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

No Pandemic this time: but what happens next?

While we sympathise with the unfortunate passengers and crew of the MV Hondius who may have been exposed to the hantavirus, our first response was rather selfish; “is this a new pandemic, and if so, how bad will it be?” We were not alone: and fortunately, as this excellent summary article from Julia Musto of the Independent, via MSN, explains: humanity seems to have dodged the bullet this time [1] Although utterly dangerous the virus just doesn’t seem to spread with the same facility as others such as SARS-CoV-2, or the influenza group. So that’s alright then.

Or is it? Because as certain as the House always winning, another pandemic will come along. Bringing the same economic, social and physical disruptions as COVID 19 did back in 2020. Or worse maybe. Surely humanity has learned some lessons from that catastrophe? Taken steps, you might think, to mitigate the worst effects and learn to pool our resources so that next time round everything will be different? Not according to Kat Lay of the Guardian [2] whose indefatigable investigations have unearthed another avoidable catastrophe in the making.

Because although a Pandemic Treaty has been signed , it cannot go into effect until a special clause called a Pabs (Pathogen access and benefits sharing) has been ratified. It hasn’t, as regular readers will be unsurprised to learn. The result is:

“If a new pathogen emerged today, the world remains largely unprepared for it. A lack of action to prevent and prepare for the next pandemic threat is a disservice to humanity,”

Kat cites the usual litany of petty squabbles, mutual jealousies and general misinformations which have led us all into this sorry plight and ends her article there.

But we, gentle readers, cannot quite leave you without adding our own thought. Natural Selection tells us that species go extinct when their key survival features are no longer adequate to their environment (what use are flippers to a whale out of water, for example?) Humanity’s key advantage was its intelligence and relatively large brain. Is this clear example of the failure to use this clear cognitive advantage a sign of even worse things to come?

[1] https://www.msn.com/en-gb/health/general/could-cruise-boat-hantavirus-be-the-next-global-pandemic/ar-AA22CAGh?

[2] https://www.theguardian.com/global-development/2026/may/05/talks-stall-on-who-pandemic-treaty-global-response-disease-outbreaks?CM

[3] MV Hondius hantavirus outbreak – Wikipedia

#hantavirus #pandemic #covid 19 #WHO #health #medicine #virus

Progress on Multiple Sclerosis: When Big Data meets Molecular Genetics

Photo by Fayette Reynolds M.S. on Pexels.com

Few of us have not met someone who is suffering from Multiple Sclerosis, that terrible wasting disease wherein the immune system seems to turn on its own body, especially in the fatty sheaths around the neurons. Leading to a progressive deterioration in mobility before confining victims finally to a wheelchair-or even worse. The experience for families and victims was extra-bad because for many years the cause seemed unknown, making hope of any cure quite unlikely. Michael Marshall of the New Scientist has been covering this story most assiduously. And so we are pleased to showcase it, because it celebrates achievements in two our our favourite fields-big data and molecular biology-and the benefits which accrue when scientists from both work together.

We urge you to read Michael’s article either by buying the hard copy mag (there’s tons else to read inside it) or paywalling past the link below [1] Suffice it to say: #1 The molecular evidence that the Epstein Barr virus (which can cause glandular fever) is involved. #2 That this has a strong effect on both B cells and T cells in the immune system, which ,when they go rogue, are essentially responsible for the terrible lesions of MS #3 That not all hosts of Epstein Barr virus go on to develop MS, because the chances of that depends on certain genetic propensities and variants and, best of all #4 the above and more, which we report so glibly, has been elucidated by the use of huge data studies : 10 million people in one, 617, 186 in another, even 471 000 B cells in another-how’s that for numbers, folks?-which were only possible because: #5 places like the UK and USA have worked to build big collaborative things the the UK Biobank and All of us. Well some of the people in those countries have anyway.

All of which leads us to few reflections, some of which will not be uncongenial to regular readers. Firstly, it seems a pretty good idea to spend money on science, especially basic research, instead of cutting it. Secondly scientists these days work best in large teams whose members come from all sorts of backgrounds and this is especially true when you throw multidisciplinarygroups of them together. And that this also seems to be true of football teams: how far would Arsenal FC. for example, have enjoyed their current success if they had insisted on retaining a staff entirely composed of plucky British lads? [2] The implications in turn for visa systems, cultural openness and plain common sense are clear in turn.

