Archive for the ‘bacteria’ Category
solutions ok – methane-eating microbes
this gives a general idea..
So here’s a relatively short one. I have/had another blog called ‘solutions ok’ which I haven’t touched in ages, I’d rather have a one-size-fits-all blog – one failure’s better than two, as they don’t say. Anyhow, here’s a little solution I read about in New Scientist – methane-eating bacteria. Not that this idea is particularly new, you’ll find videos promoting it from more than five years ago, but apparently it will soon be put into practice – at least in practice:
Later this year, researchers in the US will deploy a bioreactor filled with a specially bred strain of methane-eating bacteria at a landfill site in Washington. They hope that the field test will prove that these bacteria, known as methanotrophs, can be deployed in bioreactors such as this to harvest methane from the air, even when it is at relatively low concentrations.
So what’s a bioreactor, I ask myself. Well, it’s what it sounds like, a bound system, as with a nuclear reactor, in which controlled reactions, this time biological, can take place. If the system is made to work effectively, it presumably could be replicated globally. Methane is a more potent greenhouse gas than CO2, though not as prevalent, nor as long-lasting in the atmosphere. However, emissions of methane are rising. The main sources are agriculture, fossil fuels and waste material in landfills. These bioreactors will ultimately target all three, or so it is hoped.
The particular methanotroph to be tested is a strain, specially bred for purpose, called Methylomicrobium buryatense 5GB1C (you will be tested). They’re still working on its methane-harvesting ability, so as to deal with the relatively low levels measured at landfill sites. The idea is to suck the methane-laden air into the bioreactor, where, by means of these methanotrophs, the methane will be converted into useful proteins, plus carbon dioxide (hmmm). The net effect, in any case, will be ‘a reduction in the warming capacity of the air’.
So this isn’t the only pilot project in the works. Other projects, using methanotrophs ‘encased in hydrogels’ are planned for absorbing and converting methane from wetlands. Apparently these microbes have ‘evolved the enzymatic capacity to bind methane and oxidise it to carbon dioxide and also assimilate it to biomass’, which is a very meritorious thing, from a human perspective. All is not yet lost, apparently.
I’ll keep an eye out for other such solutions in future.
Reference
New scientist, April 19 2025, p13, ‘methane-eating bacteria ready to tackle emissions’.
immunity 2: MIT lecture – more on immunity and auto-immunity
So we’re looking at cell-mediated and auto-immunity in this second lecture. We see an image of listeria, an intracellular bacterium, pushing out the edges of the cell, so that it can move between cells without entering the extracellular space. Listeria is a food-borne bacterium which can cause severe intestinal illness. So think of a host cell with an intracellular pathogen, bacterial or viral, taking advantage of these cells to reproduce and spread. This is not good.
B cells, as described before, have an antigen receptor, initially on the plasma membrane, and sometimes secreted into the intracellular space, while T cells only have the membrane-bound form. In any case these antibodies are directed outwardly. How can a listeria-like infection, within the cells, be dealt with? This involves a process called antigen presentation, in which peptides – short sequences of amino acids – are presented and displayed on the cell surface, so that T cells, in this case, can observe what is happening within the cell. This involves another molecule previously mentioned, the major histocompatibility complex (MHC). There are two classes of MHC. Class 1 has a heavy chain – a long polypeptide – and a light chain. So, two polypeptides encoded by different genes. It has two Ig domains proximal to the plasma membrane – and it’s all inserted into this membrane – an integral membrane protein. Then at the other end, distal to the plasma membrane, is another structure, which, looking at its crystal structure, is a ‘beta sheet with two alpha helices’, shaped somewhat like a cup [a beta sheet is a common secondary structure in proteins, formed by polypeptide strands (beta strands) connected laterally by hydrogen bonds, creating a pleated, twisted, sheet-like structure]. Inside the cup is a peptide which displays some of its amino acids, away from the MHC molecule, for T cells to observe.
So these Class 1 MHCs are membrane proteins displayed on all nucleated somatic cells, and the peptides held by these MHCs are derived from the cytoplasm within the cell. They are loaded on to the MHC molecule, which is translated (using ribosomes and types of RNA) on the endoplasmic reticulum (ER), and its extracellular domain is initially present in the lumen (internal space) of the ER. Its peptides come from proteins in the cytoplasm. What happens to these proteins – including unfolded proteins and those that might be ubiquitinated [refers to a protein that has had ubiquitin, a small protein, covalently attached to it, often marking the protein for degradation or influencing its function or localisation – thanks AI, and it has of course dawned on me that this MIT course has followed on from earlier biochemistry learnin] – is that they’re processed by the proteasome [a large, cylindrical protein complex that degrades proteins tagged with ubiquitin, a process essential for maintaining cellular homeostasis and regulating various processes like cell cycle and protein quality control], which this lecturer describes as ‘a kind of shredder-like function for protein’, which cuts the proteins into peptides which can then be pumped into the ER lumen via a transporter, TAP…
The transporter associated with antigen processing (TAP) is a heterodimeric protein complex (TAP1 and TAP2) that transports peptides from the cytosol into the endoplasmic reticulum (ER), where they bind to MHC class I molecules, a crucial step in antigen presentation to cytotoxic T cells.from AI overview
From there they are loaded onto the class 1 MHC molecule. The source of these peptides is from proteins in the cytoplasm, processed by the proteasome. So now that a peptide-MHC complex has been created, it can then be trafficked to the plasma membrane of the cell, where the peptide will be displayed for T cells to observe. The types of T cell that look at these class 1 molecules are known as CD8+ T cells.
There are also class 2 MHC molecules, which have fundamentally different properties. Both molecules display peptides on the cell surface (antigen presentation), but the structure of MHC class 2 is quite different. Instead of a heavy and light chain, there are two chains of roughly equal size, and they’re encoded by different genes than the class 1 MHC. There are two Ig domains proximal to the plasma membrane, and at the end of the MHC molecule there’s a groove or pocket that holds a peptide (aka a peptide-binding cleft).
The class 2 MHC is expressed on a more restricted set of cells. They’re expressed specifically on specialised antigen-presenting cells, such as B cells and phagocytic cells [also known as phagocytes, they are specialised cells of the immune system that engulf and destroy foreign substances, pathogens, and cellular debris through a process called phagocytosis].
Phagocytosis is the process by which a cell uses its plasma membrane to engulf a large particle, giving rise to an internal compartment called the phagosome. It is one type of endocytosis. A cell that performs phagocytosis is called a phagocyte.
Endocytosis is a cellular process where a cell engulfs extracellular material, forming an internal vesicle to transport substances into the cell. This process, which includes phagocytosis (cell eating) and pinocytosis (cell drinking), is essential for nutrient uptake, cell signalling, and defence against pathogens.
Dendritic cells (DCs) are crucial immune cells that act as sentinels, capturing antigens and presenting them to T cells to initiate adaptive immune responses, effectively bridging innate and adaptive immunity (from AI overview)
References
Immunology 2 – Memory, T cells & Autoimmunity, MIT OpenCourseWare, YouTube video
the evolution of complexity
Gould’s view of the movement to complexity
I’m not sure if this is a controversial topic – perhaps it depends on whether you think complexity is in some sense superior to simplicity regarding organic life, and I suspect that we humans are a bit biased on the issue.
