Antibiotic medicine, mitochondrial medicine, cancer medicine: three stories so good we couldn’t leave out any: and a deeper question for you

Three stories we saw this morning were so compelling that it was impossible to choose just one to showcase. Each was so novel, so rich, that they raised a deeper question: where do you stop? We could have spent hours digging into any of them. Instead, we’ll let you decide for yourselves, gentle readers, as we present each in turn — and return to that last question at the end.

Ancient Antibiotic Resistance

Our first story is a tour‑de‑force article in New Scientist by Joni Wildman. You may have already seen recent media reports about dormant bacteria in ancient sediments showing signs of antibiotic resistance. Well, Joni has the definitive deep dive for anyone who wants to understand what this really means. You’ll encounter plasmids, the resistome, and even how these discoveries might help us identify the antibiotics of the future. Her article is behind a paywall, but worth it — you get the rest of the magazine too. How ancient superbugs could help us fight antibiotic resistance | New Scientist

Joni’s article is behind a paywall, but worth it, as you’ll get the rest of the mag too

How ancient superbugs could help us fight antibiotic resistance | New Scientist

Mitochondrial Transfer? Confession: before we read this excellent article by Blake Forman for Technology Networks, we didn’t know very much about mitochondrial disease(actually our basic mitochondriology was a bit weak too) But it seems that some healthy cells may be able to donate their mitochondria, those busy little subcellular power stations, to neighbours with less healthy ones. What’s more, there are promising signs that this discovery may be translatable into practicable therapies, as Blake outlines in this extremely learned article.

https://www.technologynetworks.com/biopharma/news/healthy-cells-donate-mitochondria-in-potential-treatment-for-mitochondrial-disease-416832?fbclid=IwY2xjawUodV9leH

Infections and Cancer Well, this story by Zoe Hardy of the Mail really had to go in: a new study claims that on e in eight cancers may be caused by a previous infection. No, we weren’t expecting that one either. But Zoe’s sources (International Agency for Research on Cancer, Lancet Oncology) are impeccable, their data wide and deep, and the conclusions faintly unsettling. The usual suspects are in there-HPV, Hepatitis virus, EBV and of course poor public health and sanitation. Naturally more vaccination programmes would help-but that’s becoming an uphill battle in many places these days, isn’t it? Once more, read the article and judge for yourselves:

One in eight cancers are linked to infections, new study finds, including a common stomach bug linked to bowel cancer | Daily Mail Online

All of which leads us to our main point. Each of these stories begged more reading, more digging into the data and more pondering. But in the part of the universe where we live at least there are only 24 hours in any one day, and only seven of those days in your average week. So: where do you stop? Read too much on mitochondria and you won’t have any time for green aviation technology or research on cocktails. But skim over everything and we guarantee you’ll understand none of it. It’s a conundrum which we have never satisfactorily solved. How do you do it. Gentle reader? We’d love to know.

#superbugs #antibiotics #microbiology #joni Wildman #mitochondrial disease #cell biology #inherited disorders #blake forman #cancer #infection #vaccination #zoe hardy #public health

CAR‑T gets a serious rival — and that’s good news

Long‑serving LSS readers will know the admiration we’ve expressed for CAR‑T therapy (Chimeric Antigen Receptor T‑cells) and the extraordinary advances it has brought to cancer treatment. So it was a genuine surprise this morning when our researchers stumbled upon a credible alternative approach — spotted first via the excellent science feed of Hashem Al‑Ghaili.

The substance in question is GTB‑5550, a tri‑specific natural‑killer‑cell engager developed by GT Biopharma. According to Al‑Ghaili’s summary, GTB‑5550 anchors to a specific protein on the cancer cell, binds to an activating receptor on the patient’s natural‑killer (NK) cells to form an immunological bridge, and delivers an immune‑signalling protein that drives those NK cells to multiply and sustain their attack.

The underlying science is real and verifiable: GT Biopharma has FDA clearance for Phase 1 trials, and the National Cancer Institute lists an active study in advanced solid tumours. Readers can consult the company’s announcement at [3].

What caught our eye, however, was Al‑Ghaili’s shrewd observation that this line of attack offers a potential alternative — or at least a practicable complement — to the often intricate and labour‑intensive CAR‑T process. LSS has always championed redundant capacity over just‑in‑time efficiency: think bacteriophages alongside antibiotics, quantum computing alongside AI, and now, perhaps, NK‑cell engagers alongside CAR‑T.

