird because it divides asymmetrically. These cells grow only from one end, and all their cell wall biosynthesis machinery is located on that one end. So when the cell divides, one daughter gets this machinery and the other gets nothing. The daughter that gets the machinery can keep dividing immediately, but the other daughter has to remake all that machinery from scratch, so its growth is delayed. E. coli doesn’t grow like this. When it divides, it pinches in the middle and splits everything evenly. Enzymes, metabolites, and proteins get partitioned more or less randomly between the two daughters. For the new preprint, though, researchers engineered E. coli to behave more like M. smegmatis. Here is how they did it: First, they deleted a gene called cyaA, which encodes an enzyme (adenylate cyclase) that makes a molecule called cAMP. cAMP is SUPER IMPORTANT! It is a nutrient sensor that instructs E. coli to switch on genes that help it digest non-glucose carbon sources when glucose is scarce. Without cAMP, E. coli cells growing on alternative carbon sources will starve; they won’t know how to eat the food. Next, they added back a “split” version of the cyaA gene into the cells. In other words, they split the gene in two so that each half of the enzyme is made separately. Cells can only make cAMP, and thus eat non-glucose carbon sources, if these two halves come together. To facilitate that “coming together,” the researchers also fused the split cyaA proteins to sticky proteins that clump together, and to a fluorescent protein (to make it easy to track these molecules in the cell.) So now some interesting things start to happen if you grow E. coli on a growth medium lacking glucose. As the cell grows, its cyaA “halves” start clumping together into a giant ball. Inside the aggregate, the two enzyme halves come together and make cAMP. And when the cell gets big enough and divides, the clump of cyaA RANDOMLY goes to either daughter cell #1 or #2. The daughter that gets the aggregate (called PA+ in this paper) can keep dividing. The daughter that doesn’t (PA–) cannot. It still grows a few times — about four divisions — because it inherits some leftover cAMP from its mother. But after that, the metabolite is diluted away, and the cell stops growing. PA+ cells went through about 23 divisions on average before their aggregate decayed. And the population of cells, as a whole, grew linearly. This paper is cool because there are many applications where exponential growth is too unpredictable and, perhaps, unsafe. If you want to engineer bacteria to deliver drugs, clean up waste, or live in the gut, you don’t want them to double uncontrollably. This paper shows you can make them expand in a controlled, linear way. Alas, mutations could break this whole engineered system. A mutation that restores cyaA, for example, would give cells a new way to make cAMP. Mutations that make the aggregates split between daughters would break the asymmetry, too. But still, I really enjoy proof-of-concept engineering papers like this.

Niko McCarty.

58,028 views • 11 months ago

📢 EstateX: The Next Phase Begins This week, we're pulling back the curtain on what we've been building - and announcing the first wave of ecosystem activations. What's Coming This Week: ✅ Multiple Project updates ✅ Concrete dates for key launches ✅ Behind-the-scenes reveals Now that the launch is complete, it’s time for the REAL work and business building to begin. A series of exciting developments are scheduled for release in the near future, including but not limited to: 📊 The Ecosystem Overview: 👇 (All of which will have positive flow use cases and utilities for $ESX) 🔸 20-35% of Company Revenue Buybacks - this amount of revenue generated is used to buy the $ESX token off the market 🔸 Investment Platform Transaction Fees - all transaction fees on the EstateX investment platform are paid in $ESX or used to buy $ESX off the market 🔸 ESX Blockchain Gas Fees – Every transaction fuels the network, increasing $ESX usage and demand. 🔸 RWAPad / Unicorn Club Staking – Creating $ESX lockup and growth pressure. 🔸 Whitelabel Solutions – Platform adoption by other companies drives $ESX circulation and utility. 🔸 PropXChange – Trades in tokenized real estate generate fees that flow back to $ESX. 🔸 EstateX Pay – Card transactions generate revenue that supports $ESX growth. 🔸 CapitalX Lending – Loan and interest fees contribute to $ESX buybacks. 🔸 EstateX University – Access and education fees contribute to $ESX ecosystem growth. 🔸 $AIESX Utilization – Revenue drives $ESX buybacks. 🔸 Real Estate Rental Income – Passive rental flows create consistent $ESX circulation. 🔸 Expansion Into New RWAs – Future tokenized assets add more revenue streams, boosting $ESX demand. 🔸PLUS more surprises to be revealed! 💰 Financial Perspective: Consider just one of these components: real estate tokenization. A $100M AUM (Assets Under Management) portfolio in the first 6 months of operations could generate 10% in revenue from all pillars involved. That's $10M in total revenue. With up to 35% of that revenue allocated to buybacks, that's major buy pressure from a single revenue stream. Now multiply that across the entire ecosystem. But we're doing this RIGHT. That means rolling out strategically, testing thoroughly, and ensuring each piece is bulletproof before launch. 👉 Our new standard: Underpromise, overdeliver on EVERY deadline. This week, you'll see the first glimpses of what EstateX truly is. And this is just the beginning. First announcement drops very soon. The $ESX token is LIVE! Accumulate $ESX 👉 Watch the $ESX use case video now: Join our community 👇