Bacteria and archaea are still thriving in our biosphere, in vast numbers. These two classes or domains of prokaryote differ in various ways. The eukaryotes, the third domain into which organisms have been divided, are believed to have evolved from an ancestor of modern archaea.
A question. With such forms of life thriving from billions of years ago, why become more complex? In what way would it have been more advantageous? But in thinking of advantage, aren’t we thinking outside of the prokaryotic box? Shouldn’t scientists (I’ve seen this written) confine themselves to ‘how’ questions rather than ‘why’ questions? But since I’m neither a scientist nor a philosopher, I don’t know what to think.
In any case, ‘how’ questions seem quite a bit easier to answer. One way to think about it, I suppose, is to think of ‘accidents’, or simply differences, that confer an advantage. What might be called imprecise (or just varied) replications mostly wouldn’t survive, but some would turn out to be beneficial to survival, and so, over eons – complexity.
Problem solved.
Stephen Jay Gould provides an explanation for complexity in his book Life’s Grandeur, which I find overly verbose, but I think I can simplify it, in my simple way. These early prokaryotes would’ve replicated themselves almost perfectly, but not quite. Sometimes, very rarely, they would’ve missed something, or messed something up, during replication, called binary fission in prokaryotes. This would mostly have made the next generation non-viable, because generally prokaryotes are so tiny and simple that if they were any simpler they’d come up against a ‘wall’ of non-viability. The only way a different but viable next gen could be created would be if something was added rather than subtracted.
But how could this happen? Well, the ‘addition’ might be something genetic, but let’s not go there for now – Darwin didn’t need genetics to develop his theory of natural selection, nor did he need a concept of progress, though, unsurprisingly, he fell into that trap now and again. I’ve not looked deeply into binary fission but maybe the fission might occasionally lead to something not quite the same as its predecessor, in the way that archaea are not quite the same as bacteria, or that the first eukaryotes weren’t quite the same as those ancestral archaea. That’s the funny thing about the term ‘evolved from’ – it’s so easy to say, but a lot harder to pin down precisely. Anyway, maybe some kind of genetic ‘doubling up’ made some difference, a hardiness, a more diverse diet – if prokaryotes can be said to have diets. In any case, it was all about ‘more’ – a very all-encapsulating four-letter word. For example, think of stromatolites, those colonies of cyanobacteria. Was it colonisation from the start, or did some genetic change create this kind of super-organic effect?
All of this is as hard to pin down precisely as life from non-life, but we know it happened. And we also know that once life got itself well started, it thrived pretty much everywhere, not just over our planet, but quite deeply under the surface, in the most unlikely places. And considering the vast numbers, all of them replicating, the possibility of something more complicated surviving and battening on to others in an advantageous way becomes plausible, surely.
So, prokaryotes to eukaryotes. Were there intermediate stages? Let’s look at the differences. Eukaryotes are all the life we see. Prokaryotes are invisible to us without microscopes, etc. We’ve divided them into archaea and bacteria, based on a number of differences, notably the structure of their cell walls, but these structures also differ between species of bacteria. Gould has explored the issue of ‘progress’ and complexity from a bacterial perspective in the lengthy penultimate chapter of Life’s grandeur, entitled ‘The Power of the Modal Bacter, or Why the Tail can’t Wag the Dog’. I looked up Modal Bacter online and came up empty, which is why Gould irritates me so, as a writer for ‘the general public’. I’m guessing it means the bacterial mode of life. I’m going to use Gould’s chapter for the rest of this post, which looks like being a long one. So, at the beginning of the chapter, he writes this:
… simple forms still predominate in most environments, as they always have. Faced with this undeniable fact, supporters of progress (that is, nearly all of us throughout the history of evolutionary thought) have shifted criteria and ended up grasping at straws. (The altered criterion may not have struck the graspers as such a thin reed, for one must first internalise the argument of this book – trends as changes in variation rather than things moving somewhere – to recognise the weakness).
I’m not quite sure what this means, but ‘progress’ sticks out. We can make progress in learning a language/trade/sport, but has life made progress? I would tend to agree that this term isn’t useful from an evolutionary perspective. The criterial shift is surely toward complexity, and this is surely happening in the human line of development. Unfortunately we can’t measure neural complexity in our most recent ancestors – the closest living connections we have are chimps/bonobos, and here’s something from the Cambridge University Press website:
while chimpanzee brains are markedly smaller than those of humans, their brain anatomy is so similar that a discourse comparing the two might be little different from this declaration: The chimpanzee brain is a human brain with one-third of the neurons (Herculano-Houzel & Kaas, 2011).
This odd observation – very similar anatomy with one third of neurons – is a head-scratcher. I would have thought that neural organisation, perhaps especially in the prefrontal cortex, would be key here. After all, isn’t this the point of such comparisons? We’re looking at neurology to help us understand the differences we see in the culture and behaviour of Pan troglodytes and Homo sapiens, are we not? And it’s surely fair enough to say our human behaviour is more complex, what with our language, our science, our culture, our cities and whatnot? To point this out is not to be hubristic. In pointing this out we need to be aware, and many of us are, of the downsides – our altering of the atmosphere, our responsibility for species loss, and so on. I should also point out, since I’ve mentioned hubris, that free will is a myth, as I’ve argued in more than one previous post. I didn’t choose to be human, it just happened to me. Not my achievement. Nothing to be proud or ashamed of. Just something to make sense of, as best I can.
So, bearing this in mind, human complexity is worth studying, and it’s not about patting ourselves on the back. This particular complexity of humans – and it may be that, in the vastness of the universe, different living complexities have evolved – is clearly a product of evolution. We wouldn’t be here without the ‘Modal Bacter’, as Gould calls it, or without the chain of connection that goes back to the earliest life forms.
So, it seems to me, that Gould, in trying to question, or demolish, the pedestal he believes we have placed ourselves on, and to give himself credit for so doing, is missing the point by raising up the ‘Modal Bacter’, as if it should somehow be given obeisance for being the great survivor and the great progenitor, while we are the mere accidental offshoots. Take this quote (along with my insertion):
Wind back the tape of life to the origin of modern multicellular animals in the Cambrian explosion [or indeed to the ‘Modal Bacter’ millions of years before], let the tape play again from this identical starting point, and the replay will populate the earth (and generate a right tail of life) with a radically different set of creatures. The chance that this alternative set will contain anything remotely like a human being must be effectively nil, while the probability of any kind of creature endowed with self-consciousness must also be vanishingly small.
S J Gould, Life’s grandeur, p 214
There’s an obvious flaw in the logic here. If you take the tape back to the Cambrian explosion or any other point in time and replay it, you’ll get the same result, because it’s the same tape! What he presumably means, is that if some condition was changed back in the Cambrian, or earlier, then a very different result would ensue for later generations. Or, that we humans are just ‘accidents’ resulting from particular initial, or previous, conditions. And so with all life, including his much-vaunted bacteria. Not to mention all planets, stars, etc. This should hardly be seen as a revelation. Which makes me wonder just what Gould is on about.