We just didn’t expect CAR‑T to acquire a rival quite so soon.

[1] CAR T cell – Wikipedia

[2] https://www.facebook.com/ScienceNaturePage/posts/pfbid0YtDt88h5ryQi482butNALJQQ2parbD1YsQsFRUdZp

[3] GT Biopharma, Inc. (2026). GT Biopharma Announces Potential New Indication for GTB-5550, a B7-H3-Targeted Natural Killer (NK) Cell Engager, for Multiple Myeloma. GlobeNewswire.

# Hashem Al‑Ghaili #CAR-T #GTB 5550 #cancer #immunology #medicine #health #GT Biopharma #FDA

GutSee Health: pioneering therapies may help conserve precious antibiotics

Whatever else we write about, the problem of microbial antibiotic resistance, is still the raison d’etre of our humble little blog. So while we’re always on the look-out for stories about new antibiotics, new phage techniques, what have you, we sometimes cast our net a bit wider. To bring you news of techniques which, while currently aimed at other problems, offer us the hope that they may one day be relevant to the fight against antibiotic resistance. That thereby potentially help us eke out existing stocks of antibiotics, and maybe even buy us time to develop a few more. Morever, when the pioneer is one of those brave new companies we laud so often, then we are all the more eager. So today we are showcasing the work of UK based GutSee Health. Not because they currently work to replace antibiotics per se: but because they represent a way forward which we think one day might.[1]

At present Gutsee are working on treatments to contend with such intractable problems as Irritable Bowel Syndrome and Inflammatory Bowel Disease. At present these disorders are not primarily treated with antibiotics. But if you examine their website, you will discover the formidable expertise they are developing in applied Artificial Intelligence, microbiome engineering, and phage technologies. Techniques not to replace antibiotics: but to potentially reduce the need for them, thereby conserving them for another day. Look at this from their website, with special attention to the bit which we have emphasised:

…… we are building sophisticated machine learning models to decode phage–bacteria interactions and predict therapeutic responses. This enables us to design targeted interventions that remove harmful or pro-inflammatory microbes—whether in the gut or in wounds*—while preserving healthy ecosystems.

*our emphasis

Wounds, gentle readers. You know that’s where the danger of antibiotic resistance is real: and you know why. Industrial or military wounds are notoriously vulnerable to infection, and antibiotics have long been essential in managing them. But every surgical intervention is really the imposition of a wound, albeit in a good cause, whether to cure appendicitis, deliver a baby by caesarean, transplant a heart-or carry out another of the myriad medical processes which make our lives sustainable at all. We need every possible alternative we have to address these problems, because time is growing short. It is our prediction that the work of GutSee, and many heroic pioneers like them may have a very large role to play. We wish them every possible success.

Coda We couldn’t help thinking that the above is an advertisement for a high education, high pay economy with all the public infrastructure needed to support those things. But that’s for another sort of blog on another day.

# microbial antibiotic resistance #phage #AI #start up #Gutsee #irritable bowel syndrome #health #medicine #sugery #wounds

Are you missing out on red light? A lightbulb moment for Graham Lawton and the New Scientist

It’s a funny thing to be a progressive. We ‘re always prey to the Law of Unintended Consequences. For example, we rack our brains to replace all those nasty energy intensive incandescent bulbs with lovely low energy LEDs . And suddenly there’s a new problem. Is the new light from the LEDs missing something the old incandescents were giving us for free? Something that might, just might, have been good us?

Now we take this problem seriously because it is brought to us by no less than Graham Lawton of the New Scientist, a sure guarantee of intellectual probity. Quite rightly the magazine keeps Graham and all its top writers behind a pay wall, so once again we beg you to either take a sub, or buy the magazine. But the essence of Graham’s article is that the old incandescent lights, for all their dreadful shortcomings. were throwing out long wavelength infrared light, a bit more like the natural light you find when you go outdoors. Graham presents intriguing evidence that these wavelengths stimulate mitochondria to produce energy-carrying ATP (adenosine triphosphate) which production facilitates any number of health benefits, But you’ll have to read his article to find out what those are! Not only do the new LEDs chop out most of that infrared; but the new types of window glass actually reduce its natural ingress further. If you are sitting indoors under the dominance of blue‑weighted indoor light (from computer screens for example) you may be missing out on something rather good.

