We learn something new about cancer from a great website called The Scientist

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.

[1] https://www.the-scientist.com/childhood-exposure-to-bacterial-toxin-tied-to-early-onset-colorectal-cancer-72952?fbclid=IwY2xjawSxsvNleHRuA2FlbQIxMABicmlkETBVNUo0ekNo

#cancer #medicine #science #life science #research #laboratory #start up #biotechnology

CRISPR meets Epigenetics: a marriage made in Heaven

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.

Nature | 15 min read

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).

#molecular biology #genetics #epigenetics #CRISPR Cas 9 #medicine #health #DNA #RNA

Gene Megacluster: a really big moment in antibiotic research

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 Briefing Gene 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

Nature | 4 min read
Reference: 
Nature paper

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.

#antibiotic research #antibiotic resistance #health #medicine #biotechnology #genetic engineering #research #bacteria

Round up for this week: What’s the biggest living thing. how many quantums in an atom, lupus progress-and international relations

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

https://www.theguardian.com/commentisfree/2026/jun/14/vladimir-putin-ukraine-war-borders-russian-president

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

Trees may store less planet-heating carbon than hoped, study suggests | Greenhouse gas emissions | The Guardian

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

 How many elementary particles are there?

Even if you know your fermions from your bosons, the actual number of fundamental particles — the electrons, quarks and other building blocks of physics — is still uncertain. From the 17 that feature on posters on classroom walls, “where you stop depends on your taste for complexity and mystery”, explains science writer Natalie Wolchover. “Plausible answers range from 17 to — in all seriousness — 995.5.”

Quanta | 13 min read

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

‘I’ve never been this good’ – revolutionary immune reset puts lupus in remission – BBC News

Quote of the week

He that hasteth with his feet sinneth.” (Proverbs 19:2)

#lupus #immunology #fungi #Russia #physics #quantum physics #vladimir putin #trees

Has Global Warming happened to you yet?

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.

[1] Evidence & Causes of Climate Change | Royal Society

[2] Climate Change | NOAA Climate.gov

[3] Climate – Met Office

[4] UK heat scientific report

[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.

#global warming #climate change #fossil fuels #fires #floods #droughts

Diabetes: another benefit of the BCG Vaccine?

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.

Nature | 5 min read

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.

[1] BCG vaccine – Wikipedia

[2] Vaccines and immunization


#vaccination #BCG #tuberculosis #cancer #dementia #diabetes #health #medicine #research

Chikungunya: another potential Climate Change epidemic?

News that we’re in for a record El Niño[1] this year brings a depressing thought is Climate Change going to deliver a whole new wave of tropical diseases alongside all those floods. fires and migrations? We’ve touched on this before (LSS 25 10 21,14 11 23, 2 10 25) but had rather hoped  that it had all gone away. It hasn’t, as this excellent article by Shivali Best of the Mail [2] explains in forensic detail. And it’s her work we’ll be riffing on today, with a little help other sources.[3]

Shivali takes Chikungunya virus as her theme. It’s a nasty little disease caused by an alphavirus of the Togaviridae group.  Discovered in Tanzania in 1952 it delivers a painful cocktail of symptoms including fever and severe joint pains: the latter may be extremely debilitating and long-lasting. But the real problem lies in its vectors, the famous yellow fever mosquito Aedes aegypti and the scarily named tiger mosquito (a. albopictus) Do they call it that because of its bite? Not only does climate change allow these insects to spread to lands where the cold had formerly precluded their presence. The same warming allows the virus to breed up to five times faster inside the mosquito. Before you ask: there are vaccines of sorts underway: but progress has been slowed because most of the money has been spent on wars and shopping malls.

And so Chikungunya joins the long sorry list of diseases spreading due to global warming. To which we could append Malaria, Dengue, Zika, Lyme, Tick Born Encephalitis,  Vibrio group……..enough! LSS readers are a well-informed lot. They know what’s happening. They know why. The real task before us all is how to clear up the damage, and make those culpable pay for it

[1]Prepare for El Niño, UN warns – it could be the strongest in decades – BBC News

[2]Chikungunya virus is heading for Europe: Scientists warn mosquito-borne tropical disease could spread to major cities thanks to climate change | Daily Mail

[3]Chikungunya fact sheet

#chikungunya #malaria #climate change #disease #vector #epidemic #health #mosquito

Broaden your mind with these two great brain stories from Nature Briefing

We believe that research into the human brain is the flip side of research into Artificial Intelligence. As the two will one day coincide, the more we know about both the better. So when Nature Briefing, that go-to Record for all things new and scientific, puts out not one but two (two, folks!) stories on the human brain, we felt it our solemn duty to bring you them both.

We have always believed that scaring people into doing things is counter-productive in the long term. Our worse fears are confirmed by this piece called Stress stops the Brain Joining the dots.