So let’s explore further. Here’s another of his ‘critiques’:
Under the traditional model of evolutionary history as a ‘cone of increasing diversity’, life moves ever upward to greater progress, and outward to a larger number of species – from simple Cambrian beginnings for multicellular animals to our modern levels of progress and range of diversity. Under this iconography, pathways actually followed run along predictable courses that would be at least roughly repeated in any replay.
Again I find this sort of writing overly tendentious. Either life has become more diverse in expression or it has not, and this has nothing to do with progress. And researchers are exploring this question, hopefully without recourse to ‘iconography’. It may be, as Gould argues, that vertebrates were in a ‘tenuous position’ before the Cambrian explosion and that, with some tweaking of prehistory, they wouldn’t have survived and we wouldn’t be here. So presumably this means we should be more humble and less overlordly. But is this something to be humble about, or proud of? Maybe it’s worth being aware of, just as I wouldn’t exist if my parents hadn’t met. But the fact is, they did, and vertebrates didn’t go extinct. So, if we stick with the facts, life would be a little more tractable. And no need to worry about progress or perhaps even complexity. We find complexity everywhere, from bacteria to the biosphere, and on to black holes and big bangs. It’s such a fun world to explore! And that’s the thing that easily makes me remain ‘umble. The world’s complexity isn’t my doing, obviously, and I hardly comprehend even the tiniest part of it….
References
Archaea vs. Bacteria
Stephen Jay Gould, Life’s grandeur, 1996
on the lymphatic system and its clever cells, mostly
Activation of macrophage or B cell by T helper cell
Jacinta: So we’re focussing now on the lymphatic system, ‘clear water’ remember. A most misleading definition. So there’s this network of vessels, nodes and ducts….
Canto: What’s a node?
Jacinta: It’s a point of connection, or connections. In plants, a node is a point of branching, like with leaves.
Canto: Yeah I knew that. What’s a duct?
Jacinta: Don’t kid kid. It’s like a vessel, only, somehow different. Maybe bigger? Anyway, nodes go with lymph. There are over 500 of these lymph nodes throughout our bodies. The system does a lot of clean-up work, preserving fluid balance. It’s also much implicated in the immune system of course, and it’s involved in other stuff that’s quite hard to summarise, as you know.
Canto: Something from a reliable enough website:
The lymphatic system plays a key role in intestinal function. It assists in transporting fat, fighting infections, and removing excess fluid. Part of the gut membrane in the small intestine contains tiny finger-like protrusions called villi. Each villus contains tiny lymph capillaries, known as lacteals. These absorb fats and fat-soluble vitamins to form a milky white fluid called chyle. This fluid contains lymph and emulsified fats, or free fatty acids. It delivers nutrients indirectly when it reaches the venous blood circulation. Blood capillaries take up other nutrients directly.
Jacinta: Never heard of lacteals. Have heard of chyle, but don’t know much about it. So chyle contains lymph. But what’s lymph?
Canto: It’s a not-so-clear beige-coloured milky fluid containing lots of WBCs, especially lymphocytes, of course, and fatty stuff. Well, actually, that’s not lymph, that’s chyle. Or both… So there’s this lacteal system of the small intestine, capillaries for absorbing fats – well, actually transporting them… but we need to know what bile is, and emulsification, and lipase, and glycerides and esters, and no doubt much much more.
Jacinta: Well we’ve committed ourselves to learning about the immune system and associated processes for some ineffable effing reason, so let’s soldier on.
Canto: Okay, so bile has nothing to do with Trump, at least not in this context. Bile ducts are this network of tubes inside the liver – well actually there are intrahepatic and extrahepatic bile ducts. Bile itself is a fluid made and released by the liver, for breaking fat down into fatty acids. For ‘digesting’ fat, sort of. Not particularly relevant to the immune system, but it’s all interesting en it? And it can cause problems, such as chronic bile reflux. I suspect I’ve experienced bile reflux, though not chronically. I think it’s also called acid reflux, suggesting bile is a kind of acid.
Jacinta: Or maybe not. Here’s another one of those websites that know more than us:
Bile is composed of ingredients designed to digest fat. While it isn’t an acidic formula, it’s harsh on the sensitive linings of your stomach and esophagus. Chronic bile reflux can erode these protective linings, causing painful inflammation and, eventually, tissue damage (esophagitis).
Anyway, I’m not sure how we got from chyle to bile.
Canto: Right, back to chyle and lymph. Have you heard of lymphoedema? That’s a blockage of the lymphatic system, which causes tissue swelling, mostly in the arms and legs but possibly just about everywhere.
Jacinta: Yes, and things fall apart, the centre doesn’t hold. So let’s get back to lymph nodes and the cells they contain. Within lymph nodes there are germinal centres containing a lot of B cells, or B lymphocytes. These have receptors (B cell receptors) on their membranes which are IgD antibodies, all of which have different binding domains, due to genetic recombination, which allows them to deal with differently structured antigens. Once binding occurs, signals are sent to the lymphocyte’s nucleus, resulting in what’s called receptor-mediated endocytosis. The signalling response creates pseudopods and/or clathrins which pull the membrane inside.
Canto: Ok, sorry to be boringly predicable, what are clathrins?
Jacinta: They’re proteins, very ‘clever’ proteins, as so many of them are. They mediate endocytosis, which is essentially the surrounding and cutting off of extracellular material within the cell, creating a vesicle, called an endosome I think, which might be transported to further action sites. So this is happening within the B lymphocyte. We have this B cell receptor bound to a foreign antigen, and chromosome 6 of this cell then can produce a molecule (MHC2) to ‘fit’ the antigen and fuse it to the cell membrane. This has the effect of activating the B cell, carrying an MHC2 antigen-carrying molecule on its surface, and IgD antibodies. Of course I haven’t explained how the clathrins actually carry out this transformation, because I can’t but I believe it’s all been worked out.
Canto: Yes of course, and now our lymphocyte is an antigen-presenting cell. There are three types of such cells – B lymphocytes, macrophages and dendritic cells. However, the lymphocytes still need to proliferate to be effective, and this requires a stimulus. And so enter the macrophages. These have MHC2 molecules on their surface, bound to a specific foreign antigen, and they also have MHC1 surface molecules bound to a self antigen (as do all nucleated cells). The macrophage presents this MHC2 molecule with its antigen to a type of T cell, described as a’naive’ (i.e. non-specific) T helper cell. These helper cells will have, somewhere on their surface, specific protein molecules, called CD4, that ‘fit’ with the MHC2 molecules, and other specific molecules (T cell receptors) that fit with the foreign antigen. Specific TCRs fit with specific antigens. It’s all a matter of geometry, sort of.
Jacinta: These different types of TCRs are a product of genetic recombination, which involves RAG1 and RAG2 genes, and I can only guess that the R stands for recombination… Now these helper cells have CD3 signalling molecules inside (they send signals to the nucleus), and a molecule called CD28 on their surface. The macrophage has a protein, B7, which interacts with the CD28, and this protein interaction, called a co-stimulation reaction, sends a secondary signal to the nucleus – as opposed to the first, primary signal. This is known as co-stimulation.