[1]Huge study reveals how Epstein-Barr virus may cause multiple sclerosis | New Scientist

[2]‘Everything can happen’: Trossard confident of Arsenal’s chances in final | Arsenal | The Guardian

#multiple sclerosis #Ebpstein-Barr virus #T cells #B cells #autoimmune disease #medicine #health

Hydrogen from Microbiology-another hopeful story from Nature Briefing

You might be forgiven for thinking we’re against bacteria at this blog. Got a beef with them, want more antibiotics to kill them, especially that pesky little Escherichia coli that is always clogging up the pristine pages of our little website. Nothing could be further from the truth: we are simply against bacteria that kill people, that’s all, and we admire the little creatures for all the useful things they do

Nothing more useful it seems than generating hydrogen in clean green ways that massively reduce greenhouse gas emissions. Of course we need hydrogen for all sorts of things-food, drugs, plastics-but the way it is currently made is depressingly energy intensive Which is what this remarkable team of researchers at Edinburgh University have done, re purposing E coli to make hydrogen in amazingly clean ways Get this extract from the admirable Nature Briefing:

. The new process involves growing a strain of Escherichia coli that naturally produces hydrogen when deprived of oxygen. The researchers added a palladium catalyst and substrate for the hydrogen to bind to, and when they removed oxygen, hydrogen was bound to 94% of the substrate.

And they didn’t stop there:

The team then turned waste bread into a food source that could be given to the bacteria instead of glucose, to show that this type of food waste can be repurposed. The system resulted in a three-fold decrease in greenhouse-gas equivalent emissions compared with using fossil fuels, according to the team’s modelling.

There’s a lot to be said here. First our admiration for the amazing work and intelligence of the scientists[2] whose original paper we seem for once to be able to reproduce in full. The marvellous ways old things like bread and E coli are recycled to useful purposes. And a further point which the team at the admirable Nature Briefing know well. Progress, hope even, comes from the application of the scientific method. The use of evidence and reason to judge it in that order. Nothing else, however much you might want it to be so.

[2] Native H2 pathways enable biocompatible hydrogenation of metabolic alkenes in bacteria | Nature Chemistry

#microbiology #palladium #greenhoiuse gas# hydrogen# E coli #sustainabilityn #drugs #plastics

WHO has a Cunning Plan to speed antibiotic development

“The scientific community has developed and approved new antibiotics in recent years. This is good, but unfortunately not sufficient to catch up with evolving drug-resistance bacteria, especially against those of greatest concern. We need a reliable pipeline with new antibacterial agents that are innovative, affordable, accessible to all those who need them.”

Dr Yvan Hutin, Director of Antimicrobial Resistance at WHO

Says it all really, everything that we’ve been banging on about here for the last six years and more. The problem is simple, but deadly. Although more than 90 new antibiotics are now in development, very of few of them target the really high-priority organisms that worry health care professionals: and even fewer of these are really innovative (in the way that penicillin was in its day for example) And so the World Health Organization, that most noble of entities has come up with a Cunning Plan to really get things moving. They gave divided it into three Target Product Profiles:

-our old friends the multidrug resistant gram negative bacteria such as enterobacteriales, Acinobacter baumanii and Pseudomonas aeruginosa, who’ve shown up in so many old LSS blogs we won’t bother to list them.

–Gram positives like Enterococcus faecium. We have wondered why the gram negatives have been getting all the attention, and seeing no Darwinian reason why the gram positives should not evolve resistance too, are extremely glad someone is at last paying attention to them.

-their third trope for action is bacterial meningitis, caused by organisms such as Neisseria meningitidis and Streptococcus pneumoniae among others. Particularly welcome, for of those who incur such dreadful infections, one out of six will die and of the survivors, about one in five will be left with some long term disimpairment.

Hats off to Dr Hutin in particular and the World Health Organization in general. The World Health Organization is often treated as a mere federation of its member states, but in practice it is something larger and more coherent than the sum of its parts. Individual nations see only their own budgets, their own pathogens, their own political cycles; the WHO sees the whole epidemiological chessboard. Its strength lies in that cooperative vantage point — the ability to gather data from Lagos and Lima, to convene experts from Seoul and Stockholm, and to turn a hundred local anxieties into a single, rational blueprint for global action. In a field as fragmented and under‑powered as antibiotic development, that kind of coordination isn’t bureaucracy; it’s civilisation defending itself. There’s your glass-raiser for Friday Night Cocktails, gentle readers.

WHO releases new target product profiles for urgently needed antibiotics

#antibiotics #penicillin #world health organisation #epidemiology #microbiology #health #medicine

When Bacteria Explode: a new clue in the old antibiotic arms race

Bacteria are relentlessly evolving resistance to our attacks with antibiotics and phages — but how? If we understood their tricks a little better, we might still have a chance of avoiding the lethal pandemics of antibiotic‑resistant organisms otherwise waiting in the wings. A new paper from researchers at the John Innes Centre[1] has now shed light on at least one way that whole populations of bacteria may be secretly defending themselves from our ministrations.

The team found that the bacterium Caulobacter crescentus has an extraordinary switch mechanism that can cause it to “explode” under certain conditions. When it does, it releases tiny virus‑like particles containing fragments of its own DNA. Pertinent to our quest, gentle reader, is that some of this DNA may include instructions on how to resist antibiotics — or perhaps even the bacteriophages we deploy against them. The researchers also identified the components of this switch, which go by the snappy names LypABC and CdxB. They don’t yet know exactly what flips the switch, but they have their suspicions.