EstateX

118,901 views • 8 months ago

There's a bacteriophage that turns bacteria into “liquid crystals.” Specifically, Pseudomonas aeruginosa bacteria make Pf phages, which are rod-shaped, negatively-charged, and measure about 2 micrometers in length (roughly the length of an E. coli cell). These phages leave the cells and enter their surroundings. There, they mix with polymers, also secreted by the cells, to form a crystalline matrix. Surprisingly, this is good for the cells. Although the phages kill some of them, it also makes their biofilms stickier and able to withstand certain antibiotics. These bacteria + phages are prevalent in cystic fibrosis patients; they've formed a sort of symbiotic relationship. The Pf phages are made from thousands of repeating copies of a coat protein, called CoaB, which wraps around a single-stranded, circular DNA genome. These genes are integrated directly on the bacterial chromosome. The bacteria “turn on” these phage genes when placed in a viscous environment with low oxygen levels. This is like a trigger to start forming a biofilm. And the cells make a lot of phages; about 100 billion per milliliter. These liquid crystals form because of a physics principle called “depletion attraction.” If you just mix a bunch of loose or flexible polymers together (such as long carbon chains) they will not form a liquid crystal. But if you mix stiff rods (the phages) with loose polymers at a high enough concentration, the polymers will force the phages close together to create a material that flows like a liquid despite being ordered like a crystal. See the video below. These liquid crystal biofilms are hard to get rid of. The negatively-charged phages block many antibiotics (like aminoglycosides, which are positively-charged) from entering cells. Liquid crystals also retain water, so these biofilms can survive on drier surfaces. I first heard about this from Malmesbury’s excellent newsletter, called “Telescopic Turnip.”

Niko McCarty.

50,077 views • 7 months ago

Slow Progress is the New Reality of Modern Wars There are many people commenting on Russian difficulties and coming up with numerous reasons for their alleged collapse. I absolutely do not see any collapse; on the contrary, Russia has already normalized a state of war in Ukraine, which boosts its economic and industrial growth. The difficulties faced by Russia today are the same as at the beginning of the war, with soldiers having to spend up to half of their initial salaries on their own equipment, delays in pensions, and a series of other problems that are mirrored on the Ukrainian side, even with all the support from allies. The war today is much less lethal than it was months ago, and both Russian and Ukrainian losses have significantly decreased during this phase. Lethality has fallen, but Russian advances persist. And why are they slow? Is it a Ukrainian tactic? No. They are slow because they are accompanied by the deployment of communication infrastructure like signal repeaters for drones, the advancement of artillery guided by drones, maneuvers using FAB and more recently ODAB bombs against Ukrainian drone operators' facilities, infiltration by reconnaissance teams, saboteurs, and a series of protocols they have developed. That conventional war with rapid advances no longer exists, and in the context of a battlefield dominated by drones, it is unlikely to return. Modern wars will have slow progress, as seen in the attacks and counter-attacks of the Russians and Ukrainians in this war. Contemporary military forces are still unable to see this new reality of war. When analyzing the Russian advance, it's important to consider that all these maneuvers take days to unfold, but the point is that the Russians have already adapted to this pace, not bothered whether a particular advance will take 3 weeks or 3 months. They advance continuously following tactical protocols with little threat from Ukrainian forces, which, without new equipment, have had their defensive tactics remain almost unchanged over the past two years, relying mainly on drones and making it easier for Russian studies of countermeasures. And what can Ukraine do in this situation? I see few options, but one would be to delay the Russian advance with a good number of missiles, though personally, I find it unlikely that they will reach Ukrainian hands. It wouldn't have the power to change the balance of the war, but it would guarantee more time, which is important because the battlefield is dynamic, and the implementation of new tactics based on innovative weapons can change everything overnight. A war that seems almost lost today could take a different turn in weeks. Time is crucial for Ukraine, which has fronts only about 130 km from cities like Zaporizhia and Dnipro.

Patricia Marins

39,318 views • 1 year ago

The Sabotaging Practice of Over Supply and Sameness in the NFT Space. The current zeitgeist of the NFT space is that the same artists are doing the same kind of work five times a year, with project after project leaving a trail of disappointment and discontent among collectors and all of us watching in disbelief as huge resources are extracted from the space over work that feels like it could be left as an "artist study." I understand that you can do what you want with your money as collectors, but we are killing the whole space with this incestuous practice. No artist is that prolific to be able to do 5 collections of 100+ pieces each every year and actually deliver innovation and some kind of creative evolution. Of course, they can pretend play that the work has something new, but there is no precedent nor proof that that has ever happened in the speed that it happens in the NFT space. Again, people are free to through away their resources on whatever they want but with this way of doing things, we more and more are going to start seeing the consequences. Oh! There are consequences? Yes. Maybe unintended, but there are. Let's see. Let's start with the loss of belief in the NFT space as somewhere where emerging artists can come and find support for their experiments. Why even bother to bring experiments, innovation, and new ways to think of art on the blockchain if the same people have all the collectors hypnotized with their magical flutes? Why even try to come to a space where taking risks and challenging the status quo (the mission of art!!!) is overlooked? This makes the NFT space a social club and not a space for art. I guess it is fine, but IMO it is a recipe for disaster. New collectors stay away because the art will slowly but surely become stale and un-challenging. Why even bother to come and see what is happening here if you can't, as a collector, see new weird and up-and-coming artists? The amount of noise emitted by the same artists doing the same art over and over, drowns out any new voices. Again. A recipe for disaster. The NFT space is becoming a space of disappointment and doubt. We think that collections going to zero one after the other, over and over, is not damaging? I feel we are kidding ourselves. Disappointment piles up, and again, the people who will hurt are the emerging artists, the new blood, the ones who are willing to risk the most and, in return, put fire in this cold space of sameness. I love this space—don't get me wrong—it has changed my life, and I believe it has a ton of potential, but things need to change for it to become a beacon of light in art. But we need to support new voices. We need to support new ideas. The challenge is huge. I hope to contribute all I can to this change. I hope more and more see how exciting it is to go out and try to discover what else is out there and move this space forward. But again, I understand the leaps of faith needed, but if there is a space that is based on that, it's the NFT space...so there is hope. We will see. 📺by Boldtron

alejandro cartagena

98,261 views • 2 years ago