Canto: So next, the macrophage starts secreting a molecule called interleukin-1, which binds to a specific receptor on the T helper cell, which results in a third signal to the nucleus, and activation of the T cell. The cell’s genes now produce interleukin-2, which can be secreted and will then bind to a receptor, as an ‘autocrine’, resulting in genes secreting another cytocrine, interleukin-4, and then interleukin-5. With all this, the T helper cell moves to another stage, becoming either a T helper 1 cell (stimulated by interleukin 12) or a T helper 2 cell (stimulated by interleukin 4). So, focussing on the T helper 2, it has activated interleukins 2,4 and 5, the latter two of which are especially important, after these cells have started dividing. That’s when those cytokines are produced.
Jacinta: We might be learning something. Now to the proliferation of the B lymphocyte. Interleukin 4 activates the B lymphocyte to start turning on genes for its proliferation – called clonal expansion. And they will have receptors (BCRs) specific to the foreign antigen. They’ll also have MHC2 surface molecules with exposed foreign antigens. They’re now ‘immuno-competent’ cells, and then, through the medium of interleukin 5, they will start differentiating. Some of these new types of cells are called plasma cells, which have a very prominent rough endoplasmic reticulum (RER), others are called memory B cells. Interleukin 5 and 6 stimulate plasma cells to produce and secrete antibodies specific to particular foreign antigens – or, rather, having variable regions that can adapt to and bind to those antigens.
Canto: And these antigens might be on the surface of bacteria, or not as the case may be. If they can bind to all the antigens on the bacterial (or viral) surface they can render it ineffective (neutralisation). Binding to freely circulating antigens can, however, cause problems. Such binding creates a precipitation reaction and this can be deposited in tissue resulting in a type 3 hypersensitivity. Don’t ask.
Jacinta: This is what United Staters call getting into the weeds, maybe. So that’s surely enough for now.
reading matters 12: food mysteries
New Scientist 3292 July 25 2020
Jacinta: So this cover story reminds me of something I read or heard a few years back – that if you were to list the chemical ingredients of a hen’s egg, you’d never come to the end, or something like that.
Canto: Well you’re on the right track, the cover story is titled ‘the dark matter in your diet’, but instead of a hen’s egg it starts with garlic. Both of these commonly consumed edibles, like just about everything else we eat, contain ‘nutritional dark matter’ that scientists have only recently started to focus on, surprisingly considering that we are, to a fair degree, what we eat.
Jacinta: Yes, so we all know that food components or nutrients are usually divided into fats, carbohydrates and proteins, though these three can be subdivided to a near-infinite degree, but there are also vitamins, minerals and other biochemical elements in various quantities, and with variously vital effects. Currently the US Dept of Agriculture (USDA) has a database of 188 nutritional components of food, under which some info is provided on many thousands of chemical elements.
Canto: So garlic, the USDA reckons, is found in 58,055 foodstuffs, including, uhh, garlic. Raw garlic itself is described as containing 67 nutrients, both macro and micro, some of which can only be found in very minute quantities. And yet many components, such as allin, which helps to give garlic its particular odour and flavour, aren’t listed on the database.
Jacinta: Allin is converted into allicin, through the enzyme allinase, when you crush or chop garlic. That’s when that lovely/notorious stink hits you.
Canto: Right, and this is apparently a major problem across the whole database. They added a few dozen flavonoids – plant compounds that can lower the prevalence of cardiovascular disease – in 2003, but recent researchers have been frustrated by the many gaps, and are building their own more comprehensive database, based on their own chemical analyses. It’s called FooDB, which now lists almost 400 times the number of nutritional compounds as the USDA database. 2306 for garlic, for example, compared to the USDA’s 67. But there’s a lot of work still to be done, even on garlic. Only a tiny fraction of those compounds have been quantified – we don’t know the exact concentrations. And this is a problem for the whole of FooDB, with about 85% of compounds unquantified.
Jacinta: Sounds like we need an equivalent of the old human genome project – but for every single edible product? Nice, a few hundred lifetimes’ work, if you can get the funding.
Canto: Well, it suggests that we’ve massively overlooked the complexity of our food – and not only the foods themselves, but their interaction with the microbes and enzymes in our body. But here’s the thing – brace yourself – some nutritionists disagree!
Jacinta: OMG! Scientists are disagreeing?
Canto: The counter-argument is that ‘dark matter’ in nutritional terms is a beat-up. That, though much research is still needed in nutritional epidemiology, in relation to particular conditions and so forth, we know what the essential nutrients are, so the ‘dark matter’, which tends to exist in ultra-minute quantities, would make little difference. But the researcher who coined the term ‘nutritional dark matter’, Albert-Laszlo Barabasi, begs to differ – of course. He points out, for example, that vitamin E, or its absence, can have adverse effects at minuscule quantities, and it may be that all the flip-flopping advice we’re given about nutrition may have much to do with the gaps in our knowledge. Taking garlic again, it was found that of the 67 compounds listed for it on the USDA database, 37 had health effects one way or another, but of the 2306 on FooDB, some 574 had what they called ‘potential’ health effects. In any case, it seems to me that a more complete knowledge of what’s in our food can’t be a bad thing, and will very likely be of benefit in the long run.
Jacinta: That makes sense, but isn’t everything even more complicated, when you think of how all these nutrients interact with our individual microbiota, and the enzymes that break down our food more or less efficiently, depending on how numerous and healthy they are, which no doubt varies between individuals?
Canto: Yes, Barabasi and others working on all this ‘dark matter’ are well aware of these complex interactions, but they reckon that doesn’t detract from the need to know much more about this particular component of the food-nutrient-digestion-health cycle. And Barabasi does in fact compare the current state of knowledge with the days before the human genome project, when much DNA was considered ‘junk’. It’s just not a good idea to assume that such a large proportion of nutrients are barely worth knowing about. Let’s return to garlic again. It features quite a lot in the Mediterranean diet, which seems protective against cardiovascular disease. Steak, on the other hand, can be problematic. Our gut bacteria breaks down red meat, in the process producing a compound, trimethylamine, which our liver converts into trimethylamine-N-oxide (TMAO). High levels of TMAO in the bloodstream are linked to heart and vascular problems. But allicin, from garlic, which we’ve mentioned before, and which wasn’t on the USDA database, is known to inhibit the production of trimethylamine, so a diet containing red meat – not too much mind you – can be rendered a wee bit safer, and tastier, with a nice garlic dressing.
Jacinta: And allicin appears to be an anti-carcinogen too. And luteolin, another component of garlic not on the standard database, is also reported to protect against cardiovascular disease. We love garlic! But what about processed foods. Surely there are all sorts of ways of processing, that’s to say transforming, foods and their component nutrients that won’t show up on the list of ingredients. And how do we know if those ingredient lists are accurate in the first place?
Canto: Well, baby steps I suppose. Cooking, of course, has vital transformative effects upon many foods. And I recall that when you whisk an egg it becomes ‘denatured’ – how transformative does that sound! The more you think about the interaction of foods, with all their barely recognised components, with transformative processes occurring both outside and within our bodies, the more it makes your head spin, and the more you realise that dietary science has a long long way to go.
garlic cultivars from the Phillippines
2019-nCoV: where does it come from?
