Last week, with the help of our doughty researchers, we published a small piece describing how Artificial Intelligence is being employed to design new generations of bacteriophages, some of which might be used to target antibiotic‑resistant bacteria (LSS 8.8.26). Hopeful, certainly — but intelligent readers will ask the old question: what’s the chance any of this will work anytime soon?
Well, you’ll be glad to know that human‑modified bacteriophages have already been in action, and successfully too, since the far‑off days of 2024. They weren’t using AI to design the phages then, merely modifying them using another LSS favourite: CRISPR‑Cas9 gene editing.
Our first trope concerns a report in The Lancet Microbe, a long but reasonably readable paper describing a safety and tolerability trial of SNIPR001 — a combination of four CRISPR–Cas‑equipped bacteriophages — in healthy human volunteers. Results were encouraging:
“SNIPR001 was safe and well tolerated in healthy participants, with signals suggesting targeted activity against E. coli, despite the absence of a statistically significant effect.”
Our second trope comes from the excellent Michael Le Page of New Scientist, who reports on the clinical use of the same SNIPR technology — not a trial in healthy volunteers, but in an actual patient. His piece, CRISPR‑armed phages help treat severe superbug infection, is unfortunately behind a paywall, but worth crossing. It tells the story of a 65‑year‑old man in California with a severe, antibiotic‑resistant E. coli infection whose condition markedly improved after receiving these engineered phages. The lesson is clear: artificially-modified phages can work.
Now, nobody is claiming miracle cures — not the authors of the paper, nor Michael, nor ourselves. But all of us, in our different ways, are pointing to extremely encouraging signs. And remember our original point: all of the above took place, before our famous AI‑designed bacteriophages have even gone into trial. What possibilities might open up when they are fully deployed?
At LSS we’re a pretty eclectic kind of blog. So when we think we’ve got into a rut -too much on Antibiotics, Anthropoid Ape Men, or the deeds of Mr Trump- we like to spin the wheel so that you, gentle readers, may be the first to become au fait in yet another exciting area of cutting-edge human endeavour. And today we have chosen Quantum Sensing, that quiet shy sister of the much louder Quantum Computing, which might just turn out to be the Cinderella who scooped the ball. [1]
So what is Quantum sensing? The scientific miracle that crept up on us while everyone was busy arguing about quantum computing. Instead of trying to build impossible machines, quantum sensing takes the strange behaviour of atoms, photons and spins and uses it to measure the world with a delicacy classical physics simply can’t reach.
What’s the step change? A quantum sensor doesn’t rely on bulk electronics or brute force; it relies on superposition, entanglement and other quantum states that are inherently more precise. The result is a new class of instruments that can detect the faintest magnetic fields, the tiniest vibrations, and the most subtle changes in gravity — a kind of scientific eyesight that feels almost unfair in its sharpness.
What makes quantum sensing genuinely new? Classical sensors, like rulers, are always fighting noise: thermal noise, electronic noise, environmental noise. Quantum sensors sidestep those constraints by using states of matter that are the limit — the smallest possible unit of information, the most stable possible oscillation, the purest possible signal.
Hang on-are people actually using this stuff, now, in like, August 2026? Yup: the kit is suddenly appearing in many fields: mapping quantum materials, stabilising next‑generation clocks, imaging nanoscale structures, and even probing biological systems without damaging them. It’s not an incremental upgrade; it’s a shift in what measurement science can do, when the mood takes it. [2] [3]
Why have you showcased it? because it represents science at its most elegant. Quantum sensing isn’t about building bigger machines or consuming more power; it’s about learning to see the world with new eyes. Many of the sensors themselves are tiny jewels of engineering — diamonds with engineered defects, single trapped ions, levitated nanoparticles — each one a reminder that progress sometimes comes from finesse rather than force. In a year dominated by loud technologies, quantum sensing is the quiet triumph: a discipline that turns the universe’s weirdness into clarity, and shows how much beauty there is in simply measuring the world more truthfully.
Can I buy one in my local hardware store?A: Not quite yet. Quantum sensors are still the domain of research labs, national metrology institutes and a few very specialised companies. For now, your local hardware shop will continue to offer the trusty tape measure, the spirit level and the laser rangefinder — all perfectly good tools until quantum sensing makes its way into everyday kit. Think of it as the future arriving in slow, elegant steps rather than on the shelves of B&Q.