All of this is good news for those of us following the antibiotic‑resistance story. We now have a clearer picture of how at least one type of bacterium spreads resistance among its own members. And if we know what these switches are, we have a fighting chance of intervening to turn them off. If, as the researchers suspect, the presence of a hostile phage is indeed one of the triggers, then this is a very great step forward indeed

[1]A bacterial CARD–NLR-like immune system controls the release of gene transfer agents

Emma J. Banks, Pavol Bárdy, Ngat T. Tran, Phuong M. Nguyen, Boris Stojilković, Kevin Gozzi, Abbas Maqbool & Tung B. K. Le Nature Microbiology (2026)C

[2]John Innes Centre | Excellence in plant science, genetics and microbiology

#antibiotic resistance #bacteria #dna #genes #virus #bacteriophage #health #medicine

Breakthrough for blindness, an old lesson re-learned: and a mystery question

Leber congenital amaurosis, called LCA for short, is the most common form inherited sight loss in children[1] It’s caused by defects in a cluster of genes including RPE65 and until recently was quite untreatable. Now, as Ian Sample reports for the Guardian,[2] a team of researchers have effected a major new treatment called Luxturna: a gene‑replacement therapy delivered by injecting a working copy of the RPE65 gene directly under the retina. By giving retinal cells the functional gene they’re missing, it restores the visual cycle and can improve light sensitivity, visual function, and navigation ability in people with RPE65-related Leber congenital amaurosis. Interestingly the team comprises a husband and wife called Jean Bennett and Albert Maguire who share the prestigious Breakthough Prize [3] with their colleague Katherine High.

Regular readers will share our admiration for the work of this remarkable trio. They may note moreover that the researchers have something else to teach us, something that strongly concurs with opinions often expressed in this blog:

Bennett said it was a “tremendously exciting time” for scientific and medical research, but warned that the US administration’s attacks on science could “cause damage for generations to come”, leading her to fear a brain drain that the country would struggle to recover from.

“Agendas have become politicised, government agencies that support basic and applied research have been undermined, knowledgeable advisers and experts have been dismissed or have fled and revised guidelines contradict decades of rigorous research,”

Says it all really. But don’t just sit around reading it here:tell your friends and neighbours. For us there still remains outstanding question. Is Albert Maguire by any chance a relation of Ken Maguire, one of the best pub landlords of the 1990s, being sometime manager of the superb Latymers in Hammersmith Road London W14?

[1]Leber congenital amaurosis – Moorfields Eye Hospital

[2]‘Oscar of science’ awarded to team behind gene therapy that restores lost vision | Science | The Guardian

[3]Breakthrough Prize – Wikipedia

#LCA #Blindness #gene therapy #medicine #health #science #research #pub #beer

Eyes show why evolution is never linear

Photo by Alejandro Quintanar on Pexels.com

Opponents of evolution and natural selection are fond of quoting the eye as an example of irreducible complexity which they imagine will wash away all objections to their creeds: “How could anything so complex have evolved without a very clever chap like God being behind it?” they ask, “and why would it have evolved as it only works when it’s completed?” Aside from the logical error which astute readers will have spotted at once, the story of how eyes evolved not only demonstrates how it happened, but answers so many other questions,that it’s actually rather more interesting than the stories offered as an alternative. Read this beautifully explained article in the Conversation by George Kafetzis and Dan Nillson [1] for a full exposition. Our humble summary appears below.

About 620 million years ago there lived an animal that was ancestral to all animals that would ever have two sides and move forward. It needed to steer as it swam: so it had two light sensitive areas symmetrically up front on either side. Another patch on top told light from dark, and which way up it was. And there it might have ended except for two things One group of these animals went to live in the mud as filter feeders. Having no need to swim they lost the steering eyes. Of course they kept the middle eye as it as still important to know if the Sun was shining. But when some of their descendants in turn started swimming again they needed to steer. Slowly the sides of the top eye moved apart, developed lenses and became eyes. These were the vertebrates. And this is why the eyes of all vertebrates-fish, lizards, birds and humans are so very very different from all other animals :invertebrates, such as scorpions, flies, octopuses and so on . Never giving up moving, their ancestors needed those original bilateral side eyes which slowly became more and more complex. Look at a fly if you don’t believe us. For the record the vertebrates kept the third top eye, its just that in mammals it has shrunk to the internal pineal gland where it still controls lots of light-related things like sleep and melatonin release

Its funny to think of eyes starting simple, evolving, un-evolving in some groups, and then evolving again, all according to the needs of those animals at the time. Its refreshing to find our basic LSS beliefs confirmed. Truth, or knowledge worth knowing, is complex and requires a lot of patient exposition to tease out. And it shows that simple, this-explains-it -all tales only end up obfuscating any real understanding.l. Nice to think that what happened 600 million years ago still has lessons for us today.

[1]https://theconversation.com/our-modern-vision-evolved-from-an-ancient-one-eyed-worm-creature-278120?utm_medium=email&utm_ca

#evolution #natural selection #eye #cambrian #vertebrates #invertebrates #paleonto;ogy #biology