As mentioned previously, there are lots of coronaviruses. The four most commonly found in humans have these memorable names: 229E, NL63, OC43 and HKU1. These are humanly-borne viruses that seem to be more interested in increasing spread than increasing pathogenicity. We seem to have developed enough of an immunity from these common coronaviruses for them not to be a major problem. It’s perhaps the new strains that jump from bats to humans via an intermediate species – civets in the case of SARS, dromedary camels (probably) in the case of MERS – that are most likely to be pathogenic. Researchers are on the hunt for the intermediate carrier in the case of 2019-nCoV. Snakes were first suggested, but this has now been dismissed. The most recent candidate has been the pangolin, after research from the South China Agricultural University on the genome sequences of pangolin viruses found them to be 99 percent identical to those in coronavirus patients, but this is unpublished, unverified data at present.
Civets, pangolins? These are just some of the more or less exotic wild animals that some Chinese people like to consume or use for ‘medicinal’ purposes. Traditional Chinese medicine, aka medicine that doesn’t work, has a lot to answer for. Health experts are now recommending that the Chinese government clamp down on this practice. The presence of these creatures in open Chinese markets is disturbing. A prohibition was apparently put in place by the Chinese government just last month, a matter of shutting the stable door, but how well this will be enforced is a question.
Over the past 24 hours I’ve been coughing up a storm, and I’m due to work tomorrow. Medications are reducing the inflammation, and I note that wearing a common or garden surgical mask, which we see everywhere now, will not help. To quote from Live Science:
Coronaviruses can be transmitted between humans through respiratory droplets that infected people expel when they breathe, cough or sneeze. A typical surgical mask cannot block out the viral particles contained in these droplets, but simple measures — such as washing your hands, disinfecting frequently touched surfaces and objects, and avoiding touching your face, eyes and mouth — can greatly lower your risk of infection.
Of course I don’t have such a virus, and there are no known cases of it in Australia, though at least five Australians on a cruise ship off Japan have been confirmed as having contracted it. But as to surgical masks, the point is that viruses are much smaller than bacteria (on average about 1000 times smaller). They’re not cells, with their full complement of DNA, but strands of nucleic acid (DNA or RNA) encased within protein. They’re parasitic on hosts, unlike bacteria, and they’re generally pathogenic – we don’t have ‘good’ viruses as we have good bacteria. They can live outside of hosts for a limited period of time – hence the need for hand-washing and general cleanliness. Viruses in general may take a variety of shapes and sizes, ranging from the recently-identified DNA-based pandoraviruses at 1000 or so nanometres (1 micrometer) down to 20 nanometres or less. As to coronaviruses in particular (the largest of the RNA viruses) their structure and their ‘spike proteins’ will be glanced at in the next post.
References
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5457962/
https://www.thoughtco.com/differences-between-bacteria-and-viruses-4070311
https://www.sciencealert.com/the-pangolin-is-now-a-suspect-in-the-coronavirus-outbreak
Einstein, science and the natural world: a rabid discourse
Einstein around 1915
Canto: Well, we’re celebrating this month what is surely the greatest achievement by a single person in the history of science, the general theory of relativity. I thought it might be a good time to reflect on that achievement, on science generally, and on the impetus that drives us to explore and understand as fully as possible the world around us.
Jacinta: The world that made us.
Canto: Précisément.
Jacinta: Well, first can I speak of Einstein as a political animal, because that has influenced me, or rather, his political views seem to chime with mine. He’s been described as a supra-nationalist, which to me is a kind of political humanism. We’re moving very gradually towards this supra-nationalism, with the European Union, the African Union, and various intergovernmental and international organisations whose goals are largely political. Einstein also saw the intellectual venture that is science as an international community venture, science as an international language, and an international community undertaking. And with the development of nuclear weapons, which clearly troubled him very deeply, he recognised more forcefully than ever the need for us to take international responsibility for our rapidly developing and potentially world-threatening technology. In his day it was nuclear weapons. Today, they’re still a threat – you’ll never get that genie back in the bottle – but there are so many other threats posed by a whole range of technologies, and we need to recognise them, inform ourselves about them, and co-operate to reduce the harm, and where possible find less destructive but still effective alternatives.
Canto: A great little speech Jas, suitable for the UN general assembly…
Jacinta: That great sinkhole of fine and fruitless speeches. So let’s get back to general relativity, what marks it off from special relativity?
Canto: Well I’m not a physicist, and I’m certainly no mathematician, but broadly speaking, general relativity is a theory of gravity. Basically, after developing special relativity, which dealt with the concepts of space and time, in 1905, he felt that he needed a more comprehensive relativistic theory incorporating gravity.
Jacinta: But hang on, was there really anything wrong with space and time before he got his hands on them? Why couldn’t he leave them alone?
Canto: OMG, you’re taking me right back to basics, aren’t you? If I had world enough, and time…
Jacinta: Actually the special theory was essentially an attempt – monumentally successful – to square Maxwell’s electromagnetism equations with the laws of Newton, a squaring up which involved enormous consequences for our understanding of space and time, which have ever since been connected in the concept – well, more than a concept, since it has been verified to the utmost – of the fourth, spacetime, dimension.
Canto: Well done, and there were other vital implications too, as expressed in E = mc², equivalating mass and energy.
Jacinta: Is that a word?
Canto: It is now.
Jacinta: So when can we stop pretending that we understand any of this shite?
Canto: Not for a while yet. The relevance of relativity goes back to Galileo and Newton. It all has to do with frames of reference. At the turn of the century, when Einstein was starting to really focus on this stuff, there was a lot of controversy about whether ‘ether’ existed – a postulated quasi-magical invisible medium through which electromagnetic and light waves propagated. This ether was supposed to provide an absolute frame of reference, but it had some contradictory properties, and seemed designed to explain away some intractable problems of physics. In any case, some important experimental work effectively quashed the ether hypothesis, and Einstein sought to reconcile the problems by deriving special relativity from two essential postulates, constant light speed and a ‘principle of relativity’, under which physical laws are the same regardless of the inertial frame of reference.
the general theory – get it?
Jacinta: What do you mean, ‘the initial frame of reference’?
Canto: No, I said ‘the inertial frame of reference’. That’s one that describes all parameters homogenously, in such a way that any such frame is in a constant motion with respect to other such frames. But I won’t go into the mathematics of it all here.
Jacinta: As if you could.
Canto: Okay. Okay. I won’t go any further in trying to elucidate Einstein’s work, to myself, you or anyone else. At the end of it all I wanted to celebrate the heart of Einstein’s genius, which I think represents the best and most exciting element in our civilisation.
Jacinta: Drumroll. Now, expose this heart to us.
Canto: Well we’ve barely touched on the general theory, but what Einstein’s work on gravity teaches us is that by not leaving things well alone, as you put it, we can make enormous strides. Of course it took insight, hard work, and a full and deep understanding of the issues at stake, and of the work that had already been done to resolve those issues. And I don’t think Einstein was intending to be a revolutionary. He was simply exercised by the problems posed in trying to understand, dare I say, the very nature of reality. And he rose to that challenge and transformed our understanding of reality more than any other person in human history. It’s unlikely that anything so transformative will ever come again – from the mind of a single human being.