However: Most advances in science-and the human condition- ultimately come from advances in measurement. We think this might be one such
Anyone visiting the South Coast towns of England will know we have a huge sepsis awareness campaign on at the moment, as every ambulance you see is plastered with messages on the subject. And rightly so: sepsis is the cause of enormous suffering and mortality, not to mention its toll on NHS resources. Which is why today we are showcasing the NHS sepsis framework (published only yesterday, gentle readers-we sure do scoop ‘em these days!) [1]. because down in the appendix is a little section which impinges directly on the fons et origo of this whole humble blog: microbial resistance to antibiotics, as if you haven’t guessed already. Because sepsis affords the physician the most awful, excruciating, dilemma.
It’s one of those medical emergencies where every hour counts, truly. When bacteria invade the bloodstream and the immune system spirals out of control, doctors just can’t wait days for laboratory cultures. Broad spectrum antibiotics must be thrown in immediately, because delay will be truly deadly. Maybe it’s sepsis, maybe it isn’t: but the only logical decision at that stage is to assume that it is.
Thereby creating an acute paradox. Because prescribing the antibiotics exerts evolutionary pressure on the bacteria, increasing the strain’s likelihood of developing resistance. And as we know here (LSS passim) every unnecessary course of antibiotics puts the bacteria one step ahead. Modern medicine is trying to perform two contradictory tasks: treat, but avoid overtreatment So although the report puts it in the calm precise language of an official report, sepsis management and antimicrobial resistance must be seen as two sides of the same coin.
And our thoughts? Firstly, we are full of admiration for the medical staff who are dropped into this agonising situation, recognising that they possess levels of emotional and intellectual intelligence far beyond our own limited capacities. Secondly that to shout for “more antibiotics“ is cheap rhetoric, as it just begs the question. And we’re always doing it anyway. A more fruitful answer might lie in things like better DNA sequencing, molecular diagnostics and AI assisted decisions, all of which might better identify the invading pathogen more quickly. Thus opening the possibility of a bespoke antibiotic to be delivered to the right patient at the right time. Now that would be a creative step indeed.
What happens when Belief triumphs over evidence? Here’s one example. For most of human history, childbirth was dangerous in a way modern readers struggle to imagine. In Europe in the early 19th century, maternal mortality in hospitals could reach 10–20% in bad years. Women died not from the birth itself but from the mysterious, terrifying scourge of puerperal fever. And the explanations? The usual cocky self-serving assertions like miasmas, divine wrath, atmospheric changes. Most Doctors were confident; they knew. When thinkers like Semmelweiss suggested that the cause was filthy medical practices which spread a lethal agent he called “germs,” he was hounded from his profession. The carnage continued until Pasteur and others were finally able to show the true causes, which they did using controlled experiments, rigorous data ,and logical interpretation of their findings.
Those who think such battles to be long won would do well to read the following book review from Nature Briefings. It’s called How we know: the rise of evidence based medicine, But it’s really a gateway to how we know about anything, as opposed to just believing our own first guess
In Beyond Belief, science journalist and Nature editor Helen Pearson charts the rise of evidence-based medicine and explores how rigorous research has transformed health and social policy. Pearson shares examples of success stories, in which solid evidence overturned bad practices, and the people behind them, many of whom were treated as mavericks for championing randomized trials. “Anyone can read and enjoy the book, yet there are nuggets for experienced readers,” writes public-policy researcher Peter John in his review. “The author writes as a believer, and her passion is engaging.”
At this blog we have tried many times that only reason and evidence will ultimately ameliorate the human condition. But nowhere have we done as well as this book does. And the need is not just in medicine, but in all areas such as climate physics, economics and what still passes for political life. The central problem m is that humans are wired for belief, not evidence. Intuition, anecdote, tradition, and authority shape most human decision‑making. Cognitive biases — confirmation bias, availability bias, motivated reasoning establish certainty long before any data has arrived. Yet the cost of ignoring evidence is enormous: this summer wildfires are again raging across Europe in a way unknown before 2020. Pearson’s remedy is the same old list our side has been pushing since the age of Sir Francis Bacon : demand clear causal claims, ask what the comparison group was, look for replication,, distrust single studies, favour interventions tested in real‑world conditions, accept that “what works” is often context‑dependent But try explaining all that in the bar of the Dog and Duck.