So how do we as Whigs, progressives, rationalists or whatever you want to call us, take all this? Intelligent readers will already see the other side jumping up and down with glee “See-orl dem (expletive deleted) sointissstss tryin ter cure (expletive deleted) global warmin’ wiv dem crap new bulbs, only making fings worse etc etc” In the same spirit as they disparage initiatives such as renewable energy technologies or health initiatives such as the London ULEZ zone (see next blog) Well, let’s concentrate on the rationalist word Rationalists know the world to be infinitely complex, not reducible to tabloid newspaper soundbites. Naturally every new initiative will have a cost benefit ratio(only children believe in pure unalloyed good) The new LED’s have undoubtedly brought immense benefits Only a pub philosopher would be dim enough to throw them away. But we know the tools of reason and evidence will deal with this problem as it did with the other one. That is what differentiates us.

[1] The shock revelation that light bulbs are wrecking your metabolism | New Scientist

#incandescent bulbs #LED #energy #sustainability #red light #infra red #health #medicine #lighting #ATP

Fascinating new mitochondrial discovery may help reverse ageing (one day)

It’s not the new stuff that comes up, it’s the unexpected stuff that gets us out of bed in the mornings. So when someone publishes an article like the one we’re showcasing today [1] Metabolic Signal From Dysfunctional Mitochondria Linked to Aging from the excellent Technology Networks website we sit up and take notice. Not only does the story drag the humble mitochondria[2] into the middle of the ageing process, it straddles the whole complex frontiers of genetics, epigenetics and cell physiology, long-loved favourites of ours, as veteran readers will recall.

Researchers have long known that the body slowly accumulates large populations of zombie cells, which pump out cocktails of inflammatory molecules leading to frailty, cardiovascular disease, cancer and other ailments. ( at this point the parallel with societies accumulating large populations of ageing citizens pumping out ill informed and socially damaging opinions into the body politic occurred to us, but it won’t go in the blog). Instead of removing these cells, the researchers asked, would it be possible to switch off their damaging signals? It was known that damaged mitochondia leaked DNA and RNA into cells, setting off an inflammatory response. Now detailed investigation has uncovered the key signalling mechanism, the epigenetic switch, that turns on the whole process. And it turns out to be our old friend Acetyl CoA, that standby of the biochemical textbooks of our youth. To quote the article

the researchers discovered that senescent cells increase production of acetyl-CoA, a molecule generated through mitochondrial metabolism. Acetyl-CoA enables epigenetic modifications – chemical changes that regulate whether genes are switched on or off without altering the DNA sequence itself. These modifications make inflammatory genes more accessible, allowing them to be robustly expressed.

See what we mean about straddling three fields at once? Theres good therapeutic news too in the form of a transporter molecule that goes by the snappy name of SLC25A1. Blocking this may slow down the whole process, or so the researchers hope.

Our takeaways? First, thanks to our researchers for discovering the excellent Technology networks A click on their website revealed a cornucopia of learned articles, links, communities and much else. We will be visiting them again. Secondly: epigenetics, epigenetics, epigenetics. [3] Thirdly, you never know what you don’t know, and this whole area of mitochondria in ageing has been a bit of revelation to us. We can only conclude that the more you learn, the more you discover. Or is it the other way round?

[1]Metabolic Signal From Dysfunctional Mitochondria Linked to Aging | Technology Networks

[2]Mitochondria – Wikipedia

[3]Carey, Nessa. The Epigenetics Revolution: How Modern Biology Is Rewriting Our Understanding of Genetics, Disease, and Inheritance. London: Icon Books, 2012.

#genetics #epigenetics #cell biology #mitochndria #ageing #biochemistry #health #medicine

Why antibiotic resistance will be very bad news for your Grandchildren

Photo by Monstera Production on Pexels.com

Despite our occasional diversions into such recondite fields as History and Economics, this is still front and centre an Antibiotics resistance blog, gentle readers. Which is why when an article as good as the one we’re showcasing today called Antibiotic Resistant bacteria increasingly leaving children vulnerable to common infections, global study finds by the inestimable Melissa Davey of the Guardian, we drop all else in its favour.