Jacinta: Yes it’s an interesting point, and it takes a particular development of culture to allow that kind of transformative thinking. It took Europe centuries to emerge from a sort of hegemony of dogmatism and orthodoxy. During the so-called dark ages, when warfare was an everyday phenomenon, and later too, right through to the Thirty Years War and beyond, one thing that could never be disputed amongst all that disputation was that the Bible was the word of God. Nowadays, few people believe that, and that’s a positive development in the evolution of culture. It frees us to look at morality from a broader, richer, extra-Biblical perspective..
Canto: Yes we no longer have to even pretend that our morality comes from such sources.
Jacinta: Yes and I’m thinking of other parts of the world that are locked in to this submissive way of thinking. A teaching colleague, an otherwise very liberal Moslem, told me the other day that he didn’t believe in gay marriage, because the Qu-ran laid down the law on homosexuals, and the Qu-ran, because written by God, is perfect. Of course I had to call BS on that, which made me quite sad, because I get on very well with him, on a professional and personal basis. It just highlights to me the crushing nature of culture, how it blinds even the best people to the nature of reality.
Canto: Not being capable of questioning, not even being aware of that incapability, that seems to me the most horrible blight, and yet as you say, it wasn’t so long ago that our forebears weren’t capable of questioning the legitimacy of Christianity’s ‘sacred texts’, in spite of interpreting those remarkably fluid texts in myriad ways.
Jacinta: And yet out of that bound-in world, modern science had its birth. Some modern atheists might claim the likes of Galileo and Francis Bacon as one of their own, but none of our scientific pioneers were atheists in the modern sense. Yet the principles they laid down led inevitably to the questioning of sacred texts and the gods described in them.
Canto: Of course, and the phenomenal success of the tightened epistemology that has produced the scientific and technological revolution we’re enjoying now, with exoplanets abounding, and the revelations of Homo floresiensis, Homo naledi and the Denisovan hominin, and our unique microbiome, and recent work on the interoreceptive tract leading to to the anterior insular cortex, and so on and on and on, and the constant shaking up of old certainties and opening up of new pathways, all happening at a giddying accelerating rate, all of this leaves the ‘certainty of faith’ looking embarrassingly silly and feeble.
Jacinta: And you know why ‘I fucking love science’, to steal someone else’s great line? It’s not because of science itself, that’s only a means. It’s what it reveals about our world that’s amazing. It’s the world of stuff – animate and inanimate – that’s amazing. The fact that this solid table we’re sitting at is made of mostly empty space – a solidity consisting entirely of electrochemical bonds, if that’s the right term, between particles we can’t see but whose existence has been proven a zillion times over, and the fact that as we sit here on a still, springtime day, with a slight breeze tickling our faces, we’re completely oblivious of the fact that we hurtling around on the surface of this earth, making a full circle every 24 hours, at a speed of nearly 1700 kms per hour. And at the same time we’re revolving around the sun at a far greater speed, 100,000 kms per hour. And not only that, we’re in a solar system that’s spinning around in the outer regions of our galaxy at around 800,000 kilometres an hour. And not only that… well, we don’t feel an effing thing. It’s the counter-intuitive facts about the natural world that our current methods of investigation reveal – these are just mind-blowing. And if your mind doesn’t get blown by it, then you haven’t a mind worth blowing.
Canto: And we have two metres of DNA packed into each nucleus of the trillions of cells in our body. Who’d’ve thunkit?
whatever
how did life begin? part 1 – Greenland rocks, warm little ponds and unpromising gunk
the basics of the Miller-Urey experiment: sparking interest
Jacinta: Well, we need an antidote to all that theological hocus-pocus, so how about a bit of fundamental science for dummies?
Canto: Sounds great, I just happened to read today that there are three great questions, or areas of exploration for fundamental science. The origin of the universe – and its composition, including weird black holes, dark matter and dark energy – that’s one. The others are the origin of life and the origin of consciousness. Take your pick.
Jacinta: I’ll choose life thanks.
Canto: Not a bad choice for a nihilist. So life has inhabited this planet for about three and a half billion years, or maybe more, while the planet was still cooling from its formation…
Jacinta: Isn’t it still doing that?
Canto: Well, yes of course. An interesting study conducted a few years ago found that around 54% of the heat welling up from within the earth is radiogenic, meaning that it results from radioactive decay of elements like radium and thorium. The rest is primordial heat from the time of the planet’s coalescing into a big ball of matter.
Jacinta: Gravity sucks.
Canto: Energetically so.
Jacinta: You say three and a half billion years or more – can you be a bit more specific? Are we able to home in on the where and the when of life’s origin on this planet?
Canto: Well, that would be the pot of gold, to locate the place and time of the first homeostatic replicators, to wind back history to actually witness that emergence, but I suspect there would be nothing to actually see, at least not on the time-scale of a human life. I think it’d be like the emergence of human language, only slower. You’d have to compress time somehow to witness it.
Jacinta: Fair enough, or maybe not, it seems to me that the distinction between the animate and the inanimate would be pretty clear-cut, but anyway presumably scientists have a time-frame on this emergence. What allows them to date it back to a specific time?
Canto: Well, it’s an ongoing process of honing the techniques and discovering more bits of evidence, a bit like what has happened with defining the age of our universe. For example, you’ve heard of stromatolites?
Jacinta: Yes, those funny black piles that stick out of the water and sand, somewhere in Western Australia? They’re made from really old fossilised cyanobacteria, right?
Canto: Well, that’s a start, they’re rather more complicated than that and we’re still learning about them and still discovering new deposits, all around the world, both on the shoreline and inland. But the Shark Bay stromatolites in WA were the first to be identified, and that was only in 1956. More recently though, there’s been an entirely different discovery in Greenland that’s raised a lot of excitement and controversy…
Jacinta: But hang on, these stromatolites, they say they’re really old, like more than 3 billion years, but how do they know that? As Bill Bryson would say.
Canto: Well, good question Jass, in fact it’s highly relevant to this Greenland discovery so let me talk about radiometric dating, using this example. Greenland has been attracting attention since the sixties as a potential mineral and mining resource, so the Danish Geological Survey was having a look-see around the region of Nuuk, the capital, in the south-west of the island. The principal geologist found ten successive layers of rock in the area, using standard stratigraphic techniques that you can find online, though they’re not always easy to apply, as strata are rarely neatly horizontal, what with crustal movements, fault-lines and rockfalls and erosion and such. Anyway, it was his educated guess that the bottom of these layers was extremely old, so he sent a sample to Oxford, to an expert in radiometric dating there. This was in about 1970.
Isua rocks, Greenland. Oldest rocks discovered, showing plausible traces of 3.8 billion-year-old life
Jacinta: And doesn’t it have to do with radioactive isotopes and half-lives and such?
Canto: Absolutely. Take uranium 238, which if you’ve been watching the excellent recent ABC documentary you’ll know that it decays through a whole chain of, from memory, twelve nuclides before stabilising as an isotope of lead. That decay has a half-life of 4.5 billion years – longer than the life of this planet, or at least the life of its crust. So it’s a matter of measuring the ratio of isotopes, to see how much of the natural uranium has decayed. In this case, the gneiss, the piece of bottom-strata rock that was analysed, had the highest proportion of lead in it of any naturally occurring rock ever discovered.