Beyond Belief: How Evidence Shows What Really Works by Helen Pearson (Princeton, 2026)
One thing we value here is a well‑written science story that tells us something we didn’t know — and does so in a trustworthy, responsible way. Not the sensationalist, attention‑grabbing material that flashes across our screens all too often. So when our researchers came across Colorectal Cancer and Childhood Exposure to a Common Gut Bacterium by Laura Tran in The Scientist[1], we decided to look at the source itself, to see whether it deserves a place among the canon of science‑news providers we consider worthy of your attention, gentle readers.
As you might expect, The Scientist specialises in clear, sober reporting: across the biosciences, speaking very broadly. The style is terse and informative, closely aligned in spirit with the journals and institutions it covers. There’s a strong news section, a quarterly print magazine, topic‑based browsing, and a generous set of resources. Our test search — naturally, Antibiotics — produced several well‑illustrated, highly informative pieces.
If pressed, we’d say the ideal reader is intelligent, graduate or postgraduate, and probably working somewhere in the life sciences. But there is plenty here for teachers preparing a good science lesson too. Or even two.
Our verdict: not as bite‑sized as Nature Briefing, nor as magazine‑like as New Scientist, The Scientist nevertheless earns a worthy place alongside them as a provider of news and ideas for the educated and reasonable community (that’s us, gentle readers). And in an age when so much content is shaped for attention rather than understanding, that’s a very important thing indeed.
And having satisfied ourselves that The Scientist is indeed a sober and reliable chronicler of the biosciences, we can turn to the story that brought us there in the first place. It is a quietly important one: evidence that early‑life exposure to certain strains of that perfectly ordinary gut bacterium — Escherichia coli carrying a particular genetic island — may leave a mutational fingerprint that shows up years later in colorectal tumours. No melodrama, no scare‑stories, just the steady accumulation of data: mutational signatures, epidemiology, and the slow, careful work of linking mechanism to disease. This is exactly the sort of thing the scientific enterprise does well, and exactly the sort of thing we like to bring to your attention.
CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) is a natural defence system found in bacteria, which scientists have turned into a programmable way to edit genes with extraordinary precision. In practice, it comprises two parts: a guide RNA that acts like a GPS to find the exact spot in DNA, and a Cas9 enzyme that acts like molecular scissors to cut the DNA. Once the DNA is cut, scientists can delete, fix, or replace genetic sequences inside a living cell. Our first Cover seems to have been over six years ago (LSS 23 11 20), since when we have noted a startling range practical applications from areas as diverse as horse breeding, and sickle cell medicine, to its relationship with blue sky techniques such as Base Pair editing, CART and programmable therapeutics (LSS passim).
How gratifying then to see CRISPR-based tools now partnered with epigenetics, that other old favourite of these humble pages! Once again the lead is taken by the indispensable Nature Briefing, now our go-to for all new things Scientific Their summary CRISPR’s next act: editing the epigenome tells you most of what you need to know. But some readers may well wish to click on the handy link too
A handful of start-up firms are testing therapies that target specific epigenetic markers — essentially chemical groups that sit on DNA and the proteins that it is wound around — to treat everything from high cholesterol to a rare muscular disorder. Changing these chemical markers can switch genes on or off. Some existing medications influence epigenetic markers, but these drugs act broadly and lack specificity. A new cadre of scientists has found ways to precisely alter the epigenetic signals that influence specific genes.
There is much here to gladden the hearts of all who believe in Reason and Learning. The technique seemingly so radical a few short years ago is not only becoming routine, it is embedding itself into the wider corpus of medical and scientific practice. Practicable applications are multiplying and the opportunities to reduce human and animal suffering are thereby multiplying. If anyone asks us “why do you take such an interest in the progress of the Arts, Sciences and Letters?” one answer we give is: because of things like this.
If you want to know more about epigenetics, or molecular biology in general, then we cannot do better than recommend the works of the great Professor Carey:
Carey, Nessa. The Epigenetics Revolution: How Modern Biology Is Rewriting Our Understanding of Genetics, Disease, and Inheritance.London: Icon Books, 2011. New York: Columbia University Press, 2012. ISBN: 9781848312920 (Icon Books); 9780231530712 (Columbia UP).