Acute stress makes it difficult to connect memories of past experiences with fresh information — a process crucial for making deductions. This could explain why people struggle to show insight under pressure. During psychological tests that involved making links between indirectly related pictures, brain imaging showed altered activity in the hippocampi of people who had been through a stressful mock interview compared with those of people who’d had to complete a simpler task, which suggests that their brains hadn’t inferred connections between the images as strongly.

Nature | 5 min read

Reference: Science Advances paper

Every epoch casts reality in its own image The Victorians though that everything in the world worked like a steam engine. Around 1910 they thought all was electric circuits. And Cold war people put us all down as computers. Every picture of the brain is an analogue, an attempt only as this piece The Brian is no machine makes clear.

In The Brain, In Theory, neuroscientist Romain Brette makes the case to move away from the predominant model of the brain, which treats the organ like a computer. Brette argues that engineering metaphors are often vague and misleading, and attempts to breathe life back into brain science by focusing on the study of the nervous system on biology. “Brette’s take-down of the field’s dominant theoretical frameworks is systematic,” writes neuroscientist Àlex Gómez-Marín in his review. “The book is intense and intricate. One can get lost in it, but it is worth the adventure.”

Nature | 7 min read

So our advice is study both of the above with close attention, gentle reader. It’s a no-brainer!

#neuroscience #artificial intelligence #biology #IT  #nervous system #logic #stress

Programmable Therapeutics(here’s what they’ll be talking about in 2046)


In these happy, carefree days of 2026, we almost take the success of advanced techniques like CRISPR–Cas9 and CAR‑T for granted. Yet not so long ago they were obscure experimental curiosities, known only inside specialist laboratories. So we asked ourselves: is there something equally obscure in 2026 that will be the stock‑in‑trade of doctors in 2046? We think there might be: programmable cell therapeutics.[1]

The jumping‑off point is the logic behind CAR‑T. Readers will recall how T‑cells are removed from a patient, engineered to recognise the chemical signatures of their cancer, and then reinfused to hunt down malignant cells. Researchers are now extending this idea to a wider cast of immune cells, stem cells, and progenitors, so they can tackle diseases far beyond oncology.

What makes the next generation different is the importation of ideas from electrical engineering. Instead of a single engineered receptor, cells can be fitted with ON/OFF switches, logic gates, multi‑step decision pathways, and feedback loops. In other words, cells that don’t just attack — they compute. They sense the molecular environment, decide what’s happening, and act accordingly.

And thanks to delivery tools such as viral vectors and mRNA‑carrying nanoparticles, these circuits can increasingly be installed in vivo. Rather than the expensive choreography of removing cells, re‑engineering them, and putting them back, the ambition is to program the cell to reprogram itself. Why rebuild the army in the barracks when you can train the soldiers already in the field?

Gentle readers, we are always looking for ways to put you ahead of the curve — not what is happening now, but what will be happening in five, ten, or twenty years’ time. By 2046 we could plausibly see:

  • cancer therapies that activate only in tumour microenvironments
  • gene therapies that self‑limit to avoid toxicity
  • immune cells that make multi‑step decisions
  • RNA‑based switches that restore gene expression dynamically

All this, of course, depends on continued investment in scientific research and a strong ecosystem of independent universities and research institutes. Hopeful, isn’t it.

[1]Next-generation programmable cell therapies for precision medicine | Nature Reviews Genetics

#gene editing #medicine #health #cancer #mRNA #CRISPR #CAR-T #DNA









If you are going to get wiped out by an asteroid, don’t let it spoil the weekend

For anyone who thinks dinosaurs are extinct you should try living near vast colonies of seagulls, where we do, and try to keep your car clean. But, as every schoolchild knows, most dinosaurs, especially the big scary ones, really did go extinct one day 66 million years ago when a rather large asteroid landed in the Gulf of Mexico(or do we now call it the Golf of Trump?-check before publishing-ed) But what was it like to live through that momentous day in the history of the world? Now erudite Professors Michael J Benton and Monica Grady, writing in the Conversation, have made a stab at recreating the colossal impact, through the eyes of the creatures that lived through it, from the day before until many years later when everything had played out.[1]

Well, imagine it for yourself, gentle reader. A warm Cretaceous day like many others, a Friday perhaps, with the prospect of a sunny weekend ahead…. Ankylosaurs scuttling through the undergrowth, Triceratops and T. rex vying for number one spot at the watering hole, all normal and above board, until…..well, we won’t spoil it, gentle reader. Click on the link and read for yourself.

And remember this thought. However urgent your latest report seems to be, however late the train is for the next meeting, or how long you have to wait to park at Sainsburys, trouble- unexpected, unforewarned, undeserved even- may suddenly come at you from out of a clear blue sky. And change things round more than somewhat. And finally: if we had lived there at that time, it really would have been a Friday, because everything bad happens to us twice.[2]

[1]  https://theconversation.com/what-it-would-have-been-like-to-experience-the-dinosaur-killing-asteroid-armageddon-a-blow-by-blow-account-271786?

[2] Cretaceous–Paleogene extinction event – Wikipedia

#asteroid #dinosaur #extinction #KT boundary #cretaceous #evolution #geology