Jacinta: So that means it’s likely the oldest rock? Aw, I thought Australia had the oldest. This is terrible news.
Canto: No time to be parochial when the meaning of life is at stake. May I continue? So this was an exciting discovery, but more was to come, and it’s continuing to come. The geological team were inspired to continue their explorations around the Godthaab Fjord in Greenland, and found what are called ‘mud volcanoes’, pillows of basaltic volcanic lava that had issued out into the seawater. These were again dated at about 3.7 billion years old, and this strongly suggested the existence of warm oceans at that time, with hydrothermal vents such as those recently discovered to be teeming with life…
Jacinta: Right, so that might be pushing the age of life back a few hundred million years, if it can be verified, but it still doesn’t answer the how question..
Canto: Oh, nowhere near it, but I’ve just started mate. May I continue? Not surprisingly this region is now seen as a treasure trove for those hunting out the first life forms and trying to work out how life began. It was soon found that the Isua greenstone to the north of Nuuk contains carbon with a scientifically exciting isotopic ratio. The level of carbon 13 was unexpectedly low. This is generally an indication of the presence of organic material. Photosynthesising organisms prefer the lighter carbon 12 isotope, which they capture from atmospheric or oceanic carbon dioxide. But the finding’s controversial. Many are skeptical because this is the period known as the ‘late heavy bombardment’, with asteroids crashing and smashing and vaporising and possibly even sterilising… and they haven’t discovered any fossils.
Jacinta: So, photosynthesis, that’s what created the great oxygenation, which created an atmosphere for complex oxygen-dependent organisms, is that right?
Canto: Well, that was much later, and it’s a vastly complex story with quite a few gaps in it, so maybe we’ll save it for future conversations…
Jacinta: Okay, fine, but couldn’t one of those asteroids have brought life here, or proto-life, or the last essential ingredient…?
Canto: Yes, yes, maybe, but you’re distracting me. May I please continue? Where was I? Okay, so let’s look at the various theories put forward about the origin of life – and it will bring us back to Greenland. You’ve mentioned one, called panspermia. That’s the idea that life was seeded here from space, maybe during the heavy bombardment…
Jacinta: Which isn’t an adequate explanation at all, because where did that life come from? I want to know how any life-form anywhere can spring from the inanimate.
Canto: Yes all right, don’t we all smarty-pants? One of the most interesting early speculators on the subject was one Charles Darwin, who wrote – very famously – in a letter to his good mate Joseph Hooker in 1871, and I quote:
It is often said that all the conditions for the first production of a living organism are now present, which could ever have been present.— But if (& oh what a big if) we could conceive in some warm little pond with all sorts of ammonia & phosphoric salts,—light, heat, electricity &c present, that a protein compound was chemically formed, ready to undergo still more complex changes, at the present day such matter wd be instantly devoured, or absorbed, which would not have been the case before living creatures were formed.
Now this was pretty damn good speculation for the time, and a couple of generations later two biologists, Aleksandr Oparin of Russia and John Haldane of England, independently developed a hypothesis that built on Darwin’s ideas.
Jacinta: Oh yes, they had this idea that if you added a bit of lightning to the early terrestrial atmosphere, which was full of ammonia or something, you’d get a lot of organic chemistry happening.
Canto: Well I think the ‘or something’ part is true there – their idea was that there was a lot of hydrogen, methane and water vapour in the early atmosphere, and that, combined with local heat caused perhaps by lightning, or volcanic activity or some sort of concentrated solar radiation, the combo created a soup of organic compounds, out of which somehow over time emerged a primordial replicator.
Jacinta: So far, so vague.
Canto: Okay, I’m just getting started. The Oparin-Haldane hypothesis was highly speculative, of course. The point being made was that this key event was all that was needed for natural selection to kick in. This replication must have been advantageous, and of course over time there would’ve been mutations,with the mutants competing with the originals, and the winners would’ve been the most efficient and effective harvesters of resources, and there would’ve been expansion and more mutations and modifications and so forth. And out of that would come the first self-sustaining homeostatic environment, the proto-cell, within which more sophisticated machinery for processing resources could be developed…
Jacinta: Okay so you’ve more or less succeeded in dissolving the boundary between the animate and the inanimate before my eyes, but it’s still pretty vague on the details.
Canto: In 1953, Stanley Miller took up the challenge of his supervisor, famous Nobel Prize-winning biologist Harold Urey, who noted that nobody had tested the Oparin-Haldane hypothesis experimentally. Miller created a mini-atmosphere in a bottle, using methane (CH4), hydrogen, water vapour and ammonia (NH3), and after sparking it up for a while, he managed, to the amazement of all, to produce amino acids, the building blocks of proteins. Surely the first step in producing life itself.
Jacinta: Ah yes, that was a famous experiment, but didn’t it turn out to be something of a dead end?
Canto: Well, yes and no. It has been replicated with different mixtures and ratios of gases, and amino acids, sugars and even traces of nucleic acids have been generated, but nothing that could be described as a primordial replicator. But of course this work has got a lot of biologists thinking.
Jacinta: But this was 60 years ago. That’s a lot of thought without much action.
Canto: Well, what has since been realised about the experiments of Miller and others is that they create an enormous complexity of organic molecules in a rather uncontrolled way, a kind of chemical gunk similar to what might be created when you burn the dinner. The point being that when you burn the dinner – which is something necessarily organic like a dead chook, or pig, or tragically finless shark or whatnot…
Jacinta: Or a pumpkin, or Nan’s rhubarb pie..
Canto: Yeah, okay – you get this messy complexity, all mixed with oil and vinegary acids and shite – you get this break-down into gunk, and that’s easy. What’s hard is to go in the other direction, to build up from gunk into a fully fledged chicken, or a handsomely finned shark. And that’s what these experiments were trying to do, in their small way. They were creating this primordial-soup-gunk and hoping, with a bit of experimental help, to spark life into it, and basically getting nowhere. The problem is essentially to do with randomness and order. How do we get order out of random complexity? It’s easy to go the other way, for example with explosions and machine guns and such. We see that everywhere. But building the kind of replicating order that you find even in mycoplasma, the smallest genus of bacteria, from scratch, and by chance – well, that’s mind-bogglingly improbable.
mycoplasma, one of the simplest life forms – but try making one from scratch
Jacinta: So we have to think in terms of intermediate stages.
Canto: Yes, well, there are big problems with that, too… But let’s give it a rest for now. Next time, we’ll discuss the RNA world that most biologists are convinced preceded and helped create the DNA world we live in.
N B – This piece owes much to many, but mainly to Life on the edge: the coming of age of quantum biology, by Jim Al-Khalili & Johnjoe McFadden
introducing canto and jacinta: solutions for the post-antibiotic era?
Florence Nightingale
Jacinta: Well hello Canto, let’s welcome each other to the Urbane Society of Skeptical Romantics, where we like to talk… and not much else.
Canto: Very productive and constructive talk Jacinta, but the proof will be in the pudding.
Jacinta: Well I hope it’s not a recipe for disaster. What shall we talk about today?
Canto: Well I’m thinking medicine today – the discipline, not the stuff you consume.
Jacinta: Well I don’t consume much medicine at the worst of times, being fit, positive, eternally youthful and beautiful.
Canto: That’s okay, I’ll take your share – so you know there’s a bit of a crisis with antibiotic resistance.
Jacinta: Yes, natural selection in action, or is that human-induced, unintended-consequence-style artificial selection?
Canto: Well I’m not intending to delve into the natural v artificial quagmire here, or even into the science of antibiotics. I’ve just been reading about a couple of alternative ways – one old and one new – of killing off nasty infecting bacteria in hospitals. Ever caught one of those secondary infections in hospital Jass? No of course you haven’t.
Jacinta: Last time I was in hospital I was the infection – had to be forcibly removed from the victim by a crack team of medicos and placed in isolation until deemed safe to take my chances at thriving and multiplying along with my fellow bugs.
Canto: Well I’m sure they made the right decision.
Jacinta: The jury’s still out. Tell me of the ways.
Canto: Remember Florence Nightingale?
Jacinta: One of my heroes, apart from her valetudinarianism. Though I suspect that might just have been her way of keeping everyone at a distance so she could get on with things in her way. She was a voluminous correspondent just like Darwin, another sufferer from mysterious ailments. So what about her?
Canto: She revolutionised nursing and hospital treatment, sanitation and such, right? One of her many insights was that patients convalescing from the Crimean battlefields benefitted enormously from throwing open the windows of the rather unhygienic field hospitals set up for them. Nightingale wards were built to her design, with high sash windows kept open to renew the air around the sick. This worked a treat, though it took more than a century to verify the effect experimentally, using E coli in an open rooftop environment. The bugs died within 2 hours in the open air, but in an enclosed environment they lived on.
Jacinta: Right, so this has obvious relevance to those horrible superbugs they talk about…
Canto: Like MRSA?
Jacinta: Yeah. What’s that?
Canto: Multi-resistant, or more accurately methicillin-resistant staphylococcus aureus.
Jacinta: Yeah, golden staph, just as I thought. So that’s interesting. I don’t see modern hospitals blowing in the wind really. Sounds far too hippy for the 21st century. Isn’t it all tightly controlled and air-conditioned these days? Recycled air and legionnaire’s disease? Okay, only kidding, I’ve not heard of any hospital outbreaks of that, but these hospital superbugs must surely be caused by a contaminated environment, yes? Should we bring back Nightingale wards? And why did they go out of fashion?
Canto: Well, not only did she get fresh air right, she had the windows faced to let in as much sunlight as possible, and it was only learned later that sunshine was a great germ-killer, especially in the case of tuberculosis, which ravaged all the crowded cities…
Jacinta: Yeah and picked off all those writers, like Chekhov, and the Brontës, and D H Lawrence, and Keats. Didn’t he write an ode to Florence Nightingale?
Canto: No no that was another nightingale, but at its height TB was killing one in five in the cities; but it’s probable that the sunlight was boosting levels of vitamin D, which in turn boosts the immune system. So by the turn of the century, fresh air and sunlight was all the go. TB patients were wheeled onto balconies, to be exposed to the bracing elements.
Jacinta: Ah, but of course all that changed with the discovery of antibiotics.
Canto: Right, and thanks to these miracles of modern medicine, rotten air and dark dankness came back into fashion, sort of. I mean, all sorts of infections were being vanquished by these pills and it seemed as if diseases would fall like ninepins.
Jacinta: I suspect you’re oversimplifying..
Canto: Well it must’ve seemed that way to the general public. And of course fresh air could turn into howling winds, and sunlight into clouds and rain. Controlled temperatures and conditions might’ve seemed safer, and the cleansing power of aircons was over-estimated.
Jacinta: Oh yes… Climat air-conditioning, Breezair, Bonaire – more than an air-conditioner, a tonic to the system.
Canto: But now of course the diseases are returning in resistant forms, and we’ve hit a wall in terms of antibiotic manufacture. There’s very little new stuff coming on-stream. And now, hospitals are being seen as a problem again, just as in Ms Nightingale’s day.
Jacinta: Yes, but there are new post-antibiotic treatments in the pipeline, such as phage therapies, in which bacteria are destroyed by genetically engineered viruses, and drugs that…
Canto: Okay Jass, that’s for another conversation, and these new treatments are a bit futuristic as yet. Meanwhile, we need to heed Ms Nightingale’s hygienic advice. Apparently, the recent emphasis on simple hand washing has been paying huge dividends, in reducing the incidence of MRSA and Clostridium difficile.
Jacinta: So we were getting complacent, forgetting the basics?
Canto: Well, we’d been lulled by the success of modern medicine into thinking the old precautions needn’t apply. And further studies have confirmed the cleansing power of even the mildest breezes, and hospitals have begun to open up in response.
Jacinta: But not only that, we now know more about good old-fashioned sunlight and its curative powers, don’t we?
Canto: Okay, the stage is yours.
Jacinta: Well, there was some breakthrough research done using standard UV lamps in a TB ward. Guinea pigs were used (I mean real guinea pigs), and their signs of infection were drastically reduced. Now, there are some regions of the world with high rates of TB, and of HIV, which of course weakens their immune system and makes them susceptible…
Canto: I thought TB was just about eradicated.
Jacinta: Well it’s now resurgent in some parts, so we’re back to looking at other modes of prevention. So UV lighting is proving very effective, but not applied directly, because direct exposure is quite dangerous – think of tanning beds and the like. But what is interesting is that they’ve experimented with different UV wavelengths – ultraviolet light covers the spectrum from 10 to 400 nanometres – and found a sweet spot at 207 nm. At that wavelength the UV light is absorbed by proteins and penetrates a little way into human cells but doesn’t reach any DNA to effect mutations. But it does affect bacteria, drastically. They absorb the light and die.
Canto: Very clever.
Jacinta: Quite. This sweet spot technology was first used in operating theatres, to kill airborne bacteria that could immediately settle in open incisions and the like. There’s a suggestion now that UV lamps at that wavelength should be deployed in all hospitals.
Canto: So that’s one solution, but getting back to fresh air, has anyone found a solution that eliminates the drawbacks? I mean, knocking equipment around, bringing in pollution and pathogens from outside, not to mention patients falling out of windows?
Jacinta: Well, some of those risks could easily be minimised, but there are more technological fixes. The production of hydroxyl radicals has been shown to kill bacteria…
Canto: Hydroxyl radicals? WTF?
Jacinta: Molecules with a short lifespan, produced in the atmosphere when ozone, the unstable allotrope of oxygen, reacts with water. This reaction is catalysed by organic molecules in the air, and a while back a company managed to build machines that produce these hydroxyls, for use in hospitals. They were quite effective, but the company went bust. So we’re back to good ventilation and getting patients out on balconies. And perhaps locating hospitals out of the way of cities.
Canto: Okay, so back to the future.
Jacinta: Or forward to the past.
Canto: Well thanks for this charming discussion and we look forward to many more.
Here’s an interesting commercial video about how a hydroxyl generator works
https://www.youtube.com/watch?v=a_V9HbBVM6Q
hat-tip to: Frank Swain, ‘A breath of fresh air’ in New Scientist Collection: Medical Frontiers.