Carey, Nessa. Hacking the Code of Life: How Gene Editing Will Rewrite Our Futures.London: Icon Books, 2019. New York: Columbia University Press, 2019. ISBN: 9781785784972 (Icon Books); 9780231549769 (Columbia UP).
The idea of whole and unexpected possibilities in antibiotic research excites our highest hopes-and those of readers who have accompanied us on this journey for years. None more so than this report from Nature BriefingGene Megacluster boosts antibiotic arsenal. We’ve set up their usual summary, plus links: and then we’ll try to answer a few of your questions as best we are able
A newly discovered gene ‘megacluster’ in Streptomyces bacteria enables them to produce a variety of potent antibiotic compounds. These compounds act as a multi-pronged offensive weapon against other species, with each targeting different stages of the bacterial metabolic process. It’s more difficult for bacteria to develop resistance to attacks that hit several targets, so the discovery could lead to the development of new antibiotics, experts say. The research has “discovered something new in a system so extensively studied — hidden in plain sight,” says medicinal chemist Mark Blaskovich
So, what is this gene megacluster? An unusual stretch of DNA in Streptomyces that encodes four distinct families of natural-product antibiotics, including: one compound entirely new to science, another never previously recognised as an antibiotic, and two known families deployed in a new coordinated fashion. Not a bad haul for one discovery, we think.
What does it do in Streptomyces? All four molecules target biotin (vitamin B7)—a universal cofactor required for growth, cell division, and metabolic enzyme function in most bacteria. They attack different points in the biotin pathway: production, uptake, use, and availability, aided by flanking streptavidin genes that bind up free biotin.
Why is this discovery genuinely new? Well , all sorts of reasons: here are a few of the best
–Co-location is unheard of: Antibiotic biosynthetic pathways are usually scattered across the genome. Here, four unrelated antibiotic families sit side-by-side, implying intentional evolutionary selection.
–Coordinated multi-antibiotic strategy: Natural antibiotics typically act alone. This cluster encodes a team of molecules that hit the same vulnerability from different angles—something not previously documented.
–Hidden in plain sight :Streptomyces genomes have been mined for decades, yet this megacluster was overlooked because genome-mining tools historically focused on single-product clusters. We love this bit, as regular readers will have already discerned
–It appears to be widespread. The megacluster is present across multiple Streptomyces species, suggesting an ancient, conserved strategy rather than a rare curiosity.
Could similar clusters exist in other organisms? Likely, yes. The discovery provides a road map for genome mining that looks for coordinated multi-pathway clusters, not just single biosynthetic islands Early research might do better to focus on procaryotes rather than eucaryotes-but who knows?
How could it help us to develop new antibiotics? This is the Big One for us , isn’t it? Lots of ways potentially, but as of late June 2026 three practical routes suggest themselves:
1. Direct development of the four biotin-targeting molecules. Because they attack different steps in the same essential pathway, they could be: used individually, combined as a cocktail, or engineered into hybrid molecules. Multi-target antibiotics are inherently harder for pathogens to resist. So that will teach them we’re serious this time.
2. Synthetic biology reconstruction. The megacluster’s architecture can be transplanted into: Streptomyces strains, E. coli or yeast expression systems, or modular cell-free platforms, permitting all sorts of scaling and production advantages
3. Drug discovery by analogy The discovery provides a template: look for clusters that coordinate attacks on other essential pathways (e.g., folate, isoprenoid synthesis, lipid II). Genome mining guided by this logic could uncover dozens of new multi-pronged antibiotic families.
4. Biotin-pathway inhibitors as a new class Biotin metabolism is conserved across many pathogens, including Gram-negatives—historically hard to target. These molecules could seed a new class of antibiotics that bypass existing resistance mechanisms
At this blog we tend to rate discoveries by the possibilities they open rather than the questions they answer. By that metric, this one is big indeed-and we think you’ll al agree with that.
Fungal internet Its not whales or trees:Some of the largest living things on our planet are actually vast networks of microscope white fungi growing beneath the ground on which we unthinkingly tread as The Conversation explains;
Don’t expect Putin to go quietly if he loses in Ukraine If you think current developments in the Russian Ukraine war might lead to a status quo ante bellum, think again ,as this prescient article from the Guardian makes clear
Plant a tree in ‘73, plant some more in ‘74 was a Government slogan from our long distant youth But maybe trees won’t save us from climate change as well as we thought they might as this piece from The Guardian explains
A bestiary of bosons Nothing so defeats us as the vast and baffling variety of particles ,waves and other strange things that make up the modern atom .So we welcomed this article from Nature Briefing which tries to make sense of the matter
Lupus in remission Just before we pressed the “SEND” button, our researchers insisted that this encouraging story about a new immunological technique which seems to be turning the tide on the debilitating disease of Lupus went in, Good for them. here’s the BBC
Everyone can choose how they learn about global warming. For some it is to read the science by consulting sites such as the Royal Society[1] , NOAA,[2] the Met Office [3] and other adults in the room. The second is to wait until it happens to you. Increasingly, people are choosing the second option because the climate is now delivering personal tutorials: a fire that shouldn’t have burned, a flood that shouldn’t have reached that high, a heatwave that shouldn’t have been possible at this latitude. We’ve got three examples for you today, which we present with due apologies and sympathy to the victims( it really isn’t their fault).
A. The 2022 UK 40°C heatwave
Most people who lived in Southern England that year can share memories like driving around the M25 through clouds of smoke from the burning heaths of Surrey, or seeing our beloved green South Downs turn the colour of chamois leather. Attribution studies conclude climate change made it at least 10 times more likely.[4]
B. The 2021 Pacific Northwest heatwave
You’d think the cool, rainy Pacific Coast would be the last place to expect a catastrophic climate change event. But this one was described by scientists as “virtually impossible” without global warming. [5]
C. The 2023–24 Canadian wildfires
The largest in Canadian history; attribution work shows climate change made the conditions significantly more likely and more severe.[6]
We could go on- but at this point there pops up the usual man from the Dog and Duck who yells “these are only (expletive deleted) probabilities! Just models! No one has PROVED these were caused by climate change!” To which we reply:
If you refuse to act until science gives you 100% certainty, you’ll never act on anything. Climate attribution uses the same probability standards we rely on for medicine, insurance, and engineering — the ones we trust every day without complaint. When scientists say “an event was made ten times more likely by climate change”, that’s not vague. That’s the same level of evidence we use to approve drugs, design bridges, and set insurance premiums. If you accept probability‑based evidence when it keeps planes in the sky and hospitals running, but reject it only when it concerns climate change, that’s not a scientific position — it’s a political one. It’s also disingenuous. But above all, it is very short term.
[5]Philip et al. (2022), “Rapid attribution analysis of the extraordinary heat wave on the Pacific coast of the US and Canada in June 2021.” Earth System Dynamics, 13, 1689–1713.
A couple of years ago we did a piece called Did your long-ago BCG Vaccine save you from dementia? In which we reported that the famous BCG (Bacillus Calmette-Guérin) vaccine was also proving efficacious in cases of bladder cancer and certain types of dementia. (LSS 2 12 24) Well today things just became even more intriguing. Read this from Nature Briefing, Century Old Vaccine helps control diabetes;
A tuberculosis vaccine developed in the 1920s helps to regulate blood sugar in people with certain types of diabetes, enabling them to reduce their insulin use. The findings demonstrate yet another beneficial off-target effect of the Bacillus Calmette–Guérin vaccine, derived from a weakened form of the bacterium that causes tuberculosis in cows. The shot has been approved to treat bladder cancer in the United States and is being investigated against conditions such as Alzheimer’s disease. The results were presented at the American Diabetes Association meeting on 7 June.
And the Learning Point? When we did Training and Teaching, they always told us that we had to have a learning point. So we think it’s this:
Vaccines are one of civilisation’s quiet miracles:[2] you design them for one threat, and decades later they’re still paying unexpected dividends — BCG for TB, then bladder cancer, then dementia, and now hints of protection against diabetes. That’s what real science does: it compounds. You invest once, and the benefits echo for generations. But if you decide, like the climate denier or the old‑school smoker, that evidence is optional and expertise a nuisance, you’re effectively betting your long‑term future against the only tool that has ever reliably improved it. Reality is not something you can pick and choose.