And it’s packed with goodies, it touches so many bases: if you’re antibiotics fan get a load of this:

There’s a whopping great survey of 82 countries: 106, 581 samples, over 22 years, all controlled by some of Australia’s most prestigious learned bodies. If that isn’t great statistics then you can call us David Spiegelhalter [2]

Several of this blog’s sinister old favourites such as Acinetobacter baumanii, Klebsiella have their usual run out-don’t you love ‘em?

There’s a forward prediction to 2035 which ought to make anyone pause for reflection.

Despite the efforts of brilliant journalists like Melissa, learned scientists of all stripes and even dare we say our own humble efforts, antibiotic resistance is still the ignored elephant in the room of ~~medical science.~~ Sorry we meant human existence. Yep, we meant it.

Talking of which, the all too human failings of poor diagnosis and over prescription, agricultural misuse and poor public health are driving our collective squandering of this precious, once only ever, resource.

The less discussed economic aspects are touched on. Get this: there is sometimes a reluctance to run trials on children and developing treatments for them can be less lucrative for pharmaceutical companies There’s yer problem, guvnor.

The usual hero organisations such as the WHO get a mention, and rightly so given the Herculean task they face.

And a sad, sad story about a lad called Harry whose brief life will be utterly dependent on the rest of us finally doing something about this common peril

If we were to present a class of Freshpersons with a jumping off point which summarises just about every trope in the antibiotics story, then this article would be our choice. Well done Melissa, And keep ‘em coming.

[1] https://www.theguardian.com/australia-news/2026/jul/21/antibiotic-resistant-bacteria-increasingly-leaving-children-vulnerable-to-common-infections-global-study-find

[2] David Spiegelhalter – Wikipedia

#antibiotic resistance #bacteria #microbiology #health #medicine #infection

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

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

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

More on AI and Antibiotics-and it’s good news

Once again, the source for our blog today comes from the excellent Nature Briefing, who are always in the forefront of scientific research in every field. Today we are showcasing their piece AI is taking on antibiotic resistance because we think they’re picking up on some real game-changing developments, and we really want you to know about them.

Let’s start with their usual helpful summary, as it’s a good general overview. But this time we earnestly beg you to click on the link they have provided: read below to find out why.

Antibiotics are an effective, but somewhat indiscriminate solution to some gut infections. Helpful species of gut bacteria get caught in the crossfire, which increases the likelihood that drug-resistant bacterial strains will evolve. Researchers are now designing drugs to selectively target disease-causing species with the help of artificial intelligence. Some teams are using AI to screen drug molecules for the most promising candidates quickly and cheaply. Others have developed tools that predict how drug molecules bind to protein targets to reveal a drug’s mechanism of action, reducing the need for wet-lab experiments.

Nature | 15 min read

Because if you do, you will step into a world of research where Information Science and Biological Science are meeting: which of course is more and more these days isn’t it? You will learn about:

Jonathan Stokes of McMaster University in Canada who have pioneered the use of AI to test their newest molecule called enterololin and thereby strip out all kinds of old-skool testing processes.

Regina Barzilay of MIT who with her team have done much of the AI work to set this up for Jonathan She is a remarkable woman who has been hunting down the link between antibiotics and AI since 2018-how’s that for far sightedness, folks?

You’ll be able to name check tools like Diffdock , RdKit and Chemprop which these people use to do all this-how’s that going to sound in the pub?

And a woman called Molly Bartlett who’s something called a Chemical Informatician at London’s Imperial College. As we still have a tenuous connection to that august institution we sometimes write in to their alumnus mag and tell them what a good job they’re doing, knowing we speak for all of you, gentle readers.

And much more besides, Especially if you do the decent thing and sign up to go behind the paywall.

Funny, isn’t it? If our first name were Donald (it isn’t) we might note how much this progress a) seems to come from despised places like Canadia and Englandland b) how somehow these evil foreigners still find ways to work with Unitedstatespersons c) maybe if you want to find cures for important things you may have to look at other methods in addition to earnest prayer d) if I were getting bigly older, perhaps approaching my eightieth birthday for example, I might like to have a few antibiotics around. Just a thought.

# Antibiotic research #Artificial Intelligence ~medicine #health #